Study Analysis Fails to Link Saturated Fat, Heart Disease

The saturated fat found mainly in meat and dairy products has a bad reputation, but a new analysis of published studies finds no clear link between people's intake of saturated fat and their risk of developing heart disease.

Research has shown that saturated fat can raise blood levels of "bad" LDL cholesterol, and elevated LDL is a risk factor for heart disease and stroke. Because of this, experts generally advise people to limit their intake of fatty meat, butter, and full-fat dairy.

The American Heart Association (AHA) suggests that adults get no more than 7 percent of their daily calories from the fat; for someone who eats 2,000 calories a day, that translates into fewer than 16 grams of saturated fat per day.

MORE>>>>>>>>>

More Than Half of Americans Use Internet for Health Information

More than half of Americans looked up health information on the Internet last year, U.S. government researchers reported on Tuesday.

But only 5 percent used email to communicate with their doctors, the survey by the National Center for Health Statistics found.

Researchers at the center used a survey of 7,192 adults aged 18 to 64 questioned between January and June 2009. MORE>>>>>>>>>

10 Easy Ways to Keep Your Brain Sharp

Saving your memory as you age doesn't just involve your brain; healthy choices in all areas of your life will keep your brain and your body in tip-top form. Follow these 10 easy tips to keep your brain sharp now and later. MORE>>>>>>>>>>

Fish oil supplements 'beat psychotic mental illness'

Taking a daily fish oil capsule can stave off mental illness in those at highest risk, trial findings suggest.

A three-month course of the supplement appeared to be as effective as drugs, cutting the rate of psychotic illness like schizophrenia by a quarter.

The researchers believe it is the omega-3 in fish oil - already hailed for promoting healthy hearts - that has beneficial effects in the brain.

A "natural" remedy would be welcomed, Archives of General Psychiatry says.

"The finding that treatment with a natural substance may prevent, or at least delay, the onset of psychotic disorder gives hope that there may be alternatives to antipsychotic drugs," the study authors said.

If young people can be treated successfully with fish oils, this is hugely preferable to treating them with antipsychotics
Alison Cobb
Mind

Antipsychotic drugs are potent and can have serious side effects, which puts some people off taking them.

Fish oil supplements, on the other hand, are generally well tolerated and easy to take, say the scientists.

The international team from Austria, Australia and Switzerland tested the treatment in 81 people deemed to be at particularly high risk of developing psychosis.

Natural choice

Their high risk was down to a strong family history of schizophrenia, or similar disorders, or them already showing mild symptoms of these conditions themselves.

For the test, half of the individuals took fish oil supplements (1.2 grams of omega-3 fatty acids) for 12 weeks, while the other half took only a dummy pill. Neither group knew which treatment they were receiving.

Dr Paul Amminger and his team followed the groups for a year to see how many, if any, went on to develop illness.

Two in the fish oil group developed a psychotic disorder compared to 11 in the placebo group.

Based on the results, the investigators estimate that one high-risk adult could be protected from developing psychosis for every four treated over a year.

They believe the omega-3 fatty acids found in the supplements may alter brain signalling in the brain with beneficial effects.

Alison Cobb, of the mental health charity Mind, said: "If young people can be treated successfully with fish oils, this is hugely preferable to treating them with antipsychotics, which come with a range of problems from weight gain to sexual dysfunction, whereas omega-3s are actually beneficial to their general state of health.

"These are promising results and more research is needed to show if omega-3s could be an alternative to antipsychotics in the long term."

Millions of people 'waste their time by jogging'

Researchers have discovered that the health benefits of aerobic exercise are determined by our genes - and can vary substantially between individuals.

Around 20 per cent of the population do not get any significant aerobic fitness benefit from regular exercise, according to an international study led by scientists at the University of London.

For these people, regular jogging and gym work will do little to ward off conditions like heart disease and diabetes which aerobic exercise is generally thought to resist.

Researchers say they would be better off abandoning their exercise regime and focusing on other ways of staying healthy - such as improving their diet or taking medication.

James Timmons of the Royal Veterinary College at the University of London, who led the study, said that the discovery would pave the way for more personalised treatments, with patients able to take DNA tests to find out the most effective way of keeping their own hearts healthy.

It could also be used to root out would-be recruits to the Armed Forces who will never be able to reach the required fitness standards.

Dr Timmons said the research broke new ground by using the human genome - the genetic map of the body which was decoded by scientists 10 years ago - to suggest improvements to healthcare.

"This would be one of the first examples of personalised, genomic-based medicine," he said.

As part of the research, published in the Journal of Applied Physiology, more than 500 participants in Europe and the US were asked to undergo various aerobic training programmes in line with government advice to do 30 minutes of exercise five times a week.

By the end of the 20, 12 and six week programmes the majority of people had shown a measurable improvement in how much oxygen their body consumes during exercise, a key indicator of aerobic fitness.

But 20 per cent saw their maximum oxygen increase by less than five per cent - a negligible improvement. Around 30 per cent showed no increase in insulin sensitivity, meaning that the exercise did not reduce their risk of diabetes.

A pioneering analysis of muscle tissue samples taken from the participants revealed a set of about 30 genes that predicted the increase in oxygen intake. Of these, 11 were shown to have a particular impact on how much a person could benefit from aerobic exercise.

Dr Timmons said: “We know that low maximal oxygen consumption is a strong risk factor for premature illness and death so the tendency is for public health experts to automatically prescribe aerobic exercise to increase oxygen capacity.

"Our hope is that before too long, they will be able to target that prescription just to those who may stand a greater chance of benefiting, and prescribe more effective preventive or therapeutic measures to the others.”

Research published by the British Heart Foundation this week found that one third of adults do their recommended 30 minutes of physical activity a day.

At their peak seven years ago 8.7 million Britons paid to attend gyms, although memberships have fallen since the start of the recession.

The research was conducted in association with the Human Genomics Laboratory in Louisiana and the Centre for Healthy Ageing at the University of Copenhagen.

Sunshine vitamin cuts cancer risk by 40%

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

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.

Boiled egg
Vitamin D Capsules

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 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 diseasehigh 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. , 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 -- implicate the Alzheimer's-associated protein (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 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 - 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. , 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 -- implicate the Alzheimer's-associated protein (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 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 - 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.”