Don't be so hasty to throw away slightly over-ripe apples and pears.
A group of scientists at the University of Innsbruck in Austria claim to be the first to identify the decomposition mechanism and products of apples and pears, and their findings suggest that as these fruits start to go bad their antioxidant levels dramatically increase. Key to the process is the change in color that occurs as fruits ripen.
According to lead researcher Berhard Krautler, fruit undergoes a similar decomposition process as leaves turn from green to red to yellow to brown. This color change is caused by the breakdown and disappearance of chlorophyll, which is what gives leaves and fruits their green color.
Through their research with botanists over the past several years, they claim to have identified the first decomposition products in leaves. These are colorless, polar nonfluorescing chlorophyll catabolytes (NCCs) that contain four pyrrole rings - like chlorophyll and iron.
After examining the peels of apples and pears, they found that in ripe fruits, NCCs replace the chlorophyll, especially in the peel and the flesh immediately below it.
"When chlorophyll is released from its protein complexes in the decomposition process, it has a phototoxic effect: when irradiated with light, it absorbs energy and can transfer it to other substances. For example, it can transform oxygen into a highly reactive, destructive form," reported the research team.
"However, the NCCs have the opposite effect," they said.
"These are powerful antioxidants and can thereby play an important physiological role for a plant. In the same way, when these are consumed as part of the human diet, they can play the same anti-oxidative role in humans."
Now isn't this great news at the height of autumn apple and pear season?
Saturday, November 10, 2007
Wednesday, November 7, 2007
Viruses & Obesity
No one that I know disputes the role that diet and activity play in maintaining a healthy weight - if you consume more calories than you burn in daily activity, you gain weight. But does that fully explain the amazing prevalence of obesity in the United States today?
Please don't use any of the information in this post as an excuse to pig out, because it's still theory at this point.
Richard Atkinson, MD, suggests there is a growing body of evidence demonstrating that viruses may play a role in causing obesity in humans.
Dr Atkinson is the director of Obetech Obesity Research Center in Richmond, VA. One of his recent articles, published in the October 2007 Mayo Clinic Proceedings, discusses five animal viruses and three human viruses than have been shown to cause obesity in laboratory studies.
According to Dr. Atkinson, several studies offer ample evidence that animals infected with certain human viruses experience excess weight gain and fat storage.
When researchers infected animal subjects with a human virus known as Human Ad-36, they reported measurable increases in the infected animals' body fat and the visceral fat that surrounds the organs deep within the belly. In addition, studies also demonstrated that infection with Ad-36 and the resulting weight gain could be transmitted from infected animals to uninfected animals.
Information on virus-induced obesity in human subjects is much more limited. Citing his own study conducted in 2005, Dr. Atkinson also showed a connection between obesity and exposure to the Ad-36 virus in humans.
Dr. Atkinson's study screened for antibodies to Ad-36 (a sign of exposure to this virus) in 502 people of varying body weights, both obese and non-obese, from three cities in the United States. Ad-36 antibodies were found in 30 percent of obese individuals and 11 percent of lean individuals. Study results also showed highly significant differences in body mass index (BMI) between antibody-positive and antibody-negative individuals.
Dr. Atkinson also highlighted a study that looked at 89 sets of American adult twins and screened them for Ad-36. Because twins tend to be similar in many characteristics, including body weight, the researchers looked at twin pairs where one twin tested positively for Ad-36 and the other did not.
"Antibody-positive twins were slightly, but significantly, heavier and fatter than their antibody negative co-twins," says Dr. Atkinson. "The infected twins had a higher BMI and a greater percent of body fat than the uninfected co-twins."
Dr. Atkinson's article also explores what current research has to say about the possible mechanisms underlying virus-induced obesity. Some research suggests that viral infections have a direct effect on adipocytes, cells that manufacture and store fat, turning on the enzymes of fat accumulation and recruitment of new adipocytes.
What's the next step for this research? According to Dr. Atkinson, "the body of evidence linking adenoviruses to obesity in humans is now sufficient to think about the next step. Ideally, we could prevent infection and virus-induced obesity with a vaccine for the obesity viruses."
Should this be true, development of a human vaccine of this sort would take several years, so it's way too early to give up watching your diet and getting plenty of exercise.
Please don't use any of the information in this post as an excuse to pig out, because it's still theory at this point.
Richard Atkinson, MD, suggests there is a growing body of evidence demonstrating that viruses may play a role in causing obesity in humans.
Dr Atkinson is the director of Obetech Obesity Research Center in Richmond, VA. One of his recent articles, published in the October 2007 Mayo Clinic Proceedings, discusses five animal viruses and three human viruses than have been shown to cause obesity in laboratory studies.
According to Dr. Atkinson, several studies offer ample evidence that animals infected with certain human viruses experience excess weight gain and fat storage.
When researchers infected animal subjects with a human virus known as Human Ad-36, they reported measurable increases in the infected animals' body fat and the visceral fat that surrounds the organs deep within the belly. In addition, studies also demonstrated that infection with Ad-36 and the resulting weight gain could be transmitted from infected animals to uninfected animals.
Information on virus-induced obesity in human subjects is much more limited. Citing his own study conducted in 2005, Dr. Atkinson also showed a connection between obesity and exposure to the Ad-36 virus in humans.
Dr. Atkinson's study screened for antibodies to Ad-36 (a sign of exposure to this virus) in 502 people of varying body weights, both obese and non-obese, from three cities in the United States. Ad-36 antibodies were found in 30 percent of obese individuals and 11 percent of lean individuals. Study results also showed highly significant differences in body mass index (BMI) between antibody-positive and antibody-negative individuals.
Dr. Atkinson also highlighted a study that looked at 89 sets of American adult twins and screened them for Ad-36. Because twins tend to be similar in many characteristics, including body weight, the researchers looked at twin pairs where one twin tested positively for Ad-36 and the other did not.
"Antibody-positive twins were slightly, but significantly, heavier and fatter than their antibody negative co-twins," says Dr. Atkinson. "The infected twins had a higher BMI and a greater percent of body fat than the uninfected co-twins."
Dr. Atkinson's article also explores what current research has to say about the possible mechanisms underlying virus-induced obesity. Some research suggests that viral infections have a direct effect on adipocytes, cells that manufacture and store fat, turning on the enzymes of fat accumulation and recruitment of new adipocytes.
What's the next step for this research? According to Dr. Atkinson, "the body of evidence linking adenoviruses to obesity in humans is now sufficient to think about the next step. Ideally, we could prevent infection and virus-induced obesity with a vaccine for the obesity viruses."
Should this be true, development of a human vaccine of this sort would take several years, so it's way too early to give up watching your diet and getting plenty of exercise.
Tuesday, November 6, 2007
Nutrient Synergy
Is there more to a carrot than beta carotene? Is lycopene the best we get from tomatoes? Is vitamin C the only reason to eat an orange? And when we heap our plates with wild salmon, are we serving up something other than Omega3s?
Meta-analysis of several individual vitamin studies suggests that food may be more than just a sum of its nutrient parts.
Well, duh!!
In order to publish or perish, some people in the scientific research community used the funding-dependent pharmaceutical paradigm and designed nutrition studies around individual nutrients including beta carotene, lutein, calcium, lycopene, individual vitamin and minerals, along with other phytochemical nutrients, in order to look at their health benefits in the human body.
The less creative, and usually desperate, publish or perish research folks are now doing meta-analysis on those poorly designed studies, which if nothing else, provides frequently much-needed headline material for the lay press.
University of Minnesota professor of epidemiology, David R. Jacobs, PhD, argued in a piece in yesterday's NYT that nutrition researchers should focus on whole foods and the full-spectrum of nutrients rather than only on single nutrients.
Well, duh again!!
He also argued that we need to study the effects of whole foods and the full-spectrum of nutrients on disease prevention in the healthy population, not just on sick people. He stated in the interview, "Food and nutrient synergy, rather than the biological activity of just a few key nutrients, is the real reason that certain diets, like those consumed in parts of the Mediterranean and Japan, appear to lower the risks of heart disease and other health problems."
We can only hope that those folks who are overdosing on the latest nutrient craze like it might be the second anti-aging coming (think fish oil capsules) will take Dr. Jacobs' nutrient synergy concerns to heart and eat a balanced diet with a full-spectrum multiple along with their fish oil to guarantee the nutrients that are lost during today's food processing methods.
Meta-analysis of several individual vitamin studies suggests that food may be more than just a sum of its nutrient parts.
Well, duh!!
In order to publish or perish, some people in the scientific research community used the funding-dependent pharmaceutical paradigm and designed nutrition studies around individual nutrients including beta carotene, lutein, calcium, lycopene, individual vitamin and minerals, along with other phytochemical nutrients, in order to look at their health benefits in the human body.
The less creative, and usually desperate, publish or perish research folks are now doing meta-analysis on those poorly designed studies, which if nothing else, provides frequently much-needed headline material for the lay press.
University of Minnesota professor of epidemiology, David R. Jacobs, PhD, argued in a piece in yesterday's NYT that nutrition researchers should focus on whole foods and the full-spectrum of nutrients rather than only on single nutrients.
Well, duh again!!
He also argued that we need to study the effects of whole foods and the full-spectrum of nutrients on disease prevention in the healthy population, not just on sick people. He stated in the interview, "Food and nutrient synergy, rather than the biological activity of just a few key nutrients, is the real reason that certain diets, like those consumed in parts of the Mediterranean and Japan, appear to lower the risks of heart disease and other health problems."
We can only hope that those folks who are overdosing on the latest nutrient craze like it might be the second anti-aging coming (think fish oil capsules) will take Dr. Jacobs' nutrient synergy concerns to heart and eat a balanced diet with a full-spectrum multiple along with their fish oil to guarantee the nutrients that are lost during today's food processing methods.
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