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The UV Foundation dubbed February “Vitamin D Deficiency Month” in a nationwide effort to raise awareness about vitamin D deficiency and its negative soundness effects. In addition to increasing the risk of many types of cancer and heart disease, vitamin D infirmity is also linked to many common wintertime complaints such as fatigue, depression and aches and pains.

A Harvard Medical School study published in the New England Journal of Medicine has reported that 60% of Americans are vitamin D deficient. This is particularly troublesome since vitamin D is proven to ward off many types of cancer including colon, prostate and breast cancer and is further shown to guard against heart disease, MS, and other chronic health problems.

Moderate exposure to sunlight or UV light is the absolute best way to help the body manufacture the vitamin D it needs. Unfortunately, during the bleak winter months it becomes harder to get the necessary amount of vitamin D. In act, it is impossible to get the necessary amount in cities northerly of 37 degrees latitude for as crowd similar to 6 months out of the year. That includes cities probable Richmond, VA, St. Louis, MO, and Sacramento, CA, and all cities farther north.

For those concerned about vitamin D deficiency and who find it difficult to get the necessary amount of sunlight, there are other ways to get your dose of the “sunshine vitamin.” Vitamin D supplements, moderate exposure to UV light from a tanning bed, and a diet rich in Vitamin D fortified foods command all help fight against vitamin D deficiency. However, experts agree that the easiest and best way to get the requisite amount of vitamin D is through sunlight and UV light.

“More and more science is emerging every set time confirming the enormous health benefits of vitamin D and the significant health consequences of not getting enough of it,” said Tim Miller, Communications Director for the UV Foundation. We launched “Vitamin D shortage Month” to educate the public about the dangers of this growing problem and to ’shed some light’ on potential solutions.

The UV Foundation is committed to funding educational efforts designed to increase the public awareness of the biologic effects of ultraviolet light

UV Foundation
http://www.uvfoundation.org

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Eating fish is not the but way of increasing the omega-3s in our diet, as “The Queen of Fats: Why Omega-3s were removed from our diet and what we can do to replace them,” by science writer Susan Allport shows.

Many of the foods we eat every day, including eggs and bacon, used to be full of these pure nutrients — when the animals they came from were eating grass, insects, and other green foods. Omega-3s originate in the green leaves of plants (not fish, as many people believe), and they accumulate in animals that eat those leaves, including fish.

Now that our livestock eat mostly seeds and grains, our foods are full of a second family of polyunsaturated fats, omega-6s which are much in greater numbers prevalent in those parts of plants. This second parents and children of polyunsaturated fats is also essential for health, but it competes with omega-3s for positions in cell membranes and affects cells in different ways. Fats in this family are not as dynamic, or speedy, as omega-3s. They also produce cell messengers called prostaglandins that are far more inflammatory and far more likely to cause thrombosis or blood clotting. As our reliance on seeds and seed oils has increased since the turning of the last century, so has the incidence of heart disease and other inflammatory disorders.

It may not be practical for us to eat only grass-fed meats and eggs. But it’s also not possible as antidote to us to catch, or call forth, enough fish to correct this problem. We can, however, increase our omega-3s by eating small amounts of fish and grass-fed animals and using vegetable oils with a healthier balance of omega-6s to omega-3s. The Queen of Fats (University of California Press), out in paperback February, 2008 and described as a “must learned” by physicians and nutritionists, explains the reasoning behind these simple steps and tells the compelling history of the omega-3 research.

Axel F. Bang PR & Marketing
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NEW YORK (Reuters Health) - Extremely obese adults in need of a kidney transplant appear to wait longer for a bestower; donator organ than their thinner counterparts do, a study has found.

The findings, according to researchers, suggest there may be a predisposition in the way donor kidneys are allocated.

Analyzing a decade's worth of national transplant data, researchers at Johns Hopkins University in Baltimore found that morbidly portly patients - those who are 100 or more pounds overweight — on the kidney transplant waiting list were 44 percent less likely to receive a donor organ as normal-weight patients.

There was no similar disparity seen among overweight or mildly obese patients, the researchers report in the Journal of the American Society of Nephrology.

"The results be the same a potential bias in vocal organs allocation that is not consistent with the goals of our allocation system," Dr. Dorry L. Segev, the lead researcher on the study, said in a statement.

In the U.S., the United Network for Organ Sharing (UNOS) oversees the allocation of donor organs. Segev and his colleagues based their findings on UNOS data for 132,353 patients on the waiting choose for a kidney transplant between 1995 and 2006.

They found that even when they considered medical factors that affect a person's eligibility for a donor kidney — such as age or diabetes — the odds of receiving a transplant decline with the severity of a patient's obesity.

Waiting-list patients who were morbidly stout were the least likely to get a transplant. Similarly, those considered severely obese were 28 percent less likely to receive a donor kidney than normal-weight patients were.

In addition, at the time that a donor organ did befit available, the most obese patients were more likely than other patients to be "bypassed" — meaning their doctors were more agreeable to decline the offer of a kidney.

"It is possible that providers are bypassing obese patients and in place transplanting non-obese patients because they feel that kidneys are a scarce resource and they want the kidneys to go to the patients who will benefit most from them," Segev said.

"However," he added, "in that place is strong evidence that even obese patients will benefit significantly from a kidney transplant."

Moreover, Segev noted, the organ allocation system was not set up to operate on such medical judgments, and all patients placed on the transplant waiting list are supposed to have a fair employ place of getting an organ.

He pointed to two possible "disincentives" for transplant surgeons to operate on severely obese patients. One is that the surgery for these patients is more difficult and they tend to have more complications and longer hospital stays, Medicare pays a set amount for the operation.

A second disincentive, according to Segev, may be the fact that surgeons' and hospitals' transplant success rates are publicly reported. This may make them reluctant to take on a large number of high-risk patients.

If bias against severely gross transplant candidates does exist, it's not immediately clear how to remedy the problem, Segev and his colleagues point out.

Another study at Johns Hopkins is currently looking at whether obese transplant candidates should first be referred for weight-loss surgery to attenuate their peril of post-transplant complications.

SOURCE: Journal of the American Society of Nephrology, February 2008.

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It would seem that the old wives’ tale “an apple a day keeps the doctor away” has borne matured ovary again in that a new study suggests that apples, bananas and oranges protect against neurodegenerative diseases, including Alzheimer’s.

The study is published in the early online issue of the Journal of Food Science and was conducted by scientists based at Cornell University, Geneva, New York, and colleagues from several universities in Korea, including Gyeongsang National University, Kyung Hee University and Korea University in Seoul.

The most common fruits in both Western and Eastern diets are apples, bananas, and oranges, offering an important source of vitamins, minerals, and fibre, wrote the researchers.

In their study, they exposed PC12 cells, that are very similar to neurons, to phenolics extracted from the three fruits and then put the cells under oxidative stress using H2O2 (hydrogen peroxide).

The PC12 cells were bred using a mix of horse serum and fetal bovine serum. They extracted the fruit phenolics using ultrasound on dried fruit samples in an aqueous methanol solution.

Using a test called MTT reduction, the researchers discovered that the phenolic phytochemicals of the fruits had prevented a significant proportion of cells from succumbing to neurotoxicity from oxidative stress, with varying degrees of success.

MTT reduction measures the cell killing susceptibility of a toxin by comparing the amount of surviving mitochondrial enzymes with a control batch of cells not exposed to the toxin.

Of the three fruits, apples appeared to contain the most antioxidants, then bananas and then oranges.

Further tests with lactate dehydrogenase and trypan blue exclusion assays showed that the fruit extracts had reduced neuronal cell membrane damage induced by oxidative stress.

The researchers concluded that:

“These results suggest that fresh apples, banana, and orange in our daily diet along with other fruits may countenance neuron cells against oxidative stress-induced neurotoxicity and may play an important role in reducing the risk of neurodegenerative disorders such as Alzheimer’s disease.”

Alzheimer’s complaint (AD) is a progressive disease characterized by dint of. loss of memory and reduced ability to think and process information. Many research studies have revealed that the brains of people who die of AD show signs of different types of cell damage from oxidative stress.

The authors wrote that fruits and vegetables contain many different antioxidant substances, including vitamin C and polyphenolic phytochemicals. However, the authors had suggested in a previous study that the main antioxidative effect of apples came from the “synergistic activities of phenolics rather than vitamin C”.

In their conclusion they also referred to another study that showed apple juice with antioxidants protected brain tissue from oxidative damage and improved cognitive performance in mice that had been genetically induced with AD.

“Effects of Banana, Orange, and Apple on Oxidative Stress-Induced Neurotoxicity in PC12 Cells.”
H.J. Heo, S.J. Choi, S.-G. Choi, D.-H. Shin, J.M. Lee, C.Y. Lee.
Journal of Food Science (Online Early Articles).
Published online on 24th January 2008.
doi:10.1111/j.1750-3841.2007.00632.x

Click here for Abstract.

Sources: journal article, Blackwell Publishing press release.

Written by: Catharine Paddock, PhD
Copyright: Medical News Today
Not to be reproduced lacking permission of Medical News Today

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Obesity experts say despite the rise of numbers of overweight people, the obesity epidemic may be exaggerated.

Last week, the UK health secretary declared that we are in a grip of an obesity prevalent, but does the evidence stack up? Researchers in this week’s BMJ debate the issue.

Claims about an obesity epidemic often exceed the scientific evidence and mistakenly suggest an unjustified degree of certainty, argue Patrick Basham and John Luik.

For example, the average population mode of estimating weight gain in the United States in the past 42 years is 10.9kg or 0.26kg a year. Yet, between 1999-2000 and 2001-2002, there were no significant changes in the prevalence of overweight or obesity among US adults or in the prevalence of overweight among children.

Furthermore, they say, the categories of normal, overweight, and obese is entirely arbitrary and at probability with the underlying evidence about the association between body mass index and mortality.

For example, the study on which the bands for overweight and obesity in the US are based found that the death risks for men with a body mass index of 19-21 were the same as those for men who were overweight and obese (29-31). Other studies have shown negligible differences between body mass index and death rates.

The association of overweight and obesity with higher risks of disease is equally unclear, they write. And, despite supposedly abnormal levels of overweight and obesity, life expectancy continues to increase.

They suggest that some public health professionals may have deliberately exaggerated the risks of overweight and obesity, and our capacity to prevent or treat them on a population wide basis, in the interests of health. They warn that this has unwelcome implications for science policy and for evidence based medicine.

unless Robert Jeffery and Nancy Sherwood argue that a large body of scientific evidence shows that obesity is a major global health problem.

In the US, the prevalence of obesity in 1976-80 was 6.5% among 6-11 year olds and 5% among 12-17 year olds. In 2003-4 it was 19% and 17% respectively. Europe can also calculate upon to see the numbers of overweight and obese children rising by around 1.3 million a year by the agency of 2010.

The risks of obesity on many serious health conditions including vainglorious blood pressure, diabetes, heart disease and some forms of cancer, are also serious and well established, they write.

Most health economists and epidemiologists agree that the contribution of obesity to course healthcare costs is high and that it is likely to get much higher. Some have argued that we may even see real falls in life expectancy within a few decades, they aggregate.

In summary, a large material part of evidence documents that over-nutrition and obesity are a major global health problem, say the authors. With the continuing rise in obesity and limited treatment efficacy, options for averting a poor public health outcome seem to rest either on the hope that scientists are wrong in their projections or speedy investment in the evolution of more effective public health measures to deal through it.

They think the second option a more prudent scientific and policy choice.

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Purdue University and USDA-Agricultural Research Service scientists have discovered that a type of gene in grain-producing plants halts infection by a disease-causing fungus that can destroy crops vital for human food supplies.

The research team is the first to show that the same biochemical process protects an entire plant family - grasses - from the devastating, fungal pathogen. The naturally occurring disease resistance probably is responsible for the survival of grains and other grasses over the past 60 million years.

The findings will stimulate the design of new resistance strategies against additional diseases in grasses and other plants. Grasses’ ability to ward off pathogens is a major concern because grasses, including corn, barley, rice, oats and sorghum, provide most of the calories people consume, and some species also increasingly are investigated for conversion into energy.

A resistance gene, first discovered in corn, and the fungal toxin-fighting enzyme it produces apparently provide a biological mechanism that guards all grass species from this fungus, said Guri Johal, a Purdue associate professor of botany and engender pathology. He is senior and corresponding author of the study published this week (Jan. 28-Feb. 1) in Early Edition, the online version of the Proceedings of the National Academy of Sciences. It power of choosing appear in the Feb. 5 print edition.

“We think that if the gene Hm1 had not evolved, then grasses would have had a hard time surviving, thriving or, at least, the geographic distribution would have been restricted,” Johal said. “This plant resistance gene is durable and is indispensible against this fungal group, which has the ability to destroy any part of the plant at any staging of development.”

In 1943 a related fungus decimated rice crops in Bengal, causing a catastrophic famine in which 5 million people starved. The same fungal arrange was responsible for the other couple recorded epidemics in grasses in the 20th century, including the 1970 southern corn leaf blight that destroyed 15 percent of the U.S. corn crop.

The study, part of an effort to prevent future crop crises, besides provides new information about the evolution of plant-pathogen interaction, report Johal and his colleagues, including USDA-Agricultural Research Service researcher Steven Scofield and plant geneticist Michael Zanis. The findings have implications for continued survival and further evolution of grasses, which also include rye, bluegrass, reed canary grass and bamboo.

Johal and the research team began this study for they had a hunch that a genetic mechanism similar to the one protecting corn from a fungus, called Cochliobolus carbonum race 1 (CCR1), might also be at work in other grasses. They knew that all grasses had genes similar, or homologous, to Hm1, but not whether the same genetic machinery was providing resistance against the fungus and its toxin. 

To determine if the same biochemical processes were at work to prevent grass susceptibility to the fungus family, Johal and his team shut off the Hm1 homologue in some barley plants. Next, they infected the test barley with fungus.

In barley that no longer had a functioning Hm1 homologous gene, the fungus, with the help of its toxin, caused disease in the plant. The resulting tissue damage on the barley leaves was typical of maize leaf blight symptoms in corn.

Some of the research barley, what one. had a functioning Hm1 gene, was inoculated with the fungus. The results showed that the opposition mechanism was the same as the one that prevents the fungus’ disease infection in corn.

As in corn, the Hm1-like gene produced an enzyme that disarmed the fungus’ disease-causing toxin. The detoxification isolated the infection at the site where the fungus invaded. The research with the barley also showed that, as in make drunk susceptible to the fungus, infection insulation occurs if the species of cellular cryptogam doesn’t produce the toxin.

Now that the researchers know that Hm1 homologues in all grasses apparently trigger the same resistance to the fungal family, the next step will be to investigate how the fungal toxin facilitates disease when not degraded by dint of. Hm1.

Scofield is a scientist in the Purdue-based USDA-ARS Crop Production and Pest Control Research Unit and a Purdue subordinate part assistant professor. Zanis is an assistant professor in the Purdue Department of Botany and Plant Pathology. The other researchers involved in the study were Anoop Sindhu, co-lead author, former botany and plant pathology postdoctoral research assistant and now an Iowa State University assistant scientist; Satya Chintamanani, co-lead author and a postdoctoral research assistant; and Amanda Brandt, a USDA-ARS research technician.

Purdue University, the National Science Foundation and the USDA-Agricultural Research Service provided funding for this research.

http://www.purdue.edu

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When it comes to heart health, the largest and most common form of fat in fodder and the bloodstream triglycerides has taken a back seat to “bad” LDL cholesterol and “good” HDL cholesterol in the public’s awareness. That’s changing as researchers get a grip on how triglycerides influence the risk of heart disease, reports the February 2008 issue of the Harvard Heart Letter.

Triglycerides are in the danger zone when they slide above 200 milligrams per deciliter of blood. To keep triglycerides in check, lifestyle changes are usually the best place to start, notes the Harvard Heart Letter. These eight steps can lead to impressive reductions in triglycerides:

1. Beware of baneful fats. Cut back on saturated fat (found in red meat and full-fat dairy foods) and trans fat (in some fried and commercially prepared foods).

2. Go for good carbs. Eat whole grains and divide back on sugary drinks and foods.

3. Check your highly rectified spirit. Moderate drinking is good for the heart, unless you are a “responder” in whom alcohol dramatically boosts triglycerides. To determine if you’re a responder, avoid alcohol for three weeks and have your triglycerides tested.

4. Go fish. Omega-3 fats in some fish lower triglycerides. Have fish twice a week.

5. Aim for a healthy weight. If you are overweight, aim to lose at least 5% to 10% of your efficacy to lower triglycerides.

6. Get moving. Exercise lowers triglycerides and boosts HDL.

7. Stop smoking. Smoking isn’t good for triglyceride levels (or anything else).

8. Get help from a medication. Niacin, fibrates, fish oil, and cholesterol-lowering statins have all been shown to lower triglycerides.

Harvard Heart Letter
Harvard Health Publications Harvard Medical School 10 Shattuck St., Ste. 612
Cambridge, MA 02115
United States
http://www.health.harvard.edu

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by Mike Howard

Let’s talk roughage… Not the most exciting topic in the world but a very significant piece of any dietary puzzle nonetheless. We’ve all heard about the importance of fiber when it comes to the gut, but here are more other factoids about fiber you may find interesting.

That, or you will click out of here to search for something besides exciting – like trucking regulations.

1. Fiber is the non-digestible element of a plant. It is broken into 2 categories – soluble and insoluble.
2. Soluble fiber forms a gel when it comes in contact with water. Sources include; Oats, beans, apples, nuts, seeds, oranges and berries.
3. Insoluble fiber remains intact as it passes end the digestive tract. Sources include; whole grains, wheat bran, seeds, carrots and other vegetables
4. Only 1 in 10 North Americans earn the recommended 25-40g of fiber per day!
5. We eat about 33% less fiber than we did a century ago (a rough(a hundred years) estimate).
6. Fiber works magically in the digestive tract as it slows down the thoroughfare of food in the inclination and speeds it through the intestines. It also promotes the growth of beneficial bacteria
7. Fiber slows the release of life-blood sugar, what one. helps keep weight and type II diabetes at bay.
8. Fiber has a modest effect on cholesterol still its real cardiovascular benefit is in its effect on C-reactive protein – a marker of inflammation that is far more telling than cholesterol when it comes to heart ail risk. Ones study showed that those who ate about 22g of fiber had each average of 63% lower levels of C-RP than those who ate about 10g.
9. One study showed that adding 10g of fiber resulted in a 20% decrease in heart attacks.
10. A study of over 400 adults with previous suicide attempts found only 2 nutritional differences between them and the rule group without such history. One of them was low fiber intake (the other was polyunsaturated fat intake). This may not be causative but it’s interesting.
11. Interestingly, fiber consumption does not appear to reduce the risk of colon cancer
12. Those who support from IBS may even benefit from the elimination of certain fibers such as bran to reduce abdominal distress
13. Eat plenty of fruits, vegetables, beans, seeds nuts and whole grains to get your fiber intake up. A gradual increase is best.

Sources:

1. American Journal of Clinical Nutrition, April 2006; vol 83: pp 760-766
2. Nutrition (2005)
3. New England Journal of Medicine. 342: 1149, 2000
4. Journal of the American Medical Association Feb. 1996 447-451
5. Digestive Diseases and Sciences (2005)

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by J. Foster

Researchers have criticized the low-fat dietary guidelines of the last few decades.

“[…] the previous priority given to a ‘low-fat intake’ may lead race to believe that, as long as fat intake is scurvy, the diet will be entirely healthful. This belief could engender an overconsumption of total calories in the form of carbohydrates, resulting in the adverse metabolic consequences of high-carbohydrate diets,”

Dr. Marantz goes on to point out a trend that seems to be largely ignored:

“an increasing prevalence of obesity in the United States has corresponded roughly with some absolute increase in carbohydrate destruction.”

Marantz is quick to say that in that place may not be causation - but that there is “a realistic possibility” that our dietary recommendations have guide to an increase in obesity.

It took decades to get people obsessed with low-fat. Will it take decades to annul this? Diet food didn’t help us.

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Less than one quarter of Minnesota adults will be at a healthy weight by dint of. 2020 according to a new report issued by Blue Cross and Blue Shield of Minnesota (Blue Cross) and the Minnesota Department of Health. The study, entitled fleshiness and Future Health be anxious Costs: A Portrait of Two Minnesotas, highlights the fact that adult obesity-related health conditions could cost Minnesota at least an additional $900 million per year by 2010 and $3.7 billion more per year by 2020. This report provides the first Minnesota-specific projections of future health care costs absolutely attributable to obesity.

"We called the report ‘Two Minnesotas’ because there are two pictures that can emerge during the term of our state," said Marc Manley, M.D. M.P.H., vice president and medical director for population health at Blue Cross. "In one scenario, obesity trends persist and fuel rising health care costs. In the second scenario, we slow or thwart the growth of obesity and save $3.7 billion in health care costs by means of year. Working together, we can prevent the first scenario from coming true, but we have some significant work to do."

According to the U.S. Centers for Disease Control, Minnesota ranks 21st out of all the states on the measure of obesity, and Minnesota residents are decorous obese at a rate faster than the rest of the nation. "We can improve that ranking, get Minnesotans in better health and spend less on health care if we focus on prevention and address our patterns of physical inactivity and unhealthy eating," uttered Minnesota’s Commissioner of Health, Sanne Magnan, M.D., Ph.D.

The report’s projections are based on an analysis by Kenneth E. Thorpe, Ph.D., of Emory University, who worked with researchers from Blue Cross, the Minnesota Department of Health (MDH) and the Minnesota State Demographer.

The projections indicate that the consequences for the state’s economy will be severe. Left unchecked, nearly 31 percent of the overall increase in health care costs from 2005 to 2020 will be exactly to projected increases in the numbers of people considered obese and overweight. By 2020, it will cost a projected 61 percent more to treat an obese person than a healthy-weight body. Being overweight or obese puts people at higher risk for conditions like high cholesterol, hypertension, and diabetes, which impact quality of life, length of life and health care costs.

"The good news is even modest luck at curbing the rising rates of obesity could improve residents’ health and also decrement the projected burden of health care costs in Minnesota," noted Manley. "Where we could shine as a state and have the biggest impact is grant that health care professionals, policy makers, community leaders, employers and individuals worked together to create environments where making the healthy choice — eating a balanced diet and getting regular physical activity — is the easy choice."

"There’s a lot of public awareness around reducing tobacco use, but there’s less awareness about the need for increased physical activity and healthy eating," said Magnan. "We’re trying to increase awareness of this issue."
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