A while back, I was talking with a friend of mine. He was a giant of a black man and we spoke about his blood pressure woes and his weight issues. So I asked him about his diet, his habits, and all that. He told me all about it: How he ate all the right foods, how he was trying to avoid the wrong ones, and how he recently started walking on his treadmill.
I said to him, "What do you do all day?"
He said, "I'm in the office all day."
"What do you do at lunchtime?"
"I usually have a protein shake or eat a salad with some chicken."
That's good, I tell him. But I want you to do one more thing. It's easy. While or after you eat, take a walk. Outside. In the parking lot. Once or twice a week.
OK, he says. "But why outside?"
I said, "Sunlight and vitamin D." Then, I told him a story we should all be familiar with by now, which went something like this:
Darker skin is a result of greater production of a pigment called melanin that rewards skin with a natural protection against ultraviolet light. Ultraviolet light would otherwise burn skin, destroy the body's stores of nutrients like folic acid that are needed for refurbishing DNA, increase risk of neural tube defects among other reproductive problems, and also raise risk of skin cancer.
So, in short, melanin is a good thing. Near the equator, with strong UVB rays aplenty to compensate slower vitamin D production, darker skin offers an evolutionary advantage that would only serve to sustain naked humans. But, as often is the case, reward comes with recompense. The downside of higher amounts of melanin is that the pigment interferes with the skin's ability to absorb enough UVB rays to activate Vitamin D's pre-cursor into a full-fledged hormone.
As is well-documented, humans at higher latitudes with dark skin would never have survived over the generations without shedding the extra melanin and opting for a lighter color. Lighter color would afford more UVB absorbed, more D created, stronger bones and, as evidence emerges to show, better cardiovascular health. During summer months, lighter-skinned humans who had migrated to higher latitudes collected vitamin D in fat as they gained weight, then released it into the bloodstream when they shed weight during sunlight-lacking winter months.
On the other hand, when darker-skinned humans live in a Northern latitudes of the United States -- as African Americans do -- you can bet that problems will arise.
Then, I gave him some details about asking his doctor for a 25-hydroxyvitamin D test.
A couple of weeks later, I spotted him outside walking around a parking lot. He tells me, "Thanks so much, David. I had no idea about vitamin D. Plus, my doctor says the walking and the vitamin D are helping my heart."
While attending Experimental Biology (#eb2011) over the weekend, one of the presentations had me thinking about my friend. And that was Richard Harris, Ph.D., of Georgia Health Sciences University in Augusta, presenting a study on vitamin D supplementation in African Americans.
What Dr. Harris and his fellow Georgia researchers found was that vitamin D supplementation in overweight African American adults in a single dose of 60,000 IU every for four weeks every 16 weeks improved blood vessel endothelial function – the equivalent of 2,000 IU since vitamin D has a half life of about three weeks.
It was notable that they used overweight adults, since extra weight can increase blood volume, raise blood pressure, resulting in rigid, inflamed vessels. Details are that the researchers used an inflatable cuff to increase blood flow in the brachial arteries of each of the participants, then an ultrasound to measure flow-mediated dilation.
What exactly vitamin D was able to do is what Dr. Harris calls the "million-dollar question," according to this press release. But it's likely that the hormone acted directly on endothelial cells, on a receptor perhaps, that helps dilate blood vessels when needed. The more dilation, the easier it is for blood to flow through vessels.
This study is great news, especially for this population at higher risk for cardiovascular disease factors like higher blood pressure. However, there is still too little vitamin D deficiency awareness.
Here's what I say, Why not teach African Americans why they have a greater need for vitamin D from an evolutionary perspective?
In the case of my friend, it really helped put things in perspective. There's an easy solution for this mess, which is to take a walk around the block for a few minutes when UVB rays are out (mostly just in summer months) or, simply, by just taking a vitamin D supplement as they did in the summer. Lots of benefits to come from such an easy habit of getting D daily like better blood pressure along with better bone health.
Another thing is that the Institute of Medicine's recommended daily intakes of vitamin D (although they are based as if there were no sun-produced D at all) just make little sense when they don't treat all adults the same, not bringing high-risk groups into consideration. Until more research is available and the IOM can build on current guidelines by raising them for high-risk groups, African Americans should take health into their own hands by getting tested to make sure they keep 25-hydroxyvitamin D in healthy ranges continually.
22 March 2011
Fusing aging theories: Telomere shortening causes mitochondrial dysfunction
New research is adding insight and linking three theories of aging—one that suggests telomere shortening governs lifespan, and two others that suggest dysfunctional mitochondria or oxidative stress leads to aging.
At Harvard-affiliated Dana-Farber Cancer Institute, scientists have gathered data suggesting telomere shortening is the cause of mitochondrial dysfunction and diminished antioxidant defenses. Together, they decrease the body’s energy and diminish organ function, both characteristic of old age.
As telomeres—protective caps at the end of cell chromosomes—shorten with age and begin to fray, cells activate the p53 gene, which signals an “emergency shutdown” chain of events that turns off normal cell growth and division and compromise antioxidant defenses. Going one step further, data from the carefully orchestrated mouse study, published in Nature, show that the p53 gene also represses PGC1-alpha and PGC1-beta. These PCGs are considered the master regulators of metabolism and mitochondrial function.
Repressing PCGs increases the number of dysfunctional mitochondria (with mutated mitochondrial DNA) and leads to a decrease in functional mitochondria distributed throughout in muscles and organs. The dysfunctional mitochondria in aged tissues leak greater amounts of reactive oxygen species and the lack of functional mitochondria hinders normal energy production from cell respiration (the body’s main producer of ATP energy).
“What we have found is the core pathway of aging connecting several age-related biological processes previously viewed as independent from each other,” said Ronald A. DePinho, M.D., a cancer geneticist and senior author of the paper, in a press release.
“Because telomere dysfunction weakens defenses against damage by free radicals, or reactive oxygen species,” Dr. DePinho said, “we think this exposes telomeres to an accelerated rate of damage which cannot be repaired and thereby results in even more organ deterioration. In effect, it sets in motion a death spiral.”
In an article also published in the same issue Nature, Daniel P. Kelly, M.D., scientific director and professor at Burnham Institute for Medical Research-Lake Nona, Orlando, Florida, said that the “intriguing study… unveils a potentially unifying mechanism for cellular ageing.”
Mitigating the Toll of Aging
The new study further supports current thinking that the best defense against aging is to reduce the adverse affects of overproduction of free radicals produced from dysfunctional mitochondria, which cause additional oxidative stress.
Dr. DePinho said, “The findings bear strong relevance to human aging, as this core pathway can be directly linked to virtually all known genes involved in aging, as well as current targeted therapies designed to mitigate the toll of aging on health.”
Those current targeted therapies include boosting the human body’s antioxidant defenses by eating a healthy diet, reducing calories (by around 25 percent), and supplementing with antioxidant vitamins C and E, as well as with green tea, CoQ10 and resveratrol. These practices not only help to protect against oxidative stress, thereby protecting against telomere shortening, but also help boost generation of new, healthy mitochondria.
When we asked telomere biologist Bill Andrews, Ph.D., to comment on the new study, he answered that it was “tremendous news,” as it supports the need for more research into management of telomeres by activating the genetic expression of the enzyme telomerase, which re-lengthens telomeres.
Dr. Andrews wrote, “It’s the best support ever for the fact that telomere elongation’s role in aging far exceeds the roles played by mitochondria and oxidative stress.” In effect, telomere shortening is the root cause of the others.
Mitochondria become dysfunctional when telomeres shorten and fray, a new study suggests. In an article to be published in a forthcoming issue of IsaNews magazine, Dr. Andrews writes, “Mitochondrial dysfunction causes aging—but telomere shortening has turned out to be the primary cause of mitochondrial dysfunction. And humans’ natural defenses against oxidative stress are really quite exceptional (for example, our cells produce ten times more superoxide dismutase, a potent natural antioxidant, than mice)—until telomere shortening begins to degrade those defenses inside our bodies.”
He added that while “anti-aging therapies of years past merely treated the symptoms of aging. New research is devoted to identifying a new class of therapies that treat aging at its root cause, and hold great promise of one day allowing us to feel young and healthy at 120 years of age and beyond.”
An earlier study, of which Dr. DePinho was also the senior author, gives testimony to the benefits of telomerase, as found in mice that were genetically engineered to produce the enzyme. The study found that when the telomerase was restored in the mice, their age-related symptoms disappeared and several organs including the brain were rejuvenated.
References:
Kelly DP. Cell biology: Ageing theories unified. Nature 2011;470:342-3.
Sahin E, Colla S, Liesa M et al. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature 2011;470:359-65.
Sahin E, DePinho RA. Linking functional decline of telomeres, mitochondria and stem cells during ageing. Nature 2010;464:520-8.
Jaskelioff M, Muller FL, Paik JH et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature 2011;469:102-6.
At Harvard-affiliated Dana-Farber Cancer Institute, scientists have gathered data suggesting telomere shortening is the cause of mitochondrial dysfunction and diminished antioxidant defenses. Together, they decrease the body’s energy and diminish organ function, both characteristic of old age.
As telomeres—protective caps at the end of cell chromosomes—shorten with age and begin to fray, cells activate the p53 gene, which signals an “emergency shutdown” chain of events that turns off normal cell growth and division and compromise antioxidant defenses. Going one step further, data from the carefully orchestrated mouse study, published in Nature, show that the p53 gene also represses PGC1-alpha and PGC1-beta. These PCGs are considered the master regulators of metabolism and mitochondrial function.
Repressing PCGs increases the number of dysfunctional mitochondria (with mutated mitochondrial DNA) and leads to a decrease in functional mitochondria distributed throughout in muscles and organs. The dysfunctional mitochondria in aged tissues leak greater amounts of reactive oxygen species and the lack of functional mitochondria hinders normal energy production from cell respiration (the body’s main producer of ATP energy).
“What we have found is the core pathway of aging connecting several age-related biological processes previously viewed as independent from each other,” said Ronald A. DePinho, M.D., a cancer geneticist and senior author of the paper, in a press release.
“Because telomere dysfunction weakens defenses against damage by free radicals, or reactive oxygen species,” Dr. DePinho said, “we think this exposes telomeres to an accelerated rate of damage which cannot be repaired and thereby results in even more organ deterioration. In effect, it sets in motion a death spiral.”
In an article also published in the same issue Nature, Daniel P. Kelly, M.D., scientific director and professor at Burnham Institute for Medical Research-Lake Nona, Orlando, Florida, said that the “intriguing study… unveils a potentially unifying mechanism for cellular ageing.”
Mitigating the Toll of Aging
The new study further supports current thinking that the best defense against aging is to reduce the adverse affects of overproduction of free radicals produced from dysfunctional mitochondria, which cause additional oxidative stress.
Dr. DePinho said, “The findings bear strong relevance to human aging, as this core pathway can be directly linked to virtually all known genes involved in aging, as well as current targeted therapies designed to mitigate the toll of aging on health.”
Those current targeted therapies include boosting the human body’s antioxidant defenses by eating a healthy diet, reducing calories (by around 25 percent), and supplementing with antioxidant vitamins C and E, as well as with green tea, CoQ10 and resveratrol. These practices not only help to protect against oxidative stress, thereby protecting against telomere shortening, but also help boost generation of new, healthy mitochondria.
When we asked telomere biologist Bill Andrews, Ph.D., to comment on the new study, he answered that it was “tremendous news,” as it supports the need for more research into management of telomeres by activating the genetic expression of the enzyme telomerase, which re-lengthens telomeres.
Dr. Andrews wrote, “It’s the best support ever for the fact that telomere elongation’s role in aging far exceeds the roles played by mitochondria and oxidative stress.” In effect, telomere shortening is the root cause of the others.
Mitochondria become dysfunctional when telomeres shorten and fray, a new study suggests. In an article to be published in a forthcoming issue of IsaNews magazine, Dr. Andrews writes, “Mitochondrial dysfunction causes aging—but telomere shortening has turned out to be the primary cause of mitochondrial dysfunction. And humans’ natural defenses against oxidative stress are really quite exceptional (for example, our cells produce ten times more superoxide dismutase, a potent natural antioxidant, than mice)—until telomere shortening begins to degrade those defenses inside our bodies.”
He added that while “anti-aging therapies of years past merely treated the symptoms of aging. New research is devoted to identifying a new class of therapies that treat aging at its root cause, and hold great promise of one day allowing us to feel young and healthy at 120 years of age and beyond.”
An earlier study, of which Dr. DePinho was also the senior author, gives testimony to the benefits of telomerase, as found in mice that were genetically engineered to produce the enzyme. The study found that when the telomerase was restored in the mice, their age-related symptoms disappeared and several organs including the brain were rejuvenated.
References:
Kelly DP. Cell biology: Ageing theories unified. Nature 2011;470:342-3.
Sahin E, Colla S, Liesa M et al. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature 2011;470:359-65.
Sahin E, DePinho RA. Linking functional decline of telomeres, mitochondria and stem cells during ageing. Nature 2010;464:520-8.
Jaskelioff M, Muller FL, Paik JH et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature 2011;469:102-6.
16 March 2011
Potassium iodide: Why you should avoid it
Ever since the news of Japan's nuclear crisis, there have been several claims made over the Internet that have panicked people in the U.S. about potential exposure to radiation (one culprit is this viral e-mail), which has led to me being the recipient of questions about whether or not people should be taking potassium iodide supplements to avoid absorption to radioactive iodine.
Should you take potassium iodide pills? My answer has been an unequivocal, "No, it's not necessary. There is little risk of any level of radiation exposure to worry about anywhere else other than in Japan near the reactors. If you're worried about getting cancer, try thinking more about losing weight, eating more dietary fiber, and eating more fruits and vegetables."
In the process of answering questions, I did find myself interested in learning more about radiation and health. By far the best, most in-depth article I've read on "How Radiation Threatens Health" is this one written by Nina Bai and published by Scientific American. Bai's article gives readers an excellent understanding on the typical radiation levels that people are currently exposed to (0.2 to 0.3 milliSieverts), how much they are exposed to by a typical CT scan (1 milliSievert) and what kinds of levels people should really be worried about—the kind of levels that lead to symptoms of radiation sickness ("a whole body dose of 3 sieverts, that is, 3,000 times the recommended public dose limit per year") and the kind that kills people within weeks (5 to 10 sieverts).
Yes, there are concerns over low-dose radiation over time, but as Bai's article points out, the increase of cancer risk is small and basically comes out to about an increase of eight potential cancer cases per 10,000 people. And, the point is that even if any radiation made it over the ocean and to the U.S. (which is unlikely) it would be at levels too low to cause concern.
As for potassium iodide (KI) supplements (not addressed in Bai's article), there is cause for concern because I keep reading that these are "flying off the shelves" in various articles.
The way KI works is by flooding iodine into the thyroid gland to become trapped by the thyroid's receptors, which blocks the uptake and accumulation of radioiodine that could lead to possible thyroid diseases or cancer. This is particularly important in children who are more at risk for radioiodine-induced cancer (as is what happened with the Chernobyl incident because of radioiodine0contaminated milk). The doses for preventing radioidine uptake are high: 50 to 100 milligrams for adults. If exposure is pretty certain, then supplementation with these pills make sense.
But consider that the Upper Limit for adults is 1.1 milligram per day. These pharmacologic doses could be potentially detrimental since excessive iodine can actually lead to hyper- or hypothyroidism and have been known to increase risk of thyroid cancers. Taking these doses should not be considered a safe precautionary measure, as marketed. There is a risk!
My concern is this: that the irresponsible Internet claims are leading people to actually take the high doses of the KI and that retail outlets selling them (like this one with 130 milligram per tablet!) are doing so without giving people any sense of what the risks are when taking high amounts.
Should you take potassium iodide pills? My answer has been an unequivocal, "No, it's not necessary. There is little risk of any level of radiation exposure to worry about anywhere else other than in Japan near the reactors. If you're worried about getting cancer, try thinking more about losing weight, eating more dietary fiber, and eating more fruits and vegetables."
In the process of answering questions, I did find myself interested in learning more about radiation and health. By far the best, most in-depth article I've read on "How Radiation Threatens Health" is this one written by Nina Bai and published by Scientific American. Bai's article gives readers an excellent understanding on the typical radiation levels that people are currently exposed to (0.2 to 0.3 milliSieverts), how much they are exposed to by a typical CT scan (1 milliSievert) and what kinds of levels people should really be worried about—the kind of levels that lead to symptoms of radiation sickness ("a whole body dose of 3 sieverts, that is, 3,000 times the recommended public dose limit per year") and the kind that kills people within weeks (5 to 10 sieverts).
Yes, there are concerns over low-dose radiation over time, but as Bai's article points out, the increase of cancer risk is small and basically comes out to about an increase of eight potential cancer cases per 10,000 people. And, the point is that even if any radiation made it over the ocean and to the U.S. (which is unlikely) it would be at levels too low to cause concern.
As for potassium iodide (KI) supplements (not addressed in Bai's article), there is cause for concern because I keep reading that these are "flying off the shelves" in various articles.
The way KI works is by flooding iodine into the thyroid gland to become trapped by the thyroid's receptors, which blocks the uptake and accumulation of radioiodine that could lead to possible thyroid diseases or cancer. This is particularly important in children who are more at risk for radioiodine-induced cancer (as is what happened with the Chernobyl incident because of radioiodine0contaminated milk). The doses for preventing radioidine uptake are high: 50 to 100 milligrams for adults. If exposure is pretty certain, then supplementation with these pills make sense.
But consider that the Upper Limit for adults is 1.1 milligram per day. These pharmacologic doses could be potentially detrimental since excessive iodine can actually lead to hyper- or hypothyroidism and have been known to increase risk of thyroid cancers. Taking these doses should not be considered a safe precautionary measure, as marketed. There is a risk!
My concern is this: that the irresponsible Internet claims are leading people to actually take the high doses of the KI and that retail outlets selling them (like this one with 130 milligram per tablet!) are doing so without giving people any sense of what the risks are when taking high amounts.
02 March 2011
Vitamin K2: Building bones while beating back arterial calcification
Vitamin K2's time to shine has come—move over vitamin D! Once only known for its role as a "koagulation" factor in blood clotting, vitamin K2 is emerging as another fundamental anti-aging nutrient. While vitamins D and E have garnered the majority of interest in the last decade, the impact of vitamin K2 on aging bones and hearts demands that we give it equal attention.
Whereas most vitamin and mineral supplements use vitamin K in its form of K1 (phylloquinone sourced from plants) because it is easily available and cheap, it is the natural form of K2 (menaquinone sourced from friendly bacteria) that is the most biologically active and shown to enhance both bone formation and vascular health.
The full compilation of recent research underscores the idea that K1 and K2 should be appreciated as separate nutrients with distinct physiological actions and benefits. K1 is the more familiar vitamin known for its key role in directing blood-clotting in the body and the one given as a shot at birth (a common practice in many countries to curtail hemorrhage incidents in newborns.) The picture for K2 seems to be a bit more varied and is key in regulating calcium balance.
Vitamin K2 acts by activating the bone-building hormone (carboxylating osteocalcin) to clear calcium from the arteries and use it in bone mineralization. It effectively removes calcium that would otherwise end up deposited in arterial plaques. Since protecting arteries and soft tissues from calcification is one of the most important ways to stave off the ravages of aging on the body, consuming enough vitamin K2 daily is key for a long, healthy life.
Getting Enough K2
Because vitamin K2 is synthesized by friendly bacteria in the intestine, nutrition scientists have long assumed that that deficiencies were rare. However, new data are showing that intestinally synthesized vitamin K is not absorbed as easily as previously thought. Vitamin K also preferentially accumulates in the liver where it does have a clotting factor role.
In fact, once overlooked because "time to clot" was the test for vitamin K status, it is here where we are now seeing new signs of vitamin K deficiency previously only seen with vitamin D deficiency—fragile, brittle bones and increased fractures—even with adequate calcium and vitamin D.
Most people in North America should increase amounts consumed daily. The evidence finds that only with much higher intake do bone cells get their share and the same holds true for removal of calcium in arteries.
People can obtain enough vitamin K2 by eating plenty of fermented foods such as cheese, sauerkraut, and natto (a traditional Japanese soy-based food). Supplementation is another viable option as achieved with a quality multivitamin.
Regardless of how one gets it, it’s important not to underestimate value of this underdiscussed nutrient and to understand that most people are not getting enough. Consuming sufficient amounts of K2 along with a healthy diet will increase odds of a healthier life with clear arteries and stronger bones.
Sources
McCann and Ames. Vitamin K, an example of triage theory: is micronutrients inadequacy linked to diseases of aging?. Am J Clin Nutr 90:889-907, 2009.
Vitamin K2. Monograph. Alternative Medicine Review 14(3):284-293, 2009.
Koitaya. Et al. Effect of low dose vitamin K2 (MK-4) supplementation on bioindices in postmenopausal Japanese women. J Nutr Sci Vitaminol. 55:15-21, 2009.
Gast, et al. A high menaquinone intake reduces the incidence of coronary heart disease. Nutr Metab Cardiovas Dis 19:504-510, 2009.
Shea, et al. Vitamin K supplementation and progression of coronary artery calcium in older men and women. Am J Clin Nutr 89: 1799-1807, 2009.
Shea MK, Booth SL Update on the role of vitamin K in skeletal health. Nutr Rev 66(10):549-57, 2008.
Whereas most vitamin and mineral supplements use vitamin K in its form of K1 (phylloquinone sourced from plants) because it is easily available and cheap, it is the natural form of K2 (menaquinone sourced from friendly bacteria) that is the most biologically active and shown to enhance both bone formation and vascular health.
The full compilation of recent research underscores the idea that K1 and K2 should be appreciated as separate nutrients with distinct physiological actions and benefits. K1 is the more familiar vitamin known for its key role in directing blood-clotting in the body and the one given as a shot at birth (a common practice in many countries to curtail hemorrhage incidents in newborns.) The picture for K2 seems to be a bit more varied and is key in regulating calcium balance.
Vitamin K2 acts by activating the bone-building hormone (carboxylating osteocalcin) to clear calcium from the arteries and use it in bone mineralization. It effectively removes calcium that would otherwise end up deposited in arterial plaques. Since protecting arteries and soft tissues from calcification is one of the most important ways to stave off the ravages of aging on the body, consuming enough vitamin K2 daily is key for a long, healthy life.
Getting Enough K2
Because vitamin K2 is synthesized by friendly bacteria in the intestine, nutrition scientists have long assumed that that deficiencies were rare. However, new data are showing that intestinally synthesized vitamin K is not absorbed as easily as previously thought. Vitamin K also preferentially accumulates in the liver where it does have a clotting factor role.
In fact, once overlooked because "time to clot" was the test for vitamin K status, it is here where we are now seeing new signs of vitamin K deficiency previously only seen with vitamin D deficiency—fragile, brittle bones and increased fractures—even with adequate calcium and vitamin D.
Most people in North America should increase amounts consumed daily. The evidence finds that only with much higher intake do bone cells get their share and the same holds true for removal of calcium in arteries.
People can obtain enough vitamin K2 by eating plenty of fermented foods such as cheese, sauerkraut, and natto (a traditional Japanese soy-based food). Supplementation is another viable option as achieved with a quality multivitamin.
Regardless of how one gets it, it’s important not to underestimate value of this underdiscussed nutrient and to understand that most people are not getting enough. Consuming sufficient amounts of K2 along with a healthy diet will increase odds of a healthier life with clear arteries and stronger bones.
Sources
McCann and Ames. Vitamin K, an example of triage theory: is micronutrients inadequacy linked to diseases of aging?. Am J Clin Nutr 90:889-907, 2009.
Vitamin K2. Monograph. Alternative Medicine Review 14(3):284-293, 2009.
Koitaya. Et al. Effect of low dose vitamin K2 (MK-4) supplementation on bioindices in postmenopausal Japanese women. J Nutr Sci Vitaminol. 55:15-21, 2009.
Gast, et al. A high menaquinone intake reduces the incidence of coronary heart disease. Nutr Metab Cardiovas Dis 19:504-510, 2009.
Shea, et al. Vitamin K supplementation and progression of coronary artery calcium in older men and women. Am J Clin Nutr 89: 1799-1807, 2009.
Shea MK, Booth SL Update on the role of vitamin K in skeletal health. Nutr Rev 66(10):549-57, 2008.
25 February 2011
Is there a link between telomeres and dietary fiber?
New evidence published in Archives of Internal Medicine has it that eating more dietary fiber, particularly from whole grains, could lead to a longer life. The large study found a high-fiber diet reduced risk of heart disease and cancer, as well as infectious and respiratory illnesses.
This is great news for those eating diets high in fiber. What’s also interesting is that another reason why dietary fiber is protective to health is because of its influence on telomeres. Telomeres are the protective caps at the end of chromosomes, and their length is considered the closest way to measure lifespan in humans.
As reported in a prospective cohort study published in the March 2010 issue of American Journal of Clinical Nutrition (AJCN), telomere length is positively associated with higher fiber intake in women. Dietary fiber from whole grains appears to provide the strongest benefit.
In addition, in the AJCN study, the researchers found telomere length was negatively associated with increased waist circumference and higher intake of omega-6 fatty acids in the diet.
Because the study was only observational, the authors reported that further investigation is necessary to further illuminate the link between dietary fiber and telomere length.
Whole grains examples are rolled oats, buckwheat, whole wheat, and wild rice. The grains contain the entire grain kernel, which include the bran, germ and endosperm. Less than 5 percent of Americans consume the minimum recommended amount of whole grains, which is about 3 ounce-equivalents per day, according to U.S. Department of Agriculture.
Americans barely receive half the amounts of dietary fiber recommended daily. How much dietary fiber is enough? The recommended amounts are 25 grams of fiber for women and 38 grams of fiber for men.
The AJCN study was among the first to document the relationship between diet and telomere length. The authors of the study concluded that the results provided more support that an improved diet and lifestyle would indeed help to slow the aging process.
"Telomere shortening is accelerated by oxidative stress and inflammation, and diet affects both of these processes," the authors report.
Studies have also found that the following changes in diet and lifestyle are all positively associated with telomere length:
Park Y, Subar AF, Hollenbeck A, Schatzkin A. Dietary Fiber Intake and Mortality in the NIH-AARP Diet and Health Study. Arch Intern Med 2011.
Cassidy A, De V, I, Liu Y et al. Associations between diet, lifestyle factors, and telomere length in women. Am J Clin Nutr 2010;91:1273-80.
This is great news for those eating diets high in fiber. What’s also interesting is that another reason why dietary fiber is protective to health is because of its influence on telomeres. Telomeres are the protective caps at the end of chromosomes, and their length is considered the closest way to measure lifespan in humans.
As reported in a prospective cohort study published in the March 2010 issue of American Journal of Clinical Nutrition (AJCN), telomere length is positively associated with higher fiber intake in women. Dietary fiber from whole grains appears to provide the strongest benefit.
In addition, in the AJCN study, the researchers found telomere length was negatively associated with increased waist circumference and higher intake of omega-6 fatty acids in the diet.
Because the study was only observational, the authors reported that further investigation is necessary to further illuminate the link between dietary fiber and telomere length.
Whole grains examples are rolled oats, buckwheat, whole wheat, and wild rice. The grains contain the entire grain kernel, which include the bran, germ and endosperm. Less than 5 percent of Americans consume the minimum recommended amount of whole grains, which is about 3 ounce-equivalents per day, according to U.S. Department of Agriculture.
Americans barely receive half the amounts of dietary fiber recommended daily. How much dietary fiber is enough? The recommended amounts are 25 grams of fiber for women and 38 grams of fiber for men.
The AJCN study was among the first to document the relationship between diet and telomere length. The authors of the study concluded that the results provided more support that an improved diet and lifestyle would indeed help to slow the aging process.
"Telomere shortening is accelerated by oxidative stress and inflammation, and diet affects both of these processes," the authors report.
Studies have also found that the following changes in diet and lifestyle are all positively associated with telomere length:
- not smoking
- exercising regularly
- maintaining a normal body weight
- healthy management of stress
- consuming sufficient long-chain omega-3 fatty acids from fish weekly
- maintaining a healthy vitamin D status
- consuming a quality multivitamin daily
- consuming antioxidants such as CoQ10 and green tea
Park Y, Subar AF, Hollenbeck A, Schatzkin A. Dietary Fiber Intake and Mortality in the NIH-AARP Diet and Health Study. Arch Intern Med 2011.
Cassidy A, De V, I, Liu Y et al. Associations between diet, lifestyle factors, and telomere length in women. Am J Clin Nutr 2010;91:1273-80.
Post originally written to be posted here.
22 February 2011
Pornography in the Primordial Soup
 |
| Panel of scientists debate on "What is Life?" |
Sometime between 4 and 3.5 billion years ago, the emergence of life had intense beginnings on a young planet in the midst of a so-called primordial soup—consisting of water vapor, carbon monoxide, carbon dioxide, nitrogen, and ammonia and shaped by strong winds, electrical storms, volcanic eruptions, and ultraviolet radiation.
In 1953, Stanley Miller and Harold Urey put Earth's primitive conditions to test for the first time in a famous laboratory experiment. It yielded variety of amino acids and organic compounds. The researchers realized something more: that no early form of life could have ever survived the world of today, because of the presence of oxygen that directly attacks at the bonds that holds together complex molecules.
Scientists also now know that the original blueprint of life was not DNA, but short RNA strands that may have also served as their own biological catalysts, before enzymes ever evolved, providing for self-replication. This early RNA world would eventually give rise to DNA, which used RNA as its template for encoding the genetic information to build proteins.
Still, there are several other questions that remain surrounding life's origins such as How can life be defined? Where did it happen? What came first: replication or metabolism? Could life have happened elsewhere in the universe? What would an alternative form of life and biochemistry look like?
Last weekend, to discuss the questions, a small panel of six scientists gathered at workshop at Arizona State University with a major goal of charting out the steps between the RNA world and greater complexity. Some would say theirs was a hopeless cause and a waste of time.
Then, on Saturday, February 12, a public debate took place between them with an overarching theme entitled, "What is Life?" Theoretical physicist and cosmologist Lawrence Krauss, ASU professor and director of ASU's Origins Project defended the exercise as uniquely human.
"It's a profound and deep question that hits at everything we think about," Krauss said, noting how the question has a powerful draw. "It sounds like a simple question, the answer isn't so simple. In fact, every time I think about that question, I think about pornography."
He referred to a 1964 Supreme Court case where Justice Potter Stewart once was asked to explain the definition obscene pornography. "I know it when I see it," the judge responded. Krauss said, "In some sense, life is like that."
Life: Complexity with a Specified Direction
Evolutionary biologist Richard Dawkins further elucidated the significance of the question in characteristic eloquence, "This may be the only planet in the universe that contains eyes to see it, brains to think about it, and wonder about it. I don't believe that. I suspect there is plenty of life in the universe, but this is the only kind of life we know about."
According to Dawkins, because the laws of physics apply all over the universe, it is likely that life could have materialized many times by the process of evolution by natural selection. Life, then, would have to be defined as anything that is highly statistically improbable, but that appears to have a specified direction.
"You have to add that 'specified direction' because with hindsight you could say any old heap of rubbish is statistically improbable in that there has never been a heap of rubbish exactly the same," Dawkins said. "What's special about life is that living things are statistically improbable in a direction, which you could have specified in advance. It's not always exactly the same, but birds are good at flying, fish are good at swimming, moles are good at digging. All living thins are good at something, whereas lumps of rock aren't.
Whatever life is, it is characterized by its complex molecules that must somehow create the energy to convert raw material into a structure, all while excluding anything that may be toxic to those reactions of metabolism and reproduction. This is why geneticist and Nobel Laureate Lee Hartwell argued, "Inevitably, life will be cellular. Cells will have been selected to have an optimum size and optimum structure for whatever lifestyle they happen to have."
Searching for a Second Genesis
A sort of definition of what to look for was heartening for NASA planetary scientist Chris McKay, "What Lee said was a beautiful synthesis of how we can search for life, and I want to take that to the specifics of how do we do it in near tem missions in our solar system."
There is an advantage to finding other forms of life in our own solar system, argued McKay, because "then we'd know that life is common in the universe." The task of finding other forms of life in the solar system, even on our own planet, is one promoted by cosmologist and astrobiologist Paul Davies.
Davies doesn't see things quite the same way as McKay. "How can we find this second sample of life? Chris has said one way you can do that is you can go somewhere else in the solar system and find it there. That's great. But it's also very expensive. Is there another way? Well, no planet is more Earth-like than Earth itself. Shouldn't it have occurred many times right here on our home planet? How do we know it didn't?"
While Davies looks for alternative life on Earth—a process that he boldly claims can be completed in less than a decade—biologist and entrepreneur Craig Venter is more interested in creating synthetic life.
Venter explained how he and his colleagues synthesized DNA and chromosomes and inject it into E. coli, which he likened to creating a computer program that builds its own computer, or as he puts it, "A situation where the software actually leads to building its own hardware, but we're trying to go much further. We had to learn how to boot up this bacterial genome."
Change the DNA, change the software, and you change the species, Venter explained, and as others have pointed out, his team did use a living cell, but the cell was the first one to ever have synthetic DNA.
Living Artificial Intelligence
Among these scientists, one thing was certain: the definition of life could not be agreed upon in the face of alternative forms of life in the universe, in our own solar system, on the Earth, or from creating life from scratch. But, perhaps, a definition of life isn't needed after all because, as Krauss put it, anyway, it could change.
"Let me throw it in a completely different direction," Krauss offered in the debate."When computers become conscious, which they will—my Mac is far closer than the PC—will we call them life? And they'll object if we don't, I suspect. I think the definition is a moving target."
After all, the difference from what Venter is accomplishing—with software that makes its own hardware—and computers is that computers simply haven't done that yet (made their own hardware), but when they do, which will happen in at least one or two decades, Krauss said, "they will become the dominant forms of intelligent life on the planet and biology will have to incorporate that in order to keep up."
At the end of the debate, the inevitability of life in the universe was the lesson really learned, given that there could be life lurking almost anywhere.
Be it in a biological world, a synthetic world, or another kind, life can defined as simply… we'll just know it when we see it.
To read more about the entire weekend conference on origins of life, see Dennis Overbye's article in the New York Times.
UPDATE: the science network has now published the video of this debate. Click on the video to watch below. To read more about the entire weekend conference on origins of life, see Dennis Overbye's article in the New York Times.
20 February 2011
Evolution of Lactose Tolerance in Africa
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| Sarah Tishkoff |
Sarah Tishkoff has been studying this phenomenon of recent lactose tolerance in African pastoralist populations. She shared her findings on Sunday morning at #AAASmtg in Washington DC.
The ability to digest milk as infants is with the expression of lactase-phlorizine hydrolase (lactase), which is specifically expressed by brushborder cells in the small intestine.
But shortly after weaning, the expression of lactase decreases sharply -- that is, except in populations that are lactase persistent. In 2002, an elegant genetic study found the gene for lactase in European populations.
Tishkoff showed us in charts and on a map how she performed genetic studies on the African pastoralist populations with lactase tolerance. Based on the findings, she found a perfect example of convergent evolution -- that several of the populations had developed lactose tolerance in different ways genetically -- because of strong selective pressures to drink milk.
With her latest study and archeological data, she is now tracking the origins of pastoralism. She showed us a map (Smith 1992) where it's clear that most lactose tolerance emerged only in the last few thousand years, but at different times. Her research confirms that pastoralism was brought into southern Africa only recently, most likely from the Great Lakes region.
"So, are humans still evolving? Yes," Tishkoff said.
Why was milk selective pressure so strong? There has been a lot of debate, Tishkoff said, such as whether it is the source of water, protein, or calcium. But it's not everywhere, so there has to have been a cultural transformation in each region.
"There's only some environments that can handle that cultural development," Tishkoff said, but in each case, there has to be an underlying genetic variation and the different variants suggest that perhaps for some populations had a more difficult time with the change or took longer to adapt to it than others.
The Nature of Human Skin Pigmentation
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| Nina Jablonsky |
"Human skin is colorful, it's mostly naked, it's sweaty, and it's tough yet sensitive," Jablonski said. The gradient of human skin pigmentation is very clear in the old world, as it's lighter in the northern countries and darker in Africa.
But why did human skin pigmentation evolve as it did? When you look at other apes and humans, our relatives have lightly pigmented skin covered by dark hair -- this was the ancestral pigmentation of our lineage.
"When you think of Lucy's species, you can think of lightly pigmented skin covered by dark hair," she said, noting that eventually as the hominins became more naked they developed more melanin.
When Homo ergaster 1.6 mya was foraging in the savannah, the species would have needed more naked and sweaty skin for keeping cool. In addition, Jablonski's research has found that permanent dark pigmentation evolved 1.2 mya, at the same time as these other developments -- an interesting development!.
Exposed skin could lead to disease states, so by increasing the amount of pigmentation, H. ergaster protected the species and the pigmentation was selected on.
Ultraviolet radiation (UVR) had a lot to do with the advent of darker skin pigmentation. On a map (by George Chaplin based on NASA TOMS7 satellite data) of annual average UVR, Jablonski was able to clearly show the strength of UVR.
"We evolved initially in equatorial Africa and then we had two waves of dispersal from Africa," Jablonski said. "This really changed the selective genes for human skin fundamentally."
The key thing about ultraviolet radiation is that wavelengths do different things to the human body. In general, UVR does a lot of damage, such as DNA damage leading to skin cancer.
Skin cancer generally affects people as they're older beyond their reproductive years. However, the sun has a definitive effect on folate metabolism. One of the key things we see as important, is the effect on folate metabolism on birth defects. Because folate is needed for making DNA and the competition for folate is intense in the presence of UVR, "why not increase the amount of melanin -- a superb natural sunscreen -- the evolution of permanent melanin was extremely important in high equatorial radiation levels."
However, melanin comes with a downside. It slows production of vitamin D precursor in the skin, which is essential for calcium metabolism and bone health, as well as incredibly important to the maintenance of a strong immune system.
If we look at our hairy timeline, 6 mya we had hair and light skin, then with dispersal from Africa into India and Asia, then eventually Indonesia and Europe, what did UVR have as an influence?
To Jablonski, it is the combination of needing to protect against DNA damage and folate metabolism as much as possible, but while naturally selecting for less skin pigmentation for keeping the skin light enough to absorb enough UVB rays to create vitamin D.
Indeed, we have an independent evolution of depigmentation of humans in Asia and in Europe. And we also know that the Neandertals experienced the same selection of depigmentation. There are many genes involved in pigmentation and Jablonski said she has even found in some populations, where the amount of UVR changes by season, that people have adapted to change the amount of melanin in their skin throughout the season
Nowadays, accelerated rates of movement around the world, has put humans in environments that are poorly matched, Jablonski said, which has created serious health problems such as with rickets in children, birth defects, and even metabolic syndrome.
For the purposes of education on health, we need to teach that skin color is an adaptation. It is the most visible product of evolution by natural selection on the human body. This is why we need to use it to teach evolution, Jablonski said.
Additional note posted Tuesday, Feb 22. I discovered afterward that Jablonski has a wonderful TED talk that I think everyone should watch, so I posted it below.
19 February 2011
Designing biology
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| Photo credit: Sara Fulcher on Flickr |
Arnold's lab doesn't synthesize enzymes as other labs do. She and her team "evolve them" toward a certain desired goal in the same way that nature has done it for 3.5 billion years.
Aronold presented an overview of her budding field of work to an audience at American Association for the Advancement of Science annual meeting (#AAASmtg) in Washington DC. The field of directed evolution is relatively new and includes few people at the present time, but Arnold sees high hopes for the future.
"When I started engineering proteins a long time ago, there appeared to me an algorithm that dos a really good job and that's evolution," she said. "Evolution works because the regions that life has discovered and explored are rich in function. Directed evolution exploits smooth paths in the fitness landscape."
The fact is, DNA is cheap and easy. Designing it isn't.
"We're getting really good at making DNA. The price is dropping every day," Arnold said. "But we don't know what to write. We can synthesize any sequence. We can insert new code (referring to Craig Venter's recent success), but we don't know how to write it. We don't even know how to write a single protein."
And, when it comes to enzymes for use inside a complex biological system, she says,"Details matter. We don't understand the details."
Freed from constraints of worrying about biological function, directed enzyme evolution allows Arnold's team to explore new pathways and possibilities.
Arnold presented a few of her enzymes that have been created through directed evolution. Her source materials are from every possible place -- the "heel of your shoe," for example -- and she doesn't limit herself to what's available.
 |
| Frances Arnold |
Where is directed enzyme evolution going in the future? Arnold says that functional protein can be used in several ways. One example Arnold gives is in materials chemistry, such as the work of Angela Belcher of MIT, who uses virus proteins to enrobe minerals onto protein coats.
"You can make a virus that really loves to bind to a single-walled carbon nanogen," Arnold said, which would be a boon for semiconductor technology.
There is really no end to the influence that directed enzyme evolution could have on the world, from highly specific targeting in biological systems to technology.
In short, there's no doubt of an exciting future in intelligently designing new biology.
How environmental change shaped human evolution
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| Anna Di Rienzo |
The "Out of Africa" theory has it that humans left Africa 50 Kya and then Neolithic revolution happened 14 Kya. They shifted away from foraging subsistence to horticulture. We also know that levels of human skin pigmentation changed with latitude of populations. In addition, body size and proportions changed. For example, Inuit have quite different proportions for the cold North.
Metabolic traits differ across human populations also, causing disease related traits to occur such as high blood pressure, high triglycerides, or high cholesterol. A prominent example is the rising prevalence of type 2 diabetes. "It's been long proposed that it’s a [genetic] susceptibility to change in lifestyle and diet," Di Rienzo said.
There is a prevalence of inter-ethnic differences in disease and traits. Environmental risk factors clearly play a role in shaping differences. There is a growing conseus that genetic factors also contribute. Is there evidence for genetic – in addition to cultural and physiological – adaptations? How much of the phenotypic diversity is adaptive? What is the contribution of local adaptive traits?
These question led to many studies on signals based on haplotype structure such as lactase persistence, which is common in Europe and in agropastoralist populations, but rare elsewhere. The ability to digest milk in adult life became advantages with the introduction of animal farming, Di Rienzo said. Another example is the FY allele that is fixed in most sub-saharan Africa and is virtually absent everywhere else. FY codes for a chemokine receptor (antimalarial).
Selection for polygenic traits is expected to generate subtle changes in allele frequency at multiple loci. Standard approaches are unlikely to capture these signals. The signature of selection is for monogenic (small shifts) versus polygenic traits.
Her approach is for search of information about environmental selective pressures. She searches for correlations between alledle frequency and environmental variables. She takes into account the geographic structure of human populations shaping distribution.
She used a large dataset of more than 642,000 autosomal SNPs. Environmental variables included climate, ecoregion, and subsistence. Climate includes seasons, ecoregion with temperature, humidity. The genome-wide evidence for environmental adaptations is that most of the genome doesn’t contain genes or variants that affect the function of the genes.
Natural selection acts only on variants that have both functional and phenotypic effects. Is there an excess of test SNPs relative to control SNPs among those with lowest minimum p-values?
The test SNPs used are enriched for SNPs with functional effects. Control SNPs are unlikely to have functional effects (e.g. far from genes).
In all cases, a significant excess of the test relative to control SNPs indicating that environmentals select pressures shaped the geographic distribution of variation in the human genome.
The results suggested genome-wide evidence for environmental adaptations,” Di Rienzo said.
Pancreatic lipase-related protein 2 hydrolyzes galactolipids, is the main component in plants. The truncated PLRP2 protein, which occurs at a higher frequency in those populations with higher consumption of cereal grains. PLRP2 is associated with cereal rich diet.
Two examples of patterns at individual SNPs are “foraging” and “nonforaging” and she shows a slide with patterns showing differences in Africa, Europe and other. In each geographic location, there is a shift in allele frequency that allude to differences in diet of the populations.
The shift in allele frequency is not dramatic, but small. The top signals are with categorical variables like roots & tubers, foraging, polar ecoregion, and a dry ecoregion. Top climate variables have to do with seasons.
“Selection doesn’t act on genes, it acts on phenotypes. The phenotypes are enriched with signals for environmental correlations,” Di Rienzo said.
Disease classes are influenced by environmental selective pressures. Climate influenced cancer, CVD, immune, infection. Subsistence influenced metabolic and reproduction phenotypes.
The overlaying signals of environmental correlations and genome-wide association studies show this flow:
SNP is affected by environmental correlations and GWAS, then selective pressures produce phenotype. It’s also known that pathogen diversity follows a gradient on climate factors, which can affect immune, autoimmune adaptations.
Di Rienzo made these conclusions from the data:
- Strong GWAS to climate, ecoregion and subsistence
- Signal of adaptation to environmental pressures are subtle, but consistent shifts in allele frequency
- Adaptation to local environ and common disease may have similar gene architecture
- Signals of climate correlations make a contribution to diseases of immune response and pigmentation traits
More information can be found at dbCLINE
16 February 2011
How much vitamin C do you really need?
Note: Vitamin C is fascinating topic and there's no better way to understand it than through the eyes of my boss, Dr. Rockway. I'm glad I had the pleasure of editing her article and posting it here. David
By Susie Rockway, Ph.D.
Vitamin C, or ascorbic acid (ascorbate), is the most frequently taken dietary supplement in North America. Yet, despite its widespread use, national surveys report that 15 percent of the population still doesn't get enough vitamin C to meet recommended amounts for health.
Initially, the Recommended Daily Intake (RDI) for vitamin C was set at 60 milligrams, the amount required to prevent scurvy. The deficiency disease—commonly characterized by bleeding gums and loosened teeth helped identify the vitamin as having an essential role in collagen formation.
However, more recent research has now made it clear that more dietary vitamin C is needed to saturate body tissues such as the brain, heart, liver, and adrenal glands.
Consequently, in 2000, the RDI was raised to 90 and 75 milligrams daily for men and women. The new values were based on studies suggesting that plasma vitamin C should be maintained at specific levels (~80 µmol/L) for good health and antioxidant activity.
This is how the "debate on how much of vitamin C is needed" began—with scientists discussing two questions:
While there is still not any consensus on this matter, a new, carefully designed study just published in the February issue of American Journal of Clinical Nutrition provides some clues for answering these questions.
In the study, New Zealand researchers compared "normal" mice vitamin C tissue saturation levels with "knockout" mice that were genetically engineered to lack the enzyme needed for synthesizing vitamin C in the body.
Without dietary vitamin C, they saw that tissue concentrations of ascorbate became deficient weeks before the onset of scurvy symptoms in the mice, similar to humans. During these weeks, the scientists observed that the mice exhibited signs of impaired collagen synthesis, changes in aortic wall structure, formation of atherosclerotic plaque, and activation of inflammatory processes.
Sustaining Tissue Concentration
The scientists observed that each tissue became deficient at different rates. For example, the brain maintained its vitamin C longer than other organs; however, after just two weeks of deficiency, vitamin C in the brain became depleted. To replenish these tissues to normal levels, plasma concentration had to be maintained saturated with daily ascorbate intakes.
In addition, they found that tissue levels of ascorbate became saturated more quickly when the mice ate kiwi fruit versus sodium ascorbate in water—the flavonoids present in kiwi are thought to enhance absorption of vitamin C by maintaining it in a reduced state (versus an oxidized state).
Lastly, based on the new evidence, the researchers wrote that the current RDI should receive no less than a 60 percent boost—from 75 milligrams per day to at least 120 milligrams per day—to keep not only plasma levels saturated, but also tissue levels of the brain, and organs that are unable to be measured with current methods.
The vitamin C researchers stressed the need for people to maintain an ongoing and constant vitamin C intake to sustain tissue concentration—which means consuming the scientists' recommended amounts regularly.
What Weight Has to Do with Vitamin C
Another less well-known role of vitamin C is its involvement as a cofactor in the biosynthesis of carnitine, a molecule required for burning fat as energy fuel (fatty acid oxidation).
Interestingly, there is a direct inverse relationship with obesity (adiposity) and plasma vitamin C concentrations—as plasma ascorbate levels are decreased, fatty tissue increases (adiposity increases).
This association has led researchers to wonder whether or not decreased vitamin C levels cause less carnitine to be synthesized and if there is a relationship between less carnitine and less burning of fat for fuel.
Preliminary findings are that subjects who are vitamin C depleted have lower levels of carnitine leading to a 25 percent decrease in fatty acid oxidation (per kilogram body weight) than individuals whose vitamin C status is adequate.
The researchers speculate that reduced fat oxidation seen with vitamin C depletion may result in weight gain by two mechanisms:
Sources
By Susie Rockway, Ph.D.
Vitamin C, or ascorbic acid (ascorbate), is the most frequently taken dietary supplement in North America. Yet, despite its widespread use, national surveys report that 15 percent of the population still doesn't get enough vitamin C to meet recommended amounts for health.
Initially, the Recommended Daily Intake (RDI) for vitamin C was set at 60 milligrams, the amount required to prevent scurvy. The deficiency disease—commonly characterized by bleeding gums and loosened teeth helped identify the vitamin as having an essential role in collagen formation.
However, more recent research has now made it clear that more dietary vitamin C is needed to saturate body tissues such as the brain, heart, liver, and adrenal glands.
Consequently, in 2000, the RDI was raised to 90 and 75 milligrams daily for men and women. The new values were based on studies suggesting that plasma vitamin C should be maintained at specific levels (~80 µmol/L) for good health and antioxidant activity.
This is how the "debate on how much of vitamin C is needed" began—with scientists discussing two questions:
- How much vitamin C is really needed to make an impact on plasma levels?
- Are plasma levels really the best indication of tissue saturation levels?
While there is still not any consensus on this matter, a new, carefully designed study just published in the February issue of American Journal of Clinical Nutrition provides some clues for answering these questions.
In the study, New Zealand researchers compared "normal" mice vitamin C tissue saturation levels with "knockout" mice that were genetically engineered to lack the enzyme needed for synthesizing vitamin C in the body.
Without dietary vitamin C, they saw that tissue concentrations of ascorbate became deficient weeks before the onset of scurvy symptoms in the mice, similar to humans. During these weeks, the scientists observed that the mice exhibited signs of impaired collagen synthesis, changes in aortic wall structure, formation of atherosclerotic plaque, and activation of inflammatory processes.
Sustaining Tissue Concentration
The scientists observed that each tissue became deficient at different rates. For example, the brain maintained its vitamin C longer than other organs; however, after just two weeks of deficiency, vitamin C in the brain became depleted. To replenish these tissues to normal levels, plasma concentration had to be maintained saturated with daily ascorbate intakes.
In addition, they found that tissue levels of ascorbate became saturated more quickly when the mice ate kiwi fruit versus sodium ascorbate in water—the flavonoids present in kiwi are thought to enhance absorption of vitamin C by maintaining it in a reduced state (versus an oxidized state).
Lastly, based on the new evidence, the researchers wrote that the current RDI should receive no less than a 60 percent boost—from 75 milligrams per day to at least 120 milligrams per day—to keep not only plasma levels saturated, but also tissue levels of the brain, and organs that are unable to be measured with current methods.
The vitamin C researchers stressed the need for people to maintain an ongoing and constant vitamin C intake to sustain tissue concentration—which means consuming the scientists' recommended amounts regularly.
What Weight Has to Do with Vitamin C
Another less well-known role of vitamin C is its involvement as a cofactor in the biosynthesis of carnitine, a molecule required for burning fat as energy fuel (fatty acid oxidation).
Interestingly, there is a direct inverse relationship with obesity (adiposity) and plasma vitamin C concentrations—as plasma ascorbate levels are decreased, fatty tissue increases (adiposity increases).
This association has led researchers to wonder whether or not decreased vitamin C levels cause less carnitine to be synthesized and if there is a relationship between less carnitine and less burning of fat for fuel.
Preliminary findings are that subjects who are vitamin C depleted have lower levels of carnitine leading to a 25 percent decrease in fatty acid oxidation (per kilogram body weight) than individuals whose vitamin C status is adequate.
The researchers speculate that reduced fat oxidation seen with vitamin C depletion may result in weight gain by two mechanisms:
- Indirectly, decreased carnitine leads to increased fatigue during exercise and this may lead to exercise intolerance
- Directly, by lipid (fat) accumulation
Sources
- Vissers MCM, Bozonet SM, Perason JF and Braithwaite LJ. Dietary ascorbate intake affects steady state tissue concentrations in vitamin C-deficient mice: tissue deficiency after dietary ascorbate intake affects steady state tissue concentrations in vitamin C-deficient mice: tissue deficiency after suboptimal intake and super bioavailability from a food source (kiwifruit). AJCN 93(2):292-301, 2011.
- Johnston CS, Corte C and Swan PD. Marginal vitamin C status is associated with reduced fat oxidation during submaximal exercise in young adults. Nutr & Metab 3(35):1-5, 2006.
10 February 2011
Why dark chocolate is good for her heart
Listen up, men! On this Valentine's Day, why not surprise your special lady with chocolates that are healthier for her heart? Dark chocolate eaten in moderate amounts weekly is associated with improved cardiovascular fitness in women, research suggests.
Scientists are only beginning to understand why dark chocolate is heart healthy, but a new study offers this explanation—its rich content of cocoa antioxidant compounds, called polyphenols, could enhance activity of special proteins called sterol regulatory element binding proteins (SREBPs), which are involved in cholesterol metabolism.
These activated SREBPs then bind to genes on DNA (sterol regulatory element sequences) that boost liver production of another protein called apolipoprotein A1 (ApoA1), which is the major protein component of HDL "good" cholesterol.
Correspondingly, cocoa polyphenols also decreased production of another protein in the liver called apolipoprotein B (ApoB), which is the major protein component of LDL "bad" cholesterol. The study also showed cocoa polyphenols induced activity of LDL receptors, allowing more cholesterol to be removed from the bloodstream.
The scientist’s findings—suggesting that polyphenols in dark chocolate may help maintain higher “good” cholesterol levels and lower "bad" cholesterol levels—were published in the February issue of Journal of Agricultural and Food Chemistry, published by the American Chemical Society.
The researchers write, "As cholesterol metabolism is known to be regulated by several different mechanisms, it is possible that cacao polyphenols may act on multiple pathways as a regulatory receptor agonist or ligand, similar to other plant polyphenols."
So, what's the message you give with dark chocolate? Romance, of course – but with a healthy twist for your sweetheart's heart.
Source: Yasuda A, Natsume M, Osakabe N, Kawahata K, Koga J. Cacao Polyphenols Influence the Regulation of Apolipoprotein in HepG2 and Caco2 Cells. J Agric Food Chem 2011.
Scientists are only beginning to understand why dark chocolate is heart healthy, but a new study offers this explanation—its rich content of cocoa antioxidant compounds, called polyphenols, could enhance activity of special proteins called sterol regulatory element binding proteins (SREBPs), which are involved in cholesterol metabolism.
These activated SREBPs then bind to genes on DNA (sterol regulatory element sequences) that boost liver production of another protein called apolipoprotein A1 (ApoA1), which is the major protein component of HDL "good" cholesterol.
Correspondingly, cocoa polyphenols also decreased production of another protein in the liver called apolipoprotein B (ApoB), which is the major protein component of LDL "bad" cholesterol. The study also showed cocoa polyphenols induced activity of LDL receptors, allowing more cholesterol to be removed from the bloodstream.
The scientist’s findings—suggesting that polyphenols in dark chocolate may help maintain higher “good” cholesterol levels and lower "bad" cholesterol levels—were published in the February issue of Journal of Agricultural and Food Chemistry, published by the American Chemical Society.
The researchers write, "As cholesterol metabolism is known to be regulated by several different mechanisms, it is possible that cacao polyphenols may act on multiple pathways as a regulatory receptor agonist or ligand, similar to other plant polyphenols."
So, what's the message you give with dark chocolate? Romance, of course – but with a healthy twist for your sweetheart's heart.
Source: Yasuda A, Natsume M, Osakabe N, Kawahata K, Koga J. Cacao Polyphenols Influence the Regulation of Apolipoprotein in HepG2 and Caco2 Cells. J Agric Food Chem 2011.
29 January 2011
Losing weight without developing gallstones
Gallstones are estimated to affect 1 in 10 people in North America. Those who are obese have a higher likelihood of developing gallstones. Most at risk of gallstones as a result of obesity are Native Americans, the elderly, and Caucasian women in their forties who haven’t yet reached menopause.
Gallstones are so named because they develop in the gallbladder, a small organ that stores and releases the bile made by the liver. Bile is a dark green fluid containing bile salts and cholesterol. The gallbladder releases bile into the small intestine to assist in digesting fats more efficiently. However, if the bile contains high concentrations of cholesterol, then stones too difficult for the bile salts to dissolve may develop.
Because gallstones usually form without any symptoms, most people don’t know they have them or may feel only minor symptoms such as abdominal pain after eating a fatty meal. However, if a stone becomes lodged in a bile duct causing blockage, it can result in sudden pain in the abdomen, back or right shoulder.
Cholecystitis, or gallbladder disease, which is caused by duct blockage, infection or inflammation, is one of the most common digestive diseases. Pain from duct blockage can become intense and lead to hospitalization and surgery. In the U.S. alone, gallbladder surgeries approach 700,000 annually, costing approximately $6.5 million.
Surgery costs increase if gallstones and duct blockage or infection cause the pancreas to become inflamed. The resulting pancreatitis can lead to severe or life-threatening complications. The major cause of acute pancreatitis in North America is gallstones.
Link to Obesity and Losing Weight Too Quickly
Because of obesity’s major role in the formation of gallstones, weight management is critical for decreasing the likelihood of developing them. Obesity is thought to increase risk of gallstones because of elevated production of cholesterol, which in turn increases the concentration of cholesterol in bile.
Paradoxically, losing weight actually increases risk of developing gallstones among obese people, especially amongst those who lose large amounts of weight rapidly. Although not entirely understood, nutritional and medical scientists think that losing weight too quickly may shift the balance of bile salts and cholesterol, causing increased concentrations of cholesterol. Gallstone risk may also be increased by consuming a diet too low in fat or avoiding fat, which reduces the frequency of gallbladder contractions and results in fewer chances of gallbladder emptying.
As always, individuals with a high risk for gallstones should follow medical advice in treatment. Medical researchers have studied methods that obese people can lose weight while reducing risk of gallstone developments. Statin regimens and bile salt therapies have had mixed results. A drug called ursodiol has shown much promise in helping to dissolve cholesterol in bile and prevent gallstones.
There have also been successes such as employing modifications in diet to help reduce risk of gallstones. Along with following a doctor’s advice, individuals can consider these weight-management strategies, which have shown promise based on epidemiologic studies or in clinical trials for losing weight as naturally and safely as possible.
Three Steps to Help Lower Risk of Gallstones While Losing Weight
Step 1: Avoid very low-calorie dieting, losing no more than 1-2 pounds per week.
Overall, research studies have found that obese people who lost 3 pounds or more weekly had a greater likelihood of developing gallstones. This may be because they are more likely to experience an imbalance between bile salts and cholesterol, as well as irregular gallbladder emptying.
For these reasons, people who are obese or who are at high risk for developing gallstones should also avoid skipping meals or fasting.
By eating three steady meals throughout the day and losing weight at a slower rate, obese people can reduce the weight-loss risk factor in gallstone formation. To ensure steady weight loss at 1-2 pounds per week, calorie intake should be reduced by only 500 to 1,000 calories. Weight loss is also influenced by activity, which may require eating more calories to compensate for calories burned.
Step 2: Avoid saturated fats and eat small amounts of monounsaturated or polyunsaturated dietary fat daily.
Foods high in saturated fats, trans fats and cholesterol are all associated with increased risk in gallstone formation. However, foods high in polyunsaturated or monounsaturated fats (from olive oil or high-oleic sunflower oil) may help lower cholesterol saturation and reduce risk of gallstone formation.
A randomized clinical trial on obese subjects compared a low-calorie diet (900 kcal/d) with 30 grams of fat per day with a low-calorie diet (520 kcal/d) with less than 2 grams of fat per day. After eight weeks, not one of the subjects on the diet with 30 grams of fat per day had developed gallstones. The researchers were led to conclude that dietary fat ensured regular gallbladder emptying and reduced bile cholesterol saturation.
A 10g threshold of fat per meal is now considered to be most efficient at maximizing gallbladder emptying, which can support healthy weight loss while reducing risk of formation of gallstones.
Furthermore, according to one randomized, double-blind, placebo-controlled clinical trial, fish oil in amounts of almost 12 grams per day may work comparatively to ursodiol in reducing risk of gallstone formation in low calorie diets.
Step 3: Avoid refined sugar and strive for a diet high in fiber.
In epidemiologic studies, there is a higher association of gallstones in those who ate greater amounts of refined sugars. In contrast, long-term consumption of relatively high amounts of dietary fiber has been correlated with reduced risk of gallstone diseases.
The risk appears to be even lower if the amount of fiber consumed comes from sources rich in insoluble fiber found in whole grains, fruits and vegetables. Soluble dietary fiber such as found in oats and legumes also appears to be protective, showing reduction of gallstone formation in animal studies.
Diets higher in fiber and lower in refined sugars will also assist in weight loss. Refined sugars, found in high amounts in sodas and desserts, contribute to high calorie intake, which contributes to obesity. Dietary fiber is filling, providing a satiety effect, but offers little or no calories that would contribute to weight gain.
Individuals should increase dietary fiber to recommended levels (25 to 30 grams daily) gradually.
Safe Road to Optimal Health
Once again, each of these steps is a natural dietary habit that will help lower the risk of developing gallstones and support losing weight safely. Apart from diet, getting regular exercise daily is also helpful. And, for every pound lost gradually, the ultimate achievement is reduced risk of gallstones in the future.
Beyond reduced risk of gallstones, the end-benefits of healthy weight management are profound including improved activity and mobility, improved health of organs such as the heart and brain, and reduced risk of diseases such as type 2 diabetes and cardiovascular disease. Healthy weight management improves overall health and wellness at every level.
Gallstones are so named because they develop in the gallbladder, a small organ that stores and releases the bile made by the liver. Bile is a dark green fluid containing bile salts and cholesterol. The gallbladder releases bile into the small intestine to assist in digesting fats more efficiently. However, if the bile contains high concentrations of cholesterol, then stones too difficult for the bile salts to dissolve may develop.
Because gallstones usually form without any symptoms, most people don’t know they have them or may feel only minor symptoms such as abdominal pain after eating a fatty meal. However, if a stone becomes lodged in a bile duct causing blockage, it can result in sudden pain in the abdomen, back or right shoulder.
Cholecystitis, or gallbladder disease, which is caused by duct blockage, infection or inflammation, is one of the most common digestive diseases. Pain from duct blockage can become intense and lead to hospitalization and surgery. In the U.S. alone, gallbladder surgeries approach 700,000 annually, costing approximately $6.5 million.
Surgery costs increase if gallstones and duct blockage or infection cause the pancreas to become inflamed. The resulting pancreatitis can lead to severe or life-threatening complications. The major cause of acute pancreatitis in North America is gallstones.
Link to Obesity and Losing Weight Too Quickly
Because of obesity’s major role in the formation of gallstones, weight management is critical for decreasing the likelihood of developing them. Obesity is thought to increase risk of gallstones because of elevated production of cholesterol, which in turn increases the concentration of cholesterol in bile.
Paradoxically, losing weight actually increases risk of developing gallstones among obese people, especially amongst those who lose large amounts of weight rapidly. Although not entirely understood, nutritional and medical scientists think that losing weight too quickly may shift the balance of bile salts and cholesterol, causing increased concentrations of cholesterol. Gallstone risk may also be increased by consuming a diet too low in fat or avoiding fat, which reduces the frequency of gallbladder contractions and results in fewer chances of gallbladder emptying.
As always, individuals with a high risk for gallstones should follow medical advice in treatment. Medical researchers have studied methods that obese people can lose weight while reducing risk of gallstone developments. Statin regimens and bile salt therapies have had mixed results. A drug called ursodiol has shown much promise in helping to dissolve cholesterol in bile and prevent gallstones.
There have also been successes such as employing modifications in diet to help reduce risk of gallstones. Along with following a doctor’s advice, individuals can consider these weight-management strategies, which have shown promise based on epidemiologic studies or in clinical trials for losing weight as naturally and safely as possible.
Three Steps to Help Lower Risk of Gallstones While Losing Weight
Step 1: Avoid very low-calorie dieting, losing no more than 1-2 pounds per week.
Overall, research studies have found that obese people who lost 3 pounds or more weekly had a greater likelihood of developing gallstones. This may be because they are more likely to experience an imbalance between bile salts and cholesterol, as well as irregular gallbladder emptying.
For these reasons, people who are obese or who are at high risk for developing gallstones should also avoid skipping meals or fasting.
By eating three steady meals throughout the day and losing weight at a slower rate, obese people can reduce the weight-loss risk factor in gallstone formation. To ensure steady weight loss at 1-2 pounds per week, calorie intake should be reduced by only 500 to 1,000 calories. Weight loss is also influenced by activity, which may require eating more calories to compensate for calories burned.
Step 2: Avoid saturated fats and eat small amounts of monounsaturated or polyunsaturated dietary fat daily.
Foods high in saturated fats, trans fats and cholesterol are all associated with increased risk in gallstone formation. However, foods high in polyunsaturated or monounsaturated fats (from olive oil or high-oleic sunflower oil) may help lower cholesterol saturation and reduce risk of gallstone formation.
A randomized clinical trial on obese subjects compared a low-calorie diet (900 kcal/d) with 30 grams of fat per day with a low-calorie diet (520 kcal/d) with less than 2 grams of fat per day. After eight weeks, not one of the subjects on the diet with 30 grams of fat per day had developed gallstones. The researchers were led to conclude that dietary fat ensured regular gallbladder emptying and reduced bile cholesterol saturation.
A 10g threshold of fat per meal is now considered to be most efficient at maximizing gallbladder emptying, which can support healthy weight loss while reducing risk of formation of gallstones.
Furthermore, according to one randomized, double-blind, placebo-controlled clinical trial, fish oil in amounts of almost 12 grams per day may work comparatively to ursodiol in reducing risk of gallstone formation in low calorie diets.
Step 3: Avoid refined sugar and strive for a diet high in fiber.
In epidemiologic studies, there is a higher association of gallstones in those who ate greater amounts of refined sugars. In contrast, long-term consumption of relatively high amounts of dietary fiber has been correlated with reduced risk of gallstone diseases.
The risk appears to be even lower if the amount of fiber consumed comes from sources rich in insoluble fiber found in whole grains, fruits and vegetables. Soluble dietary fiber such as found in oats and legumes also appears to be protective, showing reduction of gallstone formation in animal studies.
Diets higher in fiber and lower in refined sugars will also assist in weight loss. Refined sugars, found in high amounts in sodas and desserts, contribute to high calorie intake, which contributes to obesity. Dietary fiber is filling, providing a satiety effect, but offers little or no calories that would contribute to weight gain.
Individuals should increase dietary fiber to recommended levels (25 to 30 grams daily) gradually.
Safe Road to Optimal Health
Once again, each of these steps is a natural dietary habit that will help lower the risk of developing gallstones and support losing weight safely. Apart from diet, getting regular exercise daily is also helpful. And, for every pound lost gradually, the ultimate achievement is reduced risk of gallstones in the future.
Beyond reduced risk of gallstones, the end-benefits of healthy weight management are profound including improved activity and mobility, improved health of organs such as the heart and brain, and reduced risk of diseases such as type 2 diabetes and cardiovascular disease. Healthy weight management improves overall health and wellness at every level.
27 January 2011
No evidence of dairy and heart disease link
New research has once again confirmed after systematically analyzing 17 studies that there is simply no evidence to substantiate claims of a link between dairy and higher risk of cardiovascular disease or death.
The evidence, in fact, shows just the opposite—drinking milk slightly reduces the risk of coronary heart disease (1). In addition, multiple studies show that milk and dairy proteins (whey and casein) may actually protect the heart by helping to maintain lower blood pressure, lower blood sugar, and lead to reduced bodyweight (2-4).
The renowned, epidemiologic and nutrition researcher Walter Willet, Ph.D., and his group at Harvard, conducted this huge analysis by looking at various types of dairy intake, ranging from milk intake to total high-fat dairy products and total low-fat dairy products and correlating to risk of cardiovascular disease (CVD), coronary heart disease (CHD), stroke and all-cause mortality. This study was a meta-analysis of many prospective cohort studies in healthy men and women (4).
Although it's always a challenging task to summarize published studies' data on food intake, Willett’s group is easily recognized as having the epidemiological expertise of doing such an analysis. Results from the group's careful analysis show:
A notable strength of this methodology was the use of an advanced statistical approach for trend estimation of summarized dose-response data. This method provides uniform analysis of different studies, exposure categories and range of intakes; as well as greater power using full spectrum continuous exposure data.
These data, published in the January issue of the Journal of American Clinical Nutrition, clearly show that milk intake does not lead to cardiovascular, heart, stroke or any mortality (including cancer) and may even be beneficial in reducing cardiovascular diseases.
Several mechanisms have been discussed over the years concerning the beneficial effects of low-fat dairy intake on lowering blood pressure. For example, data from the famous DASH eating plan show systolic blood pressure reduction with a healthy diet. Inclusion of low-fat dairy products or dairy proteins showed a potential anti-hypertension effect possibly due to the natural mineral content found in dairy, particularly phosphorous.
These types of studies do not show cause and effect, but do, in fact, show that there is not an increased risk of heart disease, cardiovascular disease, stroke or all-cause mortality by drinking milk. One can only hypothesize why these associations exist—a clear possibility is that milk drinkers are taking extra dietary care by consuming natural products, perhaps in place of sugar-laden soft drinks. Diet quality is the key in reducing risk of chronic disease.
CVD is the main cause of death in the Western world claiming 17 million lives each year. Since saturated fat intake is associated with heart disease, dairy foods have often been blamed for contributing to CVD; however, the science community has yet to agree because of many conflicting studies. Although most epidemiological studies have failed to show an effect of dairy on CVD, a few have shown a positive correlation.
Likely confusion arises when results from dissimilar studies get lumped together in hopes of finding the "answer." However, combining evidence from epidemiological, case-control, prospective study designs with different age groups, genders, countries and numbers of subjects may easily explain the mixed results.
References
The evidence, in fact, shows just the opposite—drinking milk slightly reduces the risk of coronary heart disease (1). In addition, multiple studies show that milk and dairy proteins (whey and casein) may actually protect the heart by helping to maintain lower blood pressure, lower blood sugar, and lead to reduced bodyweight (2-4).
The renowned, epidemiologic and nutrition researcher Walter Willet, Ph.D., and his group at Harvard, conducted this huge analysis by looking at various types of dairy intake, ranging from milk intake to total high-fat dairy products and total low-fat dairy products and correlating to risk of cardiovascular disease (CVD), coronary heart disease (CHD), stroke and all-cause mortality. This study was a meta-analysis of many prospective cohort studies in healthy men and women (4).
Although it's always a challenging task to summarize published studies' data on food intake, Willett’s group is easily recognized as having the epidemiological expertise of doing such an analysis. Results from the group's careful analysis show:
- a statistically significant inverse association between milk intake and cardiovascular disease.
- no significant relationship between CHD, stroke, and all-cause mortality (including cancer) and total dairy of all types (high-fat, low-fat)
A notable strength of this methodology was the use of an advanced statistical approach for trend estimation of summarized dose-response data. This method provides uniform analysis of different studies, exposure categories and range of intakes; as well as greater power using full spectrum continuous exposure data.
These data, published in the January issue of the Journal of American Clinical Nutrition, clearly show that milk intake does not lead to cardiovascular, heart, stroke or any mortality (including cancer) and may even be beneficial in reducing cardiovascular diseases.
Several mechanisms have been discussed over the years concerning the beneficial effects of low-fat dairy intake on lowering blood pressure. For example, data from the famous DASH eating plan show systolic blood pressure reduction with a healthy diet. Inclusion of low-fat dairy products or dairy proteins showed a potential anti-hypertension effect possibly due to the natural mineral content found in dairy, particularly phosphorous.
These types of studies do not show cause and effect, but do, in fact, show that there is not an increased risk of heart disease, cardiovascular disease, stroke or all-cause mortality by drinking milk. One can only hypothesize why these associations exist—a clear possibility is that milk drinkers are taking extra dietary care by consuming natural products, perhaps in place of sugar-laden soft drinks. Diet quality is the key in reducing risk of chronic disease.
CVD is the main cause of death in the Western world claiming 17 million lives each year. Since saturated fat intake is associated with heart disease, dairy foods have often been blamed for contributing to CVD; however, the science community has yet to agree because of many conflicting studies. Although most epidemiological studies have failed to show an effect of dairy on CVD, a few have shown a positive correlation.
Likely confusion arises when results from dissimilar studies get lumped together in hopes of finding the "answer." However, combining evidence from epidemiological, case-control, prospective study designs with different age groups, genders, countries and numbers of subjects may easily explain the mixed results.
References
- Soedamah-Authu SS, Ding EL, Al-Delaimy WK, Hu FB, Engberink MF, Willet WC and Geleijnse JM. Milk and dairy consumption and incidence of cardiovascular disease and all-cause mortality: dose-response meta-analysis of prospective cohort studies. Am J Clin Nutr 2011; 93: 158-71.
- Petersen BL, Ward LS, Bastian ED, Jenkins AL, Campbell J, Vuksan V. A whey protein supplement decreases post-prandial glycemia. Nutr J 2009;8:47.
- Frestedt JL, Zenk JL, Kuskowski MA, Ward LS, Bastian ED. A whey-protein supplement increases fat loss and spares lean muscle in obese subjects: a randomized human clinical study. Nutr Metab (Lond) 2008;5:8.
- Fluegel SM, Shultz TD, Powers JR, Clark S, et al. Whey beverages decrease blood pressure in prehypertensive and hypertensive young men and women. International Dairy Journal; 1010; 753-760.
22 January 2011
CoQ10 Adds to Mediterranean Diet’s Anti-Aging Benefits
Elderly men and women who supplement Mediterranean-style meals with coenzyme Q10 (coQ10) enjoy greater antioxidant protection and could slow aging, a Spanish study finds (1).
In a randomized crossover trial, University of Cordoba researchers assigned 20 healthy adults (ages 65 and older) to one of the three dietary protocols for the duration of four weeks: a traditional Western-style diet rich in saturated fats, a Mediterranean-style diet rich in olive oil, or a Mediterranean-style diet supplemented with coQ10 (200 mg/day in capsules).
The scientists found that the combination (Mediterranean-style meals and coQ10) improved antioxidant activity and reduced cellular oxidative stress in the subjects more successfully than the Mediterranean-style or Western-style diet alone.
The Mediterranean-style diet protocols also exhibited greater heart-protective benefits in comparison to the Western-style diet. The scientists noticed a significantly greater decrease in HDL cholesterol (the “good” cholesterol) levels in response to the Western-style meals.
Writing in the December issue of AGE, the authors concluded that the effect of the Mediterranean-style diet rich in olive oil, in combination with coQ10, may have “favorable effects on the aging process” and on the prevalence of age-related conditions.
Previous studies, noted by the authors, have found that the olive-oil rich diet supplemented with coQ10 also improves capillary blood flow and helps maintain healthy blood pressure.
Mediterranean-style diet
A Mediterranean-style diet generally includes greater amounts of fruits, vegetables, whole grains, and olive oil; at least two servings of fish and seafood per week; moderate amounts of poultry, eggs, cheese and yogurt; and fewer meats and sweets.
In this study, the Mediterranean-style diet consisted of 15 percent of calories as protein, 47 percent as carbohydrate, and 38 percent as fat (24 percent monounsaturated fats [from virgin olive oil], 10 percent saturated fat, and 4 percent polyunsaturated fatty acid).
The Western-style diet consisted of 15 percent calories as protein, 47 percent as carbohydrate, and 38 percent as fat (12 percent monounsaturated fats, 22 percent saturated fats, and 4 percent polyunsaturated fats).
Several other studies have pointed to anti-aging benefits from the Mediterranean-style diet. One such study, just published by researchers at Rush University, of Chicago, in the American Journal of Clinical Nutrition linking the diet to a healthier brain in older age (2).
CoQ10 and Oxidative Stress
CoQ10 is a major fat-soluble antioxidant found in all cell membranes, especially within mitochondrial membranes. It’s one of the cell’s most potent scavengers of free radicals, neutralizing the lipid peroxyl radicals that damage cell membranes, proteins and DNA.
Antioxidants are the body’s first line of defense against free radicals and byproducts of metabolism that could lead to cellular decline and dysfunction.
The ability of humans to synthesize coQ10 declines 20 percent for every decade of life after the age of 21. This reduction leads to deficiency, weakness and fatigue throughout the body.
Lower coQ10 levels in tissues and cells can allow for more damage on nearby lipids, proteins and DNA. Because coQ10 is chiefly instrumental (along with selenium) for the regeneration of vitamin E, another potent fat-soluble antioxidant, the diminished coQ10 levels also lead to declines in levels of vitamin E.
Sources:
1. Yubero-Serrano EM, Delgado-Casado N, Delgado-Lista J et al. Postprandial antioxidant effect of the Mediterranean diet supplemented with coenzyme Q(10) in elderly men and women. Age (Dordr ) 2010.
2. Tangney CC, Kwasny MJ, Li H, Wilson RS, Evans DA, Morris MC. Adherence to a Mediterranean-type dietary pattern and cognitive decline in a community population. Am J Clin Nutr 2010.
In a randomized crossover trial, University of Cordoba researchers assigned 20 healthy adults (ages 65 and older) to one of the three dietary protocols for the duration of four weeks: a traditional Western-style diet rich in saturated fats, a Mediterranean-style diet rich in olive oil, or a Mediterranean-style diet supplemented with coQ10 (200 mg/day in capsules).
The scientists found that the combination (Mediterranean-style meals and coQ10) improved antioxidant activity and reduced cellular oxidative stress in the subjects more successfully than the Mediterranean-style or Western-style diet alone.
The Mediterranean-style diet protocols also exhibited greater heart-protective benefits in comparison to the Western-style diet. The scientists noticed a significantly greater decrease in HDL cholesterol (the “good” cholesterol) levels in response to the Western-style meals.
Writing in the December issue of AGE, the authors concluded that the effect of the Mediterranean-style diet rich in olive oil, in combination with coQ10, may have “favorable effects on the aging process” and on the prevalence of age-related conditions.
Previous studies, noted by the authors, have found that the olive-oil rich diet supplemented with coQ10 also improves capillary blood flow and helps maintain healthy blood pressure.
Mediterranean-style diet
A Mediterranean-style diet generally includes greater amounts of fruits, vegetables, whole grains, and olive oil; at least two servings of fish and seafood per week; moderate amounts of poultry, eggs, cheese and yogurt; and fewer meats and sweets.
In this study, the Mediterranean-style diet consisted of 15 percent of calories as protein, 47 percent as carbohydrate, and 38 percent as fat (24 percent monounsaturated fats [from virgin olive oil], 10 percent saturated fat, and 4 percent polyunsaturated fatty acid).
The Western-style diet consisted of 15 percent calories as protein, 47 percent as carbohydrate, and 38 percent as fat (12 percent monounsaturated fats, 22 percent saturated fats, and 4 percent polyunsaturated fats).
Several other studies have pointed to anti-aging benefits from the Mediterranean-style diet. One such study, just published by researchers at Rush University, of Chicago, in the American Journal of Clinical Nutrition linking the diet to a healthier brain in older age (2).
CoQ10 and Oxidative Stress
CoQ10 is a major fat-soluble antioxidant found in all cell membranes, especially within mitochondrial membranes. It’s one of the cell’s most potent scavengers of free radicals, neutralizing the lipid peroxyl radicals that damage cell membranes, proteins and DNA.
Antioxidants are the body’s first line of defense against free radicals and byproducts of metabolism that could lead to cellular decline and dysfunction.
The ability of humans to synthesize coQ10 declines 20 percent for every decade of life after the age of 21. This reduction leads to deficiency, weakness and fatigue throughout the body.
Lower coQ10 levels in tissues and cells can allow for more damage on nearby lipids, proteins and DNA. Because coQ10 is chiefly instrumental (along with selenium) for the regeneration of vitamin E, another potent fat-soluble antioxidant, the diminished coQ10 levels also lead to declines in levels of vitamin E.
Sources:
1. Yubero-Serrano EM, Delgado-Casado N, Delgado-Lista J et al. Postprandial antioxidant effect of the Mediterranean diet supplemented with coenzyme Q(10) in elderly men and women. Age (Dordr ) 2010.
2. Tangney CC, Kwasny MJ, Li H, Wilson RS, Evans DA, Morris MC. Adherence to a Mediterranean-type dietary pattern and cognitive decline in a community population. Am J Clin Nutr 2010.
19 January 2011
Sweet Sugar Alcohols
You’ve probably noticed sugar alcohols before in chewing gum, candies, baked goods, ice cream and diet drinks. These products are also often labeled “sugar free”, “low in calories”, “diabetic-friendly”, and even “tooth-friendly”. Suspicious? We don’t blame you—when you see the words sugar and alcohol together, there’s plenty of reason to start asking questions. However, upon learning a little about these ingredients you’ll find they have unique benefits.
Sugar alcohol sounds worse than it is because chemists create names based on structures—it’s not the type of alcohol that makes you drunk! Sugar alcohols are so named because they are little carbon rings with OH (oxygen-hydrogen) groups on them, also called polyols. These polyols are naturally found in many plants and are easily recognized by the human body (in fact, human cells produce their own sugar alcohols such as sorbitol).
Fewer calories, greater flavor
The truth is that sugar alcohols, when used in correct amounts, can be safe, natural and healthy. They do provide sweetness and energy, but they have fewer calories than sugar (1-3 per gram versus 4 per gram). This results in a low impact on blood sugar and insulin levels, which is why sugar alcohols are often used in products intended for diabetics.
Some sugar alcohols can also be fermented by friendly probiotic bacteria that make up a healthy intestinal flora. A healthy intestinal flora helps support your immune system and can help improve digestion. In addition, sugar alcohols are seldom able to be metabolized by oral bacteria, which is why they’re “tooth-friendly”. They avoid promotion of tooth decay and cavities.
When used in foods, sugar alcohols can be especially useful. They provide bulk and texture that makes foods and candies more enjoyable to consumers. They enhance and deliver a lasting flavor of sweetness as well as provide a “cooling effect”. Particularly in baked goods, they help prevent browning when exposed to heat and also help those foods stay moist over time.
Maltitol
Not all sugar alcohols are the same. There are many with varying attributes. Maltitol, for example, acts in a different way than, say, xylitol. Maltitol is a disaccharide like sucrose (table sugar) and has almost the same level of sweetness and other properties. This makes it very useful for replacing table sugar while offering fewer calories and avoiding promotion of tooth decay.
When consumed, maltitol is broken down by enzymes to glucose and sorbitol. The glucose is easily absorbed, but the sorbitol is resistant to digestion. Because of its resistance to digestion, sorbitol works in similar fashion to prebiotic fiber, fermenting and feeding that helpful intestinal bacteria.
With maltitol, however, there is a concern about overconsumption, especially in people who are unused to sugar alcohols. Consuming an excess of 10g may cause bloating. And, in absence of soluble fiber, consumption of 20g or more can cause loose stool or diarrhea. You’d have the same laxative effect from eating too many fruits like plums, prunes, apples, pears and cherries. These fruits are all high in sorbitol.
Xylitol and Erythritol
What about xylitol and erythritol? These sugar alcohols are not quite as sweet as sugar or maltitol. And they have a stronger cooling effect than any of the other sugar alcohols. You’d recognize their flavor from sugar-free chewing gum. Like maltitol and sorbitol, they offer fewer calories than sugar and don’t promote tooth decay.
Unlike their counterparts, however, xylitol and erythritol are unlikely to ferment and cause bloating or diarrhea. They are considered non-fermentable because intestinal bacteria have difficulty digesting them. After consumption, most erythritol is absorbed easily into the bloodstream, while xylitol is absorbed more slowly.
Xylitol is notable because it’s found to be more effective than other sugar alcohols in reducing cavities. According to recent studies, primarily from Finland, xylitol may not only reduce potential cavities from forming, but even strengthen teeth. Its mechanism is thought to occur by attracting and “starving” cavity-producing bacteria. The Finnish were the first to extract xylitol from birch, but it’s found in many plants, fruits and vegetables, especially berries, plums and raspberries.
Erythritol is naturally found in grapes, melons and mushrooms, as well as in fermented foods like wine, beer and cheese. Because of its ultra-low impact on blood sugar, you’ll also find erythritol often paired with sugars to lessen its blood-sugar effects in foods, with other sugar alcohols, or with natural sweetening herbs such as stevia in natural sweetener packets.
Reference: Brown A. Understanding Food: Principles and Preparation, 3rd ed. Wadsworth, Cengage Learning. 2008.
Sugar alcohol sounds worse than it is because chemists create names based on structures—it’s not the type of alcohol that makes you drunk! Sugar alcohols are so named because they are little carbon rings with OH (oxygen-hydrogen) groups on them, also called polyols. These polyols are naturally found in many plants and are easily recognized by the human body (in fact, human cells produce their own sugar alcohols such as sorbitol).
Fewer calories, greater flavor
The truth is that sugar alcohols, when used in correct amounts, can be safe, natural and healthy. They do provide sweetness and energy, but they have fewer calories than sugar (1-3 per gram versus 4 per gram). This results in a low impact on blood sugar and insulin levels, which is why sugar alcohols are often used in products intended for diabetics.
Some sugar alcohols can also be fermented by friendly probiotic bacteria that make up a healthy intestinal flora. A healthy intestinal flora helps support your immune system and can help improve digestion. In addition, sugar alcohols are seldom able to be metabolized by oral bacteria, which is why they’re “tooth-friendly”. They avoid promotion of tooth decay and cavities.
When used in foods, sugar alcohols can be especially useful. They provide bulk and texture that makes foods and candies more enjoyable to consumers. They enhance and deliver a lasting flavor of sweetness as well as provide a “cooling effect”. Particularly in baked goods, they help prevent browning when exposed to heat and also help those foods stay moist over time.
Maltitol
Not all sugar alcohols are the same. There are many with varying attributes. Maltitol, for example, acts in a different way than, say, xylitol. Maltitol is a disaccharide like sucrose (table sugar) and has almost the same level of sweetness and other properties. This makes it very useful for replacing table sugar while offering fewer calories and avoiding promotion of tooth decay.
When consumed, maltitol is broken down by enzymes to glucose and sorbitol. The glucose is easily absorbed, but the sorbitol is resistant to digestion. Because of its resistance to digestion, sorbitol works in similar fashion to prebiotic fiber, fermenting and feeding that helpful intestinal bacteria.
With maltitol, however, there is a concern about overconsumption, especially in people who are unused to sugar alcohols. Consuming an excess of 10g may cause bloating. And, in absence of soluble fiber, consumption of 20g or more can cause loose stool or diarrhea. You’d have the same laxative effect from eating too many fruits like plums, prunes, apples, pears and cherries. These fruits are all high in sorbitol.
Xylitol and Erythritol
What about xylitol and erythritol? These sugar alcohols are not quite as sweet as sugar or maltitol. And they have a stronger cooling effect than any of the other sugar alcohols. You’d recognize their flavor from sugar-free chewing gum. Like maltitol and sorbitol, they offer fewer calories than sugar and don’t promote tooth decay.
Unlike their counterparts, however, xylitol and erythritol are unlikely to ferment and cause bloating or diarrhea. They are considered non-fermentable because intestinal bacteria have difficulty digesting them. After consumption, most erythritol is absorbed easily into the bloodstream, while xylitol is absorbed more slowly.
Xylitol is notable because it’s found to be more effective than other sugar alcohols in reducing cavities. According to recent studies, primarily from Finland, xylitol may not only reduce potential cavities from forming, but even strengthen teeth. Its mechanism is thought to occur by attracting and “starving” cavity-producing bacteria. The Finnish were the first to extract xylitol from birch, but it’s found in many plants, fruits and vegetables, especially berries, plums and raspberries.
Erythritol is naturally found in grapes, melons and mushrooms, as well as in fermented foods like wine, beer and cheese. Because of its ultra-low impact on blood sugar, you’ll also find erythritol often paired with sugars to lessen its blood-sugar effects in foods, with other sugar alcohols, or with natural sweetening herbs such as stevia in natural sweetener packets.
Reference: Brown A. Understanding Food: Principles and Preparation, 3rd ed. Wadsworth, Cengage Learning. 2008.
17 January 2011
Brussels sprouts in olive oil
For some fun, I've decided to take pics of some foods I eat and write a bit about them.
For example, these Brussels sprouts in olive oil.
I made a bunch of them for my family and me. They all declined, even my grandma. So I ended up eating them for dinner and for breakfast!
But seriously, they're not only delicious (an acquired taste, I guess), but they're also packed with fiber, carotenoids, vitamins, and minerals.
In addition, like other cruciferous vegetables they do contain some sulfur-rich chemicals that are potentially cancer-protective.
These chemicals are called glucosinolates. When they are chewed they end up as hydrolysis products like indole-3-carbinol.
The breakdown products appear to stimulate the body to eliminate carcinogens more easily and/or by inhibiting cells from becoming cancerous.
They might even induce genomic effects, increasing production of glutathione S-transferases, which metabolize isothiocynates and several other compounds including known carcinogens.
According to epidemiological evidence, eating cruciferous veggies can lower risk of lung, colorectal, prostate, and breadt cancer.
That's why I try to eat cruciferous at least twice a week.
Why the Brussels sprouts? Why not enjoy other cruciferous like broccoli, cabbage, cauliflower, and bok choy?
Mainly, it's because I love the sprouts, especially with olive oil as pictured here. The complexity of its flavor is what I go for really.
But also because they have roughly four times as much glucosinolates than other types of cruciferous veggies.
That's a heavy dose of cancer protection for each sprout!
- Posted using BlogPress from my iPhone
10 January 2011
Vitamin D status affected by obesity
People who are overweight or obese are more likely to have lower circulating levels of vitamin D and may have trouble with conversion to its hormonally active form, a Norwegian study suggests.
These findings, published in the Journal of Nutrition, may partially explain why carrying extra pounds raises risk of several poor health outcomes linked to low vitamin D. The hormonally active form is critical for maintaining cell health, strong bones, a strong immune system, and a healthy heart and brain.
University of Oslo researchers observed almost 1,800 people for six years—about 62 percent obese and 11 percent morbidly obese as indicated by Body Mass Index (BMI)—and found an inverse relationship between higher BMI and serum concentrations of circulating 25(OH)2D and the hormonally active 1,25(OH)2D.
A seasonal variation of both vitamin D metabolites in the obese subjects provided clues that excess weight disturbed the complicated conversion (hydroxylation) of the circulating 25(OH)2D to hormonaly active 1,25(OH)2D in the kidneys.
The authors suggest that measurement of both serum concentrations, 25(OH)2D to 1,25(OH)2D, in overweight and obese persons may be valuable because of “the reduced bioavailability” of the fat-soluble vitamin that “accumulates in excess body fat and muscular tissue.”
The research confirms prior studies’ findings that people who are overweight or obese may need to obtain higher amounts of vitamin D from sun exposure, diet or supplementation. In addition, achieving a healthier BMI is predicted as a way to improve vitamin D status.
Several other factors affect vitamin D status, and include lack of sunlight exposure, skin with higher melanin content (darker skin), older age, low dietary intake, and impaired ability to absorb vitamin D from the diet.
Source: Lagunova Z, Porojnicu AC, Vieth R, Lindberg FA, Hexeberg S and Moan J. Serum 25-Hydroxyvitamin D is a Predictor of Serum 1,25-Dihydroxyvitamin D in Overweight and Obese Patients. J Nutr 2011; 141: 112-117. doi: 10.3945/jn.109.119495.
My thoughts:
I found this to be an interesting paper. The point is that one of the big reasons for why obesity leads to poor health is because it wrecks your ability to use a powerful hormone, vitamin D. People overweight need more vitamin D to cope, plus will improve vitamin D status when they lose weight. A big deal.
These findings, published in the Journal of Nutrition, may partially explain why carrying extra pounds raises risk of several poor health outcomes linked to low vitamin D. The hormonally active form is critical for maintaining cell health, strong bones, a strong immune system, and a healthy heart and brain.
University of Oslo researchers observed almost 1,800 people for six years—about 62 percent obese and 11 percent morbidly obese as indicated by Body Mass Index (BMI)—and found an inverse relationship between higher BMI and serum concentrations of circulating 25(OH)2D and the hormonally active 1,25(OH)2D.
A seasonal variation of both vitamin D metabolites in the obese subjects provided clues that excess weight disturbed the complicated conversion (hydroxylation) of the circulating 25(OH)2D to hormonaly active 1,25(OH)2D in the kidneys.
The authors suggest that measurement of both serum concentrations, 25(OH)2D to 1,25(OH)2D, in overweight and obese persons may be valuable because of “the reduced bioavailability” of the fat-soluble vitamin that “accumulates in excess body fat and muscular tissue.”
The research confirms prior studies’ findings that people who are overweight or obese may need to obtain higher amounts of vitamin D from sun exposure, diet or supplementation. In addition, achieving a healthier BMI is predicted as a way to improve vitamin D status.
Several other factors affect vitamin D status, and include lack of sunlight exposure, skin with higher melanin content (darker skin), older age, low dietary intake, and impaired ability to absorb vitamin D from the diet.
Source: Lagunova Z, Porojnicu AC, Vieth R, Lindberg FA, Hexeberg S and Moan J. Serum 25-Hydroxyvitamin D is a Predictor of Serum 1,25-Dihydroxyvitamin D in Overweight and Obese Patients. J Nutr 2011; 141: 112-117. doi: 10.3945/jn.109.119495.
My thoughts:
I found this to be an interesting paper. The point is that one of the big reasons for why obesity leads to poor health is because it wrecks your ability to use a powerful hormone, vitamin D. People overweight need more vitamin D to cope, plus will improve vitamin D status when they lose weight. A big deal.
09 January 2011
Tucson shooting suspect's possible schizophrenia
I am deeply shocked and saddened as I know many of you are by the news of the senseless shooting that happened in Tucson.
As a resident of Chandler, Ariz., I also found that the incident hit a little too close to home; so, admittedly, I was quick (as many others were) to turn to news reports that offered possible reasons for the heinous act -- politics of the day often pointed out as a motive.
After all, Jared Loughner did target a congresswoman and his Web rantings did wreak of politics. Also, Loughner listed several political books among his favorite reads including Mein Kampf, Animal Farm, and The Communist Manifesto.
However, one book not as often mentioned by the media that caught my eye was this one: One Flew Over the Cuckoo's Nest -- this novel, by Ken Kesey, is one I think reveals more about Loughner than the others.
In short, here's the novel's plot: the setting is a mental hospital, and the tale (in a nutshell) is of a "sane" patient, McMurphy, who has a skewed sense that he has entered a world of psychological control, one that he must escape whatever the cost.
After a failed attempt at freedom and the death of his friend, McMurphy finally takes matters into his own hands, and attacks the "Big Nurse" who symbolically represents all the oppression and brainwashing. It's a kind of suicide act, which eventually has him paying the ultimate price when he is given a lobotomy.
I'm reminded of McMurphy when I read Loughner's disconnected comments in a YouTube video he made before the incident about an imagined fear that the government is "implying mind control and brain wash" of the people, controlling their "grammar structure", and tricking them into believing lies about the U.S. flag.
I'm also reminded of schizophrenia. I'm no psychologist, so a thorough diagnosis is obviously warranted, but I've had the experience of having a person close to me be diagnosed with schizophrenia, and witnessed first-hand the irrational fears they have of the world.
So to me, it appears that Loughner exhibits classic signs of this mental disorder, and that he may have a delusion, or an abnormal interpretation of reality, where the U.S. is one big Cuckoo's nest.
Loughner may have acted in what appears to have been politically motivated, but I think we need to think deeper, and it may serve us all to cease from pointing fingers at political rhetoric (although I agree it should be toned down). Let's look at what's really going on here: mental illness. Loughner did something sick, because he is sick.
What should really be part of our conversation today is how we as a society can do a better job at recognizing the signs of mental illness, such as schizophrenia, and how we can best provide care and treatment to those that suffer from it.
Schizophrenia affects around 2.2 million people in the U.S. alone. Proper diagnosis must be performed by a qualified individual, but we should all at least be somewhat aware of what symptoms to look for and here they are from WebMD:
- Social withdrawal
- Depersonalization
- Loss of appetite
- Loss of hygiene
- Delusions
- Hallucinations
- The sense of being controlled by outside forces
At times, schizophrenia can lead sufferers to behave psychotically, become depressed, cause self-harm, make threats of suicide or violence, commit suicide or acts of violence. The risk of violence from a person with schizophrenia is small, but it can become greater with substance abuse.
We need to spread the message: people who think someone they know someone that may have one or more symptoms of schizophrenia, or know someone with the disorder who has discussed suicide or violence, should help them receive medical care immediately.
In ending this post, I'll just say that my thoughts are with U.S. Rep. Gabrielle Giffords -- who I just learned may have a chance at recovery despite a bullet through her brain -- as well as with the thirteen people who were injured, and the families of the six people who died.
As a resident of Chandler, Ariz., I also found that the incident hit a little too close to home; so, admittedly, I was quick (as many others were) to turn to news reports that offered possible reasons for the heinous act -- politics of the day often pointed out as a motive.
After all, Jared Loughner did target a congresswoman and his Web rantings did wreak of politics. Also, Loughner listed several political books among his favorite reads including Mein Kampf, Animal Farm, and The Communist Manifesto.
However, one book not as often mentioned by the media that caught my eye was this one: One Flew Over the Cuckoo's Nest -- this novel, by Ken Kesey, is one I think reveals more about Loughner than the others.
In short, here's the novel's plot: the setting is a mental hospital, and the tale (in a nutshell) is of a "sane" patient, McMurphy, who has a skewed sense that he has entered a world of psychological control, one that he must escape whatever the cost.
After a failed attempt at freedom and the death of his friend, McMurphy finally takes matters into his own hands, and attacks the "Big Nurse" who symbolically represents all the oppression and brainwashing. It's a kind of suicide act, which eventually has him paying the ultimate price when he is given a lobotomy.
I'm reminded of McMurphy when I read Loughner's disconnected comments in a YouTube video he made before the incident about an imagined fear that the government is "implying mind control and brain wash" of the people, controlling their "grammar structure", and tricking them into believing lies about the U.S. flag.
I'm also reminded of schizophrenia. I'm no psychologist, so a thorough diagnosis is obviously warranted, but I've had the experience of having a person close to me be diagnosed with schizophrenia, and witnessed first-hand the irrational fears they have of the world.
So to me, it appears that Loughner exhibits classic signs of this mental disorder, and that he may have a delusion, or an abnormal interpretation of reality, where the U.S. is one big Cuckoo's nest.
Loughner may have acted in what appears to have been politically motivated, but I think we need to think deeper, and it may serve us all to cease from pointing fingers at political rhetoric (although I agree it should be toned down). Let's look at what's really going on here: mental illness. Loughner did something sick, because he is sick.
What should really be part of our conversation today is how we as a society can do a better job at recognizing the signs of mental illness, such as schizophrenia, and how we can best provide care and treatment to those that suffer from it.
Schizophrenia affects around 2.2 million people in the U.S. alone. Proper diagnosis must be performed by a qualified individual, but we should all at least be somewhat aware of what symptoms to look for and here they are from WebMD:
- Social withdrawal
- Depersonalization
- Loss of appetite
- Loss of hygiene
- Delusions
- Hallucinations
- The sense of being controlled by outside forces
At times, schizophrenia can lead sufferers to behave psychotically, become depressed, cause self-harm, make threats of suicide or violence, commit suicide or acts of violence. The risk of violence from a person with schizophrenia is small, but it can become greater with substance abuse.
We need to spread the message: people who think someone they know someone that may have one or more symptoms of schizophrenia, or know someone with the disorder who has discussed suicide or violence, should help them receive medical care immediately.
In ending this post, I'll just say that my thoughts are with U.S. Rep. Gabrielle Giffords -- who I just learned may have a chance at recovery despite a bullet through her brain -- as well as with the thirteen people who were injured, and the families of the six people who died.
26 December 2010
Hydroponics and health
I've had friends of mine try to get me into hydroponics before, but I haven't ever been truly interested until today, when @TheEconomist tweeted links to these videos on "vertical farming," the brainchild of Dickson Despommier, professor of public health in environmental health sciences at Columbia University.
The magazine reports mainly on this urban-type agriculture as a way to bring local, sustainable food to places like New York City, the logistical problems, and what this might mean for battling climate change. There was also mention of how hydroponics allows for introduction of nutrients in the water, reduces need for fertilizing, and how it being a closed system recycles water.
And, the interview (below) with Despommier speaks to how this idea could potentially turn the "parasitism" of cities into productive ecosystems.
These are neat topics, although I still wonder about how realistic it is on a grand scale based on concerns about use of artificial lighting, expense, and so on.
However, from a nutritional standpoint, urban agriculture does lend to great possibilities for producing food that is healthier, cleaner and safer. As I see it, the possibilities for human health is endless.
Urban agriculture allows for much more control over heavy metals with use of refined minerals in the hydroponics fertilizer. Plus, you could standardized to reasonable exactness, the amounts the plants would receive of minerals. Then, with a controlled environment, the potential of having a standardized product comes into the picture too.
This might sound really lame to some people, but it's a nutritionist's dream -- Can you imagine walking into a grocery store and seeing fruits and vegetables with standardized nutrition facts panels complete with quantities of minerals, and possibly vitamins and phytonutrients?
You could also do a much better job controlling and enhancing the flavor of plants, which is highly dependent on what comes through the water. By adding in concentrated extracts, for example, of vanilla or orange, you could give plants certain notes or essences.
Anyway, I might have to head down to Tucson, Arizona, to check out what's currently largest system of hydroponics in the country -- and maybe have a bite of something tasty.
I might also have to order me some kind of home hydroponics system.
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