Sunshine vitamin cuts cancer risk by 40%

By Daily Mail Reporter
Last updated at 10:02 AM on 22nd January 2010

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Having a higher level of vitamin D in your blood means you are less like to develop bowel cancer than those with low levels, according to scientists.

A study published in the British Medical Journal has concluded that those with the highest levels of the vitamin were at 40 per cent lower risk of developing the disease compared with those with the lowest levels.

Scientists looked at vitamin D quantities in 1,248 people with bowel cancer and 1,248 controls in the largest ever study of the subject.

Two sources of Vitamin D: Eggs and supplement pills. Having a higher level of vitamin D in your blood means you are 'less like to develop bowel cancer'

The research was carried out by scientists at the International Agency for Research on Cancer (IARC) in Lyon, France, and Imperial College London, and was funded by World Cancer Research Fund (WCRF).

It comes after medical experts expressed concern yesterday about the rising number of cases of rickets - caused by vitamin D deficiency - and called for it to be added to milk and other food products.

The main source of vitamin D is sunlight, through skin exposure, but it is also present in a small number of foods, such as oily fish or cod liver oil.

According to the research team, although the latest study provides evidence of a link between vitamin D and bowel cancer it does not prove that taking vitamin D supplements prevents the disease.

More...

• The return of rickets: Victorian disease on the rise due to poor diet and lack of exercise

More studies are needed to find out the potential impact on other cancers and the effects of taking extra vitamin D doses, scientists said.

Dr Panagiota Mitrou, science programme manager for WCRF, said: 'This is the biggest ever study on this subject and there is now quite a lot of evidence from studying populations that people who have low levels of vitamin D are more likely to develop bowel cancer.

'The next step is to carry out new clinical trials to try to confirm whether vitamin D supplementation can reduce the risk of bowel cancer and whether there are any harmful effects of higher levels of vitamin D.

'Looking at the figures in this latest study, it suggests that increasing the UK's vitamin D intake by ten per cent could prevent seven per cent of cases.

'And when you think that there are about 37,500 cases diagnosed in the UK every year, that could have a big impact.

'But we need to emphasise that, for the moment, the findings need to be treated with caution and they are certainly not enough evidence to suggest that we should be taking supplements to increase levels of vitamin D.

'The best advice for reducing risk of bowel cancer remains to stop smoking, maintain a healthy weight, be regularly physically active, to eat more fibre and less red and processed meats and to cut down on alcohol.'

Dr Mazda Jenab, the lead author of the study from the International Agency for Research on Cancer, said: 'Our results support a role for vitamin D in the etiology of colorectal cancer, but this has to be balanced with caution regarding the potential toxic effects of too much vitamin D and the fact that very little is known about the association of vitamin D with either increased or reduced risk of other cancers.'

More blood pressure worry: It's linked to dementia

If the cardiologist's warnings don't scare you, consider this: Controlling blood pressure just might be the best protection yet known against dementia.

In a flurry of new research, scientists scanned people's brains to show hypertension fuels a kind of scarring linked to later development of Alzheimer's disease and other dementias. Those scars can start building up in middle age, decades before memory problems will appear.

The evidence is strong enough that the National Institutes of Health soon will begin enrolling thousands of hypertension sufferers in a major study to see if aggressive treatment — pushing blood pressure lower than currently recommended — better protects not just their hearts but their brains.

"If you look ... for things that we can prevent that lead to cognitive decline in the elderly, hypertension is at the top of the list," Dr. Walter Koroshetz, deputy director of NIH's National Institute of Neurological Disorders and Stroke, told The Associated Press.

Age is the biggest risk factor for Alzheimer's disease and other forms of dementia that affect about one in eight people 65 or older.

Scientists have long noticed that some of the same triggers for heart disease — high blood pressure, obesity, diabetes — seem to increase the risk of dementia, too. But for years, they thought that link was with "vascular dementia," memory problems usually linked to small strokes, and not the scarier classic Alzheimer's disease.

Now those lines are blurring as specialists realize that many if not most patients have a mix of the two dementias. Somehow, factors like hypertension — blood pressure readings of 140 over 90 or higher — that weaken arteries also seem to spur Alzheimer's disease-like processes.

One suspect: Scarring known as white matter lesions. White matter acts as the brain's telephone network, a system of axons, or nerve fibers, that allow brain cells to communicate with each other. Even slightly elevated blood pressure can damage the tiny blood vessels that nourish white matter, interrupting those signals.

Among the strongest new studies:

_MRI scans showed women 65 and older with high blood pressure had significantly more white matter lesions in their brains eight years later. The study included 1,403 women who were enrolled in a memory subset of the landmark Women's Health Initiative that tracked postmenopausal health. The worse their blood pressure, the higher volume of white matter damage, says the study published online last month in the Journal of Clinical Hypertension.

"This is a silent disease in the brain," says lead researcher Dr. Lewis Kuller of the University of Pittsburgh. "It's evolving over time and it leads to very bad outcomes."

_The journal Stroke just published similar evidence from a Johns Hopkins University-led study that tracked 983 people for more than 15 years, starting in middle age. The longer people spent with uncontrolled high blood pressure, the more white matter damage they accumulated. The researchers could see a change with each 20-point jump in too-high systolic pressure, the top number in a blood-pressure reading.

Clearly, hypertension alone doesn't doom someone to later dementia. Far more people, nearly one in three U.S. adults, have hypertension.

And there are plenty of other reasons to lower blood pressure: Hypertension is a leading cause of heart attacks, strokes and kidney failure.

But while some studies have found hypertension treatment lowered the dementia risk, others haven't.

Enter the NIH's SPRINT study, which in a few months is to begin enrolling 7,500 hypertension patients age 55 and older around the country. The test: Whether aggressive treatment to lower systolic blood pressure below 120 — what's considered normal — will prove healthier than today's guidelines that urge getting it below 140, or 130 for diabetics.

The main focus is on heart and kidney health. But all participants will be screened for dementia, and a subset will undergo repeated cognitive testing and MRI scans to tell if lowering blood pressure also protects against a slide toward dementia. Another question: If older patients can tolerate bigger than usual blood pressure drops without side effects, such as falls.

With dementia rising fast as the population grays, even a small effect from better blood pressure control could have a big public health impact, says Dr. William Thies of the Alzheimer's Association.

Other dementia-preventing efforts, such as targeting the sticky amyloid plaques in Alzheimer's patients brains, haven't panned out so far — while hypertension control has little downside, notes Pittsburgh's Kuller.

"Until I can tell you how to get rid of amyloid in your brain, take care of the blood pressure."

Studies demonstrate link among Alzheimer's disease, Down syndrome and atherosclerosis

And that's not all. Down syndrome, artery-clogging cardiovascular disease, and possibly even diabetes, appear to share a common disease mechanism with Alzheimer's disease,

Dr. Potter and colleagues at the Florida Alzheimer's Disease Research Center, USF Health Byrd Alzheimer's Institute, recently reported.

The researchers' two papers - one in Molecular Biology of the Cell and the other in PLoS ONE -- implicate the Alzheimer's-associated protein beta amyloid (amyloid protein), which damages the microtubule transport system responsible for moving chromosomes, proteins and other cargo around inside cells. Both studies were done in mice and humans cell cultures modeling Alzheimer's disease. Together, the laboratory discoveries suggest that protecting the microtubule network from this amyloid damage might be an effective way to prevent or even reverse Alzheimer's disease and associated disorders.

The first paper, by Antoneta Granic and colleagues published online Dec. 23 in Molecular Biology of the Cell, provides the mechanism behind previous work by Dr. Potter's laboratory showing that all Alzheimer's disease patients harbor some cells with three copies of chromosome 21, known as trisomy 21, instead of the usual two. Trisomy 21 is a characteristic shared by all the cells in people with the birth defect Down syndrome as well. This earlier work demonstrated that Alzheimer's disease could be considered a late onset form of Down syndrome.

By age 30 to 40, all people with Down syndrome develop the same brain pathology seen in Alzheimer's disease, including a nerve-killing buildup of sticky amyloid protein clumps. This contributes to accelerated nerve cell loss and dementia.

With the study reported in MBC, Dr. Potter and his colleagues now show that the Alzheimer's-associated amyloid protein is the culprit that interferes with the microtubule transport system inside cells. The microtubules are responsible for segregating newly duplicated chromosomes as cells divide.

"Beta amyloid basically creates potholes in the protein highways that move cargo, including chromosomes, around inside cells," said Dr. Potter, who holds the Eric Pfeiffer Endowed Chair for Research on Alzheimer's Disease.

When the microtubule network is disrupted, chromosomes can be incorrectly transported as cells divide and the result is new cells with the wrong number of chromosomes and an abnormal assortment of genes. For example, Down syndrome cells contain three copies of the beta amyloid gene on chromosome 21 - leading to more accumulation of the "bad" amyloid protein over a lifetime, Dr. Potter says. "Alzheimer's disease probably is caused in part from the continuous development of new trisomy 21 nerve cells, which amplify the disease process by producing extra beta amyloid."

The second paper by lead author Jose Abisambra and colleagues, published Dec. 31 in the online journal PLoS ONE, describes another consequence of the damaged microtubule network caused by the amyloid protein.

Many Alzheimer's disease patients also commonly develop vascular diseases and diabetes. Whether this coincidence is bad luck or due to shared disease processes is intensely debated. Research teams have investigated the role that low-density lipoprotein (LDL), the bad cholesterol that causes atherosclerosis, cardiovascular disease and stroke, may play in the development of Alzheimer's with mixed results. However, the USF group focused on the amyloid protein's potential effects on LDL metabolism. The receptor needed to detect and use LDL is among the proteins transported by the microtubules.

As previously reported by their colleagues in the MBC paper, the second USF team found that the amyloid protein inflicts damage to the microtubule network. As a consequence, the receptor needed to pull LDL circulating throughout the bloodstream into the body's cells has trouble getting to the cell surface to retrieve this bad cholesterol. This interference with LDL metabolism may allow bad cholesterol to build up in into plaques that choke off blood supply to the brain and heart in people with Alzheimer's, Dr. Potter said.

Similarly, other key proteins - including insulin receptors and receptors for brain signaling molecules -- are also likely locked inside cells when the transport system is damaged by amyloid or other factors. "The insulin receptors are needed to get blood sugar inside the cell where it can be used for energy. The nerve cell signaling receptors help promote memory and learning," Dr. Potter said. "So, if these receptors are unable to function properly, it may lead to diabetes and problems with learning and memory."

"We're beginning to understand how conditions like cardiovascular disease and diabetes may manifest some of the same underlying disease processes as Alzheimer's disease," he said, "rather than being independent diseases that just happen to develop in the same patient."

More information: Journal articles cited:

1. "Alzheimer Ab Peptide Induces Chromosome Mis-segregation and Aneuploidy, including Trisomy 21; Requirement for Tau and APP," Antoneta Granic, Jaya Padmanabhan, Michelle Norden, and Huntington Potter. Molecular Biology of the Cell, Dec. 23, 2009.

2. "LDLR Expression and Localization Are Altered in Mouse and Human Cell Culture Models of Alzheimer's Disease," Jose Abisambra, Tina Fiorella, Jaya Padmanabhan, Peter Neame, Inge Wefes, and Huntington Potter, PLoS ONE, Volume 5, Issue 1. (January 2010).

Provided by University of South Florida Health

Studies demonstrate link among Alzheimer's disease, Down syndrome and atherosclerosis

And that's not all. Down syndrome, artery-clogging cardiovascular disease, and possibly even diabetes, appear to share a common disease mechanism with Alzheimer's disease,

Dr. Potter and colleagues at the Florida Alzheimer's Disease Research Center, USF Health Byrd Alzheimer's Institute, recently reported.

The researchers' two papers - one in Molecular Biology of the Cell and the other in PLoS ONE -- implicate the Alzheimer's-associated protein beta amyloid (amyloid protein), which damages the microtubule transport system responsible for moving chromosomes, proteins and other cargo around inside cells. Both studies were done in mice and humans cell cultures modeling Alzheimer's disease. Together, the laboratory discoveries suggest that protecting the microtubule network from this amyloid damage might be an effective way to prevent or even reverse Alzheimer's disease and associated disorders.

The first paper, by Antoneta Granic and colleagues published online Dec. 23 in Molecular Biology of the Cell, provides the mechanism behind previous work by Dr. Potter's laboratory showing that all Alzheimer's disease patients harbor some cells with three copies of chromosome 21, known as trisomy 21, instead of the usual two. Trisomy 21 is a characteristic shared by all the cells in people with the birth defect Down syndrome as well. This earlier work demonstrated that Alzheimer's disease could be considered a late onset form of Down syndrome.

By age 30 to 40, all people with Down syndrome develop the same brain pathology seen in Alzheimer's disease, including a nerve-killing buildup of sticky amyloid protein clumps. This contributes to accelerated nerve cell loss and dementia.

With the study reported in MBC, Dr. Potter and his colleagues now show that the Alzheimer's-associated amyloid protein is the culprit that interferes with the microtubule transport system inside cells. The microtubules are responsible for segregating newly duplicated chromosomes as cells divide.

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"Beta amyloid basically creates potholes in the protein highways that move cargo, including chromosomes, around inside cells," said Dr. Potter, who holds the Eric Pfeiffer Endowed Chair for Research on Alzheimer's Disease.

When the microtubule network is disrupted, chromosomes can be incorrectly transported as cells divide and the result is new cells with the wrong number of chromosomes and an abnormal assortment of genes. For example, Down syndrome cells contain three copies of the beta amyloid gene on chromosome 21 - leading to more accumulation of the "bad" amyloid protein over a lifetime, Dr. Potter says. "Alzheimer's disease probably is caused in part from the continuous development of new trisomy 21 nerve cells, which amplify the disease process by producing extra beta amyloid."

The second paper by lead author Jose Abisambra and colleagues, published Dec. 31 in the online journal PLoS ONE, describes another consequence of the damaged microtubule network caused by the amyloid protein.

Many Alzheimer's disease patients also commonly develop vascular diseases and diabetes. Whether this coincidence is bad luck or due to shared disease processes is intensely debated. Research teams have investigated the role that low-density lipoprotein (LDL), the bad cholesterol that causes atherosclerosis, cardiovascular disease and stroke, may play in the development of Alzheimer's with mixed results. However, the USF group focused on the amyloid protein's potential effects on LDL metabolism. The receptor needed to detect and use LDL is among the proteins transported by the microtubules.

As previously reported by their colleagues in the MBC paper, the second USF team found that the amyloid protein inflicts damage to the microtubule network. As a consequence, the receptor needed to pull LDL circulating throughout the bloodstream into the body's cells has trouble getting to the cell surface to retrieve this bad cholesterol. This interference with LDL metabolism may allow bad cholesterol to build up in into plaques that choke off blood supply to the brain and heart in people with Alzheimer's, Dr. Potter said.

Similarly, other key proteins - including insulin receptors and receptors for brain signaling molecules -- are also likely locked inside cells when the transport system is damaged by amyloid or other factors. "The insulin receptors are needed to get blood sugar inside the cell where it can be used for energy. The nerve cell signaling receptors help promote memory and learning," Dr. Potter said. "So, if these receptors are unable to function properly, it may lead to diabetes and problems with learning and memory."

"We're beginning to understand how conditions like cardiovascular disease and diabetes may manifest some of the same underlying disease processes as Alzheimer's disease," he said, "rather than being independent diseases that just happen to develop in the same patient."

More information: Journal articles cited:

1. "Alzheimer Ab Peptide Induces Chromosome Mis-segregation and Aneuploidy, including Trisomy 21; Requirement for Tau and APP," Antoneta Granic, Jaya Padmanabhan, Michelle Norden, and Huntington Potter. Molecular Biology of the Cell, Dec. 23, 2009.

2. "LDLR Expression and Localization Are Altered in Mouse and Human Cell Culture Models of Alzheimer's Disease," Jose Abisambra, Tina Fiorella, Jaya Padmanabhan, Peter Neame, Inge Wefes, and Huntington Potter, PLoS ONE, Volume 5, Issue 1. (January 2010).

Provided by University of South Florida Health

Non-stick chemical linked to thyroid disease

A chemical used to make non-stick coatings for saucepans and as a stain and water repellent for carpets and fabrics has been linked with thyroid problems in adults.

Scientists who tested the blood of 4,000 US adults between 1996 and 2006 for the presence of the chemical perfluorooctanoic acid (PFOA) found the 25 per cent with the highest levels had twice the incidence of thyroid problems.

PFOA has been produced for 50 years and is used in a wide variety of materials. It is thought to enter the body in the diet or as dust breathed in through the lungs.

Animal studies have shown that the chemical can affect thyroid function, which is essential for maintaining heart rate, regulating body temperature and supporting other bodily functions. Researchers from the Unversity of Exeter, who conducted the study published in Environmental Health Perspectives, said they had demonstrated an association but had not proved causality. “Our results highlight the need for further research,” they said.

Reaction from other experts was sceptical. Ieuan Hughes, professor of paediatrics at the University of Cambridge and chair of the Committee on the Toxicity of Chemicals in the Environment, said the evidence for the link was “tenuous.”

Can Flame-Retardant Chemicals Cause Infertility?

Women with high levels of a common type of flame retardant in their blood took longer to become pregnant than women with low levels. PBDEs, or polybrominated diphenyl ethers are found in common household items including plastics, fabrics, carpets, insulated wires, and foam furniture.

Researchers at the University of California, Berkeley found that for each 10-fold increase in the concentration of PBDEs in the blood, a woman's odds of conceiving decreased by 30 percent. For women actively attempting to become pregnant, the odds of conceiving dropped by 50 percent in any given month.

"We aren't looking at infertility, just subfertility, because all the women in our study eventually became pregnant," the study's lead author, Kim Harley, adjunct assistant professor of maternal and child health and associate director of the Center for Children's Environmental Health Research at UC Berkeley's School of Public Health, said in a statement. "Had we included infertile couples in our study, it is possible that we would have seen an even stronger effect from PBDE exposure.

"There have been numerous animal studies that have found a range of health effects from exposure to PBDEs, but very little research has been done in humans," Harley said. "This latest paper is the first to address the impact on human fertility, and the results are surprisingly strong. These findings need to be replicated, but they have important implications for regulators."

Although there are 209 different mixtures for PBDEs, only three formulations � pentaBDE, octaBDE, and decaBD � were developed for commercial use as flame retardants. They became common in the 1970s when new fire safety standards were implemented throughout the United States.

The EPA banned two of the PBDE mixtures in 2005 (pentaBDE and octaBDE), and the third will be phased out in 2013.

"The good news is these chemicals have or are being phased out," Hardley told the San Francisco Chronicle. "The bad news is their legacy will continue because of their presence in a lot of items in our homes."

"Every month, it seems, there are new studies linking this class of chemicals to problematic health concerns," Judy Levin, pollution prevention coordinator for the Center for Environmental Health in Oakland, told the Chronicle. "A bigger question is why are chemicals allowed to be placed in commerce and into our bodies before their toxicity is fully understood?"

How can you avoid PBDEs? Use these tips from the Environmental Working Group:

MORE>>>>>>>>

Bipolar Diagnosis Jumps in Tots

The number of children aged 2 to 5 who have been diagnosed with bipolar disorder and prescribed powerful antipsychotic drugs has doubled over the past decade, according to research released on Friday.

The research suggests that while it is still rare to prescribe powerful psychiatric drugs to 2-year-olds, the practice is becoming more frequent.

The data, compiled from 2000 to 2007, and published in the Journal of the American Academy of Child & Adolescent Psychiatry, could inform testimony at the upcoming Boston-area murder trials of the parents of 4-year-old Rebecca Riley. The girl died of an overdose of mood-stabilizing medication in 2006.

A Boston child psychiatrist, Kayoko Kifuji, diagnosed Riley with bipolar disorder and attention deficit hyperactivity disorder when she was 30 months old, and placed her on several powerful drugs: Depakote, an antiseizure medication also used for bipolar disorder, and clonidine, a blood pressure medication.

Kifuji's testimony may be crucial to the fate of Michael and Carolyn Riley, who face first-degree murder charges. A grand jury and a review by the state's medical licensing board cleared the doctor of wrongdoing.

Prosecutors claim the Rileys deliberately overmedicated their daughter to subdue her. The couple say they were following Kifuji's instructions and their daughter died of pneumonia.

The case has shone the spotlight again on a debate within the psychiatric profession about whether bipolar disorder can be diagnosed in very young children and whether it is wise to prescribe powerful medications.

Bipolar disorder, characterized by severe mood swings, was once thought to emerge only during adolescence or later. But Dr. Joseph Biederman, a child psychiatrist at Harvard University, transformed views on the subject by arguing that children could have the disorder at extremely young ages.

He is credited with spearheading a more than 40-fold increase in the number of children diagnosed with bipolar disorder over the past decade.

Biederman was accused in 2008 by Republican U.S. Senator Charles Grassley of failing to fully disclose payments by drug companies, including some that produced medication for bipolar disorder. Biederman declined to be interviewed about the latest study.

"The psychiatric diagnosis of very young children is anything but an exact science," said Harry Tracy, a psychologist and publisher of NeuroInvestment, a monthly publication specializing in central nervous system disorders.

"Such disparate causes as ADHD, depression, bipolar disorder, sexual abuse, and family dysfunction can produce very similar symptoms in a toddler."

The report's author, Mark Olfson, professor of clinical psychiatry at Columbia University, said about 1.5 percent of all privately insured children between the ages of 2 and 5, or one in 70 children, received some sort of psychotropic drug�whether an antipsychotic, a mood stabilizer, a stimulant or an antidepressant�in 2007.

If a child is diagnosed with bipolar disorder between the ages of 2 and 5, about half are prescribed an antipsychotic, such as Eli Lilly & Co's Zyprexa, AstraZeneca Plc's Seroquel, and Johnson & Johnson's Risperdal. They are prescribed to about one in 3,000 2-year-olds, according to his report.

"There might be a role for these drugs but only after you've tried other interventions, with the parents, or with the parents and child together, but that is not happening when you examine the billing records," Olfson said.

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A spanked child may be a better adult: study

Young children spanked by their parents may perform better at school later on and grow up to be happier, according to a controversial new study that is drawing scorn from critics.

The U.S.-based research states that spanking children up to six years old made them more successful in school, more optimistic about life, more likely to take voluntary work, and more keen to attend university than their never-spanked counterparts.

The findings were drawn from interviews of more than 2,600 people, including a core group of 179 teenagers. The teens were asked how old they were when they were spanked and how often it happened. Their answers were compared with information they gave about their behaviour that could have been influenced by smacking.

Lead researcher Marjorie Gunnoe, a psychology professor at Michigan's Calvin College, said her research is not a green light for parents to spank their children, but rather a red light for those groups who want corporal punishment banned.

"There isn't enough evidence that kids who are not spanked look better than kids who are spanked," said Prof. Gunnoe, a mother of two children (she has spanked only one). "Some need the extra deterrent ... for young children, the external motivator is more effective."

However this latest research, which Prof. Gunnoe admitted was previously rejected by two professional journals, including the Journal of Family Psychology, contradicts other findings that spanking is counterproductive.

Dr. Diane Sacks, former president of the Canadian Paediatric Society, says research has proven that spanking, whether short or long-term, leads to "bad, physical behaviour."

"Many studies show that when children are spanked in order to teach, they don't learn," said Dr. Sacks, a pediatrician with 35 years experience. "When afraid, children learn poorly. Fear is a very bad teacher."

Instead, Dr. Sacks suggests non-physical methods to control the child. Time-outs, keeping the child out of the situation, or a firm "no" are much better forms of discipline.

Grant Wilson, president of the Canadian Children's Rights Council, suggested that the study's results may have been influenced by Calvin College's Christian affiliation, adding that some religious groups have opposed abolition of corporal punishment.

"People get confused over what discipline is -- it's not hitting children," Mr. Wilson said. "There are better methods of parenting rather than hitting.... It's not OK to hit children."

The spanking study had Prof. Gunnoe interviewing teenagers between ages 12 and 18. Their answers to a questionnaire about their childhood discipline was compared with their current behaviour, possibly affected by spanking. These measures covered topics around good behaviour such as academic aspirations, doing well in school and optimism for the future. The bad outcomes included violence, depression and anti-social behaviour.

Teenagers who had been spanked between ages two to six performed slightly better on the positive behaviors, but no worse on the negative measures than those who had never been spanked, the study found.

Only the teenagers who were still being spankYoung children spanked by their parents may perform better at school later on and grow up to be happier, according to a controversial new study that is drawing scorn from critics.

The U.S.-based research states that spanking children up to six years old made them more successful in school, more optimistic about life, more likely to take voluntary work, and more keen to attend university than their never-spanked counterparts.

The findings were drawn from interviews of more than 2,600 people, including a core group of 179 teenagers. The teens were asked how old they were when they were spanked and how often it happened. Their answers were compared with information they gave about their behaviour that could have been influenced by smacking.

Lead researcher Marjorie Gunnoe, a psychology professor at Michigan's Calvin College, said her research is not a green light for parents to spank their children, but rather a red light for those groups who want corporal punishment banned.

"There isn't enough evidence that kids who are not spanked look better than kids who are spanked," said Prof. Gunnoe, a mother of two children [she has spanked only one]. "Some need the extra deterrent ... for young children, the external motivator is more effective."

However this latest research, which Prof. Gunnoe admitted was previously rejected by two professional journals, including the Journal of Family Psychology, contradicts other findings that spanking is counterproductive.

Dr. Diane Sacks, former president of the Canadian Paediatric Society, says research has proven that spanking, whether short or long-term, leads to "bad, physical behaviour."

"Many studies show that when children are spanked in order to teach, they don't learn," said Dr. Sacks, a pediatrician with 35 years experience. "When afraid, children learn poorly. Fear is a very bad teacher."

Instead, Dr. Sacks suggests non-physical methods to control the child. Time-outs, keeping the child out of the situation, or a firm "no" are much better forms of discipline.

Grant Wilson, president of the Canadian Children's Rights Council, suggested that the study's results may have been influenced by Calvin College's Christian affiliation, adding that some religious groups have opposed abolition of corporal punishment.

"People get confused over what discipline is -- it's not hitting children," Mr. Wilson said. "There are better methods of parenting rather than hitting.... It's not OK to hit children."

The spanking study had Prof. Gunnoe interviewing teenagers between ages 12 and 18. Their answers to a questionnaire about their childhood discipline was compared with their current behaviour, possibly affected by spanking. These measures covered topics around good behaviour such as academic aspirations, doing well in school and optimism for the future. The bad outcomes included violence, depression and anti-social behaviour.

Teenagers who had been spanked between ages two to six performed slightly better on the positive behaviors, but no worse on the negative measures than those who had never been spanked, the study found.

Only the teenagers who were still being spanked showed clear behavioural problems, receiving the worst scores.

However, the results were less clear for the teenagers spanked between ages seven to 11. Against the never-spanked group, they scored slightly worse on the negative behaviours, being more prone to violence and anti-social behaviour. But they also scored well on the positive measures.

The study also compared teenagers from different ethnic groups and genders, but found little difference between them.ed showed clear behavioural problems, receiving the worst scores.

However, the results were less clear for the teenagers spanked between ages seven to 11. Against the never-spanked group, they scored slightly worse on the negative behaviours, being more prone to violence and anti-social behaviour. But they also scored well on the positive measures.

The study also compared teenagers from different ethnic groups and genders, but found little difference between them.

Read more: http://www.nationalpost.com/news/story.html?id=2409510#ixzz0d0zf8i2o
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Study Finds Exposure to Chemical Pollutants Increases Fat

Researchers have for the first time found a connection between exposure to certain chemicals and insulin resistance, according to a study published in the online edition of Environmental Health Perspectives.

A group of European scientists examined whether exposure to persistent organic pollutantsobesity and difficulty regulating blood levels of fat and sugar. (POPs) contributed to insulin resistance, which has been increasing around the world. More than 25 percent of U.S. adults suffer from metabolic conditions stemming from insulin resistance that include fatigue,

Researchers fed rats a high-fat diet of either crude or refined fish oil from farmed Atlantic salmon over 28 days. The crude fish oil contained average levels of POPs that people are exposed to through fish consumption, while the refined oil contained none. Both had equal fat levels.

They found that rats exposed to the crude fish oil developed belly fat and could not regulate fat properly. They had higher levels of cholesterol and several fatty acids in their livers. Those exposed to the refined fish oil experienced none of those symptoms.

Researchers said the findings provide "compelling evidence" of a causal relationship between POP exposure common in the food chain and insulin resistance, and highlight the need to understand the interactions of POPs and fat-containing foods such as fish, dairy products and meat.

How to deal with POPs is particularly challenging because they persist in the environment for long periods and can build up in animals' tissues.

The 2001 Stockholm Convention, which the United States has ratified but not signed, lists and bans numerous POPs from manufacture and use. The researchers say their evidence reinforces the need to have international agreements aimed at limiting the release of POPs into the environment in an effort to protect public health.

Studies demonstrate link among Alzheimer's disease, Down syndrome and atherosclerosis

Nearly 20 years ago Huntington Potter kicked up a storm of controversy with the idea that Down syndrome and Alzheimer's were the same disease. Now the evidence is in: He was right.

And that's not all. Down syndrome, artery-clogging cardiovascular disease, and possibly even diabetes

, appear to share a common disease mechanism with Alzheimer's disease,

Dr. Potter and colleagues at the Florida Alzheimer's Disease Research Center, USF Health Byrd Alzheimer's Institute, recently reported.

The researchers' two papers - one in Molecular Biology of the Cell and the other in PLoS ONE -- implicate the Alzheimer's-associated protein beta amyloid (amyloid protein), which damages the microtubule transport system responsible for moving chromosomes, proteins and other cargo around inside cells. Both studies were done in mice and humans cell cultures modeling Alzheimer's disease. Together, the laboratory discoveries suggest that protecting the microtubule network from this amyloid damage might be an effective way to prevent or even reverse Alzheimer's disease and associated disorders.

The first paper, by Antoneta Granic and colleagues published online Dec. 23 in Molecular Biology of the Cell, provides the mechanism behind previous work by Dr. Potter's laboratory showing that all Alzheimer's disease patients harbor some cells with three copies of chromosome 21, known as trisomy 21, instead of the usual two. Trisomy 21 is a characteristic shared by all the cells in people with the birth defect Down syndrome as well. This earlier work demonstrated that Alzheimer's disease could be considered a late onset form of Down syndrome.

By age 30 to 40, all people with Down syndrome develop the same brain pathology seen in Alzheimer's disease, including a nerve-killing buildup of sticky amyloid protein clumps. This contributes to accelerated nerve cell loss and dementia. With the study reported in MBC, Dr. Potter and his colleagues now show that the Alzheimer's-associated amyloid protein is the culprit that interferes with the microtubule transport system inside cells. The microtubules are responsible for segregating newly duplicated chromosomes as cells divide.
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"Beta amyloid basically creates potholes in the protein highways that move cargo, including chromosomes, around inside cells," said Dr. Potter, who holds the Eric Pfeiffer Endowed Chair for Research on Alzheimer's Disease.

When the microtubule network is disrupted, chromosomes can be incorrectly transported as cells divide and the result is new cells with the wrong number of chromosomes and an abnormal assortment of genes. For example, Down syndrome cells contain three copies of the beta amyloid gene on chromosome 21 - leading to more accumulation of the "bad" amyloid protein over a lifetime, Dr. Potter says. "Alzheimer's disease probably is caused in part from the continuous development of new trisomy 21 nerve cells, which amplify the disease process by producing extra beta amyloid."

The second paper by lead author Jose Abisambra and colleagues, published Dec. 31 in the online journal PLoS ONE, describes another consequence of the damaged microtubule network caused by the amyloid protein.

Many Alzheimer's disease patients also commonly develop vascular diseases and diabetes. Whether this coincidence is bad luck or due to shared disease processes is intensely debated. Research teams have investigated the role that low-density lipoprotein (LDL), the bad cholesterol that causes atherosclerosis, cardiovascular disease and stroke, may play in the development of Alzheimer's with mixed results. However, the USF group focused on the amyloid protein's potential effects on LDL metabolism. The receptor needed to detect and use LDL is among the proteins transported by the microtubules.

As previously reported by their colleagues in the MBC paper, the second USF team found that the amyloid protein inflicts damage to the microtubule network. As a consequence, the receptor needed to pull LDL circulating throughout the bloodstream into the body's cells has trouble getting to the cell surface to retrieve this bad cholesterol. This interference with LDL metabolism may allow bad cholesterol to build up in into plaques that choke off blood supply to the brain and heart in people with Alzheimer's, Dr. Potter said.

Similarly, other key proteins - including insulin receptors and receptors for brain signaling molecules -- are also likely locked inside cells when the transport system is damaged by amyloid or other factors. "The insulin receptors are needed to get blood sugar inside the cell where it can be used for energy. The nerve cell signaling receptors help promote memory and learning," Dr. Potter said. "So, if these receptors are unable to function properly, it may lead to diabetes and problems with learning and memory."

"We're beginning to understand how conditions like cardiovascular disease and diabetes may manifest some of the same underlying disease processes as Alzheimer's disease," he said, "rather than being independent diseases that just happen to develop in the same patient."

More information: Journal articles cited:

1. "Alzheimer Ab Peptide Induces Chromosome Mis-segregation and Aneuploidy, including Trisomy 21; Requirement for Tau and APP," Antoneta Granic, Jaya Padmanabhan, Michelle Norden, and Huntington Potter. Molecular Biology of the Cell, Dec. 23, 2009.

2. "LDLR Expression and Localization Are Altered in Mouse and Human Cell Culture Models of Alzheimer's Disease," Jose Abisambra, Tina Fiorella, Jaya Padmanabhan, Peter Neame, Inge Wefes, and Huntington Potter, PLoS ONE, Volume 5, Issue 1. (January 2010).

Provided by University of South Florida Health