Dietary Guidelines Aim to Reduce Alzheimer’s Risk

By 2050, Alzheimer’s rates will affect 100 million people worldwide. the International Conference on Nutrition and the Brain presented seven dietary principles to reduce the risk of Alzheimer’s

Alzheimer’s disease affects nearly half of North Americans by age 85, it will triple over the next four decades unless preventive measures are developed, warned the American Academy of Neurology. By 2050, Alzheimer’s rates will affect 100 million people worldwide.

Although treatments for the disease remain unsatisfactory, scientific studies suggest that preventive strategies are now feasible.

According to a special report presented at the International Conference on Nutrition and the Brain in Washington on July 19 and 20, 2013, the seven dietary principles to reduce the risk of Alzheimer’s are as follows:
1. Minimize your intake of saturated fats and trans fats. Saturated fat is found primarily in dairy products, meats, and certain oils (coconut and palm oils). Trans fats are found in many snack pastries and fried foods and are listed on labels as “partially hydrogenated oils.”

2. Vegetables, legumes (beans, peas, and lentils), fruits, and whole grains should be the primary staples of the diet.

3. One ounce of nuts or seeds (one small handful) daily provides a healthful source of vitamin E.

4. A reliable source of vitamin B12, such as fortified foods or a supplement providing at least the recommended daily allowance (2.4 mcg per day for adults) should be part of your daily diet.

5. When selecting multiple vitamins, choose those without iron and copper, and consume iron supplements only when directed by your physician.

6. While aluminum’s role in Alzheimer’s disease remains a matter of investigation, it is prudent to avoid the use of cookware, antacids, baking powder, or other products that contribute dietary aluminum.

7. Include aerobic exercise in your routine, equivalent to 40 minutes of brisk walking three times per week.

 

 

Antipsychotic Drugs Raise Diabetes Risk in Children

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an increased risk for type 2 diabetes associated with the use atypical antipsychotic medications

Prescribing antipsychotic drugs to kids and young adults having behavioral problems or mood disorders could put them at a risk for acquiring type 2 diabetes, a study has showed.

The Vanderbilt University Medical Center study shows that young people using medications like risperidone, quetiapine, aripiprazol and olanzapine led to increased risk of developing type 2 diabetes within the first year of taking the drug.

Senior author Wayne A. Ray, Ph.D., professor of Preventive Medicine, said that while other studies have shown an increased risk for type 2 diabetes associated with the use atypical antipsychotic medications; this is the first large, well-designed study to look at the risk in children.

Ray said that as they wanted to address this question of risk for indications for which there were therapeutic alternatives, they deliberately excluded those taking antipsychotics for schizophrenia and other psychoses; thus, our entire sample consisted of patients for whom there were alternatives to antipsychotics.

State-provided, de-identified medical records were examined for TennCare youths ages 6-24 from 1996 through 2007.

During that time children and youth who were prescribed treatment with atypical antipsychotics for attention, behavioral or mood disorders, were compared with similar youth prescribed approved medications for those disorders.

Even with the further elimination of certain disorders that are commonly associated with diabetes, like polycystic ovarian syndrome, those taking antipsychotics had triple the risk of developing type 2 diabetes in the following year, with the risk increasing further as cumulative dosages increased. The increased risk persisted for at least a year after the medications were stopped.

Ray and his colleagues point out developing type 2 diabetes are still rare in this age group. Of the nearly 29,000 children and youth in the antipsychotic medication group and 14,400 children in the control group, 106 were ultimately diagnosed and treated for type 2 diabetes.

The study has been published in the journal JAMA Psychiatry.

 

Long-term study backs early HIV drugs for children

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WHO recommended antiretroviral therapy be started immediately

A landmark five-year trial has strengthened evidence that early use of antiretroviral drugs helps children combat the AIDS virus, doctors reported today.

Conducted in South Africa, the so-called CHER trial made history in 2007, after only two years, when it discovered that early treatment slashed the risk of disease and death from AIDS by 75 percent.

The astonishing finding prompted the World Health Organisation (WHO) to overhaul its treatment guidelines in 2010 for youngsters with the AIDS virus.

The WHO recommended that antiretroviral therapy be started immediately when HIV is diagnosed in children less than a year old, rather than wait until a threshold of virus infection is reached.

Now completed, the CHER trial takes early-use-is-good a step further, according to results reported in The Lancet.

Children who began an immediate course of drugs were able to interrupt their treatment, giving them a break from the powerful, potentially toxic drugs, researchers found.

Yet even with this interruption, the infants did far better than those who started treatment later.

On average, the children who received the deferred treatment began the drugs about 20 weeks after diagnosis.

Those who began an immediate course of 40 weeks of drugs were able to take a 33-week break before starting treatment afresh. And those who took an immediate 96-week course enjoyed a break of 70 weeks.

The trial was conducted at two sites in South Africa among 377 infants with HIV who were less than 12 weeks old.

The research marks the latest advance in knowledge about antiretroviral drugs, which revolutionised the fight against AIDS from 1996.

The drugs are a lifeline to millions, for they can roll back the virus to below detectable levels.

But if the drugs are stopped, the virus rebounds from boltholes, called reservoirs, in cells in the body.

Two other trials — both small in scale and at a very early stage — have recently raised hopes that hitting HIV with drugs very soon after infection can wipe out this hiding place.

An estimated 34 million people are infected with HIV worldwide, and about 1.8 million die each year.

Infants are especially vulnerable. If untreated, around half of infected newborns die before their second birthday.

The new work revives hopes that flourished in the late 1990s, before the reservoir problem was identified, that patients could get a temporary holiday from AIDS drugs.

“This important finding indicates we may be able to temporarily stop treatment and spare infants from some of the toxic effects of continuous ART [antiretroviral therapy] for a while, if we can monitor them carefully,” said Mark Cotton, a professor at Stellenbosch University near Cape Town, who helped lead the study.

Caution, though, was sounded in a commentary by Robert Colebunders of the Institute of Tropical Medicine in Antwerp, Belgium, and Victor Musiime of Makerere University College of Health Sciences in Kampala, Uganda.

Treatment interruption is a risky option in poor countries which lack laboratory facilities to monitor levels of CD4 immune cells, they said.

 

New avian influenza strain found in China

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A new strain of bird flu that can infect and kill animals has been discovered in chickens

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a new virus called H7N7 in chickens

A new strain of bird flu that can infect and kill animals has been discovered in chickens in poultry markets in China, according to a new study.

Having studied samples from birds for the H7N9 virus, researchers at the University of Hong Kong said genetic tests suggested that the virus entered domestic ducks from wild birds and then infected chickens, which are probably the origin of infection in humans, says the study published Wednesday in the journal `Nature`, Xinhua reported.

The research team also discovered a new virus called H7N7 in chickens. Laboratory tests showed H7N7 was also able to cause severe pneumonia in ferrets – a domesticated form of the European polecat – which are usually used as proxies for humans in flu research.

Zhu Huachen, one of the leading authors of the paper, told Xinhua that H7 viruses probably transferred from ducks to chickens on at least two independent occasions and that re-assortment with H9N2 viruses generated the H7N9 outbreak lineage.

Although the H7N7 virus carries only some of the molecular markers present in the human H7N9 isolates, the authors suggested the current pandemic threat could extend beyond H7N9 viruses, and that long-term influenza surveillance was essential for early warning of new viruses and inter-species transmission events.

The H7N9 bird flu has killed 45 people on the Chinese mainland since the first human infection was confirmed in late March this year, a health official said last week.

 

Deadly new MERS virus traced to bats

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(MERS) has been discovered in the bat in close proximity to the first known case of the disease in Saudi Arabia

 

The deadly MERS virus that has claimed many lives has been traced to an insect-eating bat in Saudi Arabia, researchers claim.

A 100 per cent genetic match for Middle East Respiratory Syndrome (MERS) has been discovered in the bat in close proximity to the first known case of the disease in Saudi Arabia, researchers said.

The discovery points to the likely animal origin for the disease, although researchers say that an intermediary animal is likely also involved.

Led by team of investigators from the Center for Infection and Immunity (CII) at Columbia University`s Mailman School of Public Health, Eco Health Alliance, and the Ministry of Health of Saudi Arabia, the study is the first to search for an animal reservoir for MERS in Saudi Arabia, and the first to identify such a reservoir by finding a genetic match in an animal.

“There have been several reports of finding MERS-like viruses in animals. None were a genetic match. In this case we have a virus in an animal that is identical in sequence to the virus found in the first human case.

Importantly, it`s coming from the vicinity of that first case,” said W Ian Lipkin, director of the Center for Infection and Immunity and a co-author of the study.

MERS was first described in September 2012 and continues to spread. Close to 100 cases have been reported worldwide, 70 of them from Saudi Arabia. The causative agent, a new type of corona virus, has been determined, however, the origin of the virus has been unknown until now.

The researchers collected more than 1,000 samples from seven bat species in regions where cases of MERS were identified in Bisha, Unaizah, and Riyadh.

Extensive analysis was performed using polymerase chain reaction and DNA sequencing revealed the presence of a wide range of alpha and beta corona viruses in up to a third of bat samples.

One fecal sample from an Egyptian Tomb Bat (Taphozous perforatus) collected within a few kilometers of the first known MERS victim`s home contained sequences of a virus identical to those recovered from the victim.

Bats are the reservoirs of viruses that can cause human disease including rabies and SARS. In some instances the infection may spread directly to humans through inadvertent inhalation of infected aerosols, ingestion of contaminated food, or, less commonly, a bite wound, researchers said.

In other instances bats can first infect intermediate hosts. The researchers suggest that the indirect method for transmission is more likely in MERS.

“There is no evidence of direct exposure to bats in the majority of human cases of MERS,” said Ziad Memish, Deputy Minister of Health, Saudi Arabia, and lead author of the study.

The study appears in the journal Emerging Infectious Diseases.

 

 

New cytometry cell analyzer facilitate multi color experiments

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cytometry cell analyzer BD LSRFortessa X-20 that can be configured with up to five lasers to detect up to 20 parameters

 

BD Biosciences, a part of global medical technology company BD (Becton, Dickinson and Company), has launched a high-performance research flow cytometry cell analyzer BD LSRFortessa X-20 that can be configured with up to five lasers to detect up to 20 parameters simultaneously.

According to the company, the BD LSRFortessa X-20 cell analyzer delivers high-performance multi color analysis with the most compact footprint in its class at 30”x29” and a height of 30”. Recognizing that space is a valuable commodity in today’s research environment, BD Biosciences designed the new cell analyzer to be compact without compromising the power needed

While popular laser choices include blue, red, violet, yellow-green and UV, a wide range of up to 34 available laser choices are available as excitation sources. Each excitation source is supported by new polygon detector arrays, and each polygon can support up to eight detectors for maximum flexibility in optical configuration, the company said in a statement.

The new cell analyzer enables customers to configure BD flow cytometers and cell sorters to fit precise research and assay needs. This program is tailored to meet the needs of researchers at the leading edge of biomedical discovery.

“The new BD LSRFortessa X-20 cell analyzer will enable researchers to conduct complex experiments with the additional parameters and increased sensitivity they need,” said Alberto Mas, president, BD Biosciences. “Uncovering dim staining and rare cell populations is extremely valuable to complex multi color assays, which are tools for advanced disease or drug development research.”

 

Biggest heart attack risks for Indians revealed

Indian researchers have conducted a data mining exercise to find out important risk factors in increasing the chances of an individual having a heart attack.

The authors confirm that the usual suspects high blood cholesterol, intake of alcohol and passive smoking play the most crucial role in `severe,` `moderate` and `mild` cardiac risks, respectively.

Subhagata Chattopadhyay of the Camellia Institute of Engineering in Kolkata used 300 real-world sample patient cases with various levels of cardiac risk – mild, moderate and severe and mined the data based on twelve known predisposing factors: age, gender, alcohol abuse, cholesterol level, smoking (active and passive), physical inactivity, obesity, diabetes, family history, and prior cardiac event.

He then built a risk model that revealed specific risk factors associated with heart attack risk.

Chattopadhyay explained that the essence of this work essentially lies in the introduction of clustering techniques instead of purely statistical modeling, where the latter has its own limitations in `data-model fitting` compared to the former that is more flexible.

He said that the reliability of the data used, should be checked, and this has been done in this work to increase its authenticity. I reviewed several papers on epidemiological research, where I`m yet to see these methodologies, used.

The study has been published in International Journal of Biomedical Engineering and Technology.

 

Genes inherited from mother may induce ageing process

Genes inherited from mother may induce ageing process

A new research has found that ageing is determined not only by the accumulation of changes during our lifetime but also by the genes we acquire from our mothers.

There are many causes of ageing that are determined by an accumulation of various kinds of changes that impair the function of bodily organs.

Of particular importance in ageing, however, seems to be the changes that occur in the cell`s power plant – the mitochondrion.

This structure is located in the cell and generates most of the cell`s supply of ATP which is used as a source of chemical energy.

“The mitochondria contains their own DNA, which changes more than the DNA in the nucleus, and this has a significant impact on the ageing process,” Nils-Goran Larsson, Ph.D., professor at the Karolinska Institute and principal investigator at the Max Planck Institute for Biology of Ageing, and leader of the current study alongside Lars Olson, Ph.D., professor in the Department of Neuroscience at the Karolinska Institute, said.

“Many mutations in the mitochondria gradually disable the cell`s energy production,” Larsson said.

For the first time, the researchers have shown that the aging process is influenced not only by the accumulation of mitochondrial DNA damage during a person`s lifetime, but also by the inherited DNA from their mothers.

“Surprisingly, we also show that our mother`s mitochondrial DNA seems to influence our own aging,” Larsson said.

“If we inherit m DNA with mutations from our mother, we age more quickly,” the researcher added.

The study is published in the journal Nature.

 

Pringles Potato Chips contain Cancer causing Chemical – Facts

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One of the most hazardous ingredients in potato chips is not intentionally added, but rather is a byproduct of the processing.

 

To understand the nature of Pringles and other stackable chips, forget the notion that they come from actual potatoes in any recognizable way.

The Pringles Company (in an effort to avoid taxes levied against “luxury foods” like chips in the UK) once even argued that the potato content of their chips was so low that they are technically not even potato chips.

 

So if they’re not made of potatoes, what are they exactly? The process begins with slurry of rice, wheat, corn, and potato flakes that are pressed into shape.

This dough-like substance is then rolled out into an ultra-thin sheet cut into chip-cookies by a machine.

According to io9:

“The chips move forward on a conveyor belt until they’re pressed onto molds, which give them the curve that makes them fit into one another.

Those molds move through boiling oil … Then they’re blown dry, sprayed with powdered flavors, and at last, flipped onto a slower-moving conveyor belt in a way that allows them to stack.

From then on, it’s into the cans … and off towards the innocent mouths of the consumers.”

I suspect nearly everyone reading this likely enjoys the taste of potato chips. However, they are clearly one of the most toxic processed foods you can eat—whether they’re made from actual potato shavings or not.

Potato Chips are Loaded with Cancer-Causing Chemical

One of the most hazardous ingredients in potato chips is not intentionally added, but rather is a byproduct of the processing.

Acrylamide, a cancer-causing and potentially neurotoxic chemical, is created when carbohydrate-rich foods are cooked at high temperatures, whether baked, fried, roasted or toasted. Some of the worst offenders include potato chips and French fries, but many foods cooked or processed at temperatures above 212°F (100°C) may contain acrylamide. As a general rule, the chemical is formed when food is heated enough to produce a fairly dry and brown/yellow surface. Hence, it can be found in:

Potatoes: chips, French fries and other roasted or fried potato foods

  • Grains: bread crust, toast, crisp bread, roasted breakfast cereals and various processed snacks
  • Coffee; roasted coffee beans and ground coffee powder. Surprisingly, coffee substitutes based on chicory actually contains 2-3 times MORE acrylamide than real coffee

Beware: Baked Chips May Be WORSE than Fried!

If you think you can avoid the health risks of potato chips by choosing baked varieties, which are typically advertised as being “healthier,” think again. Remember that acrylamide is formed not only when foods are fried or broiled, but also when they are baked. And according to U.S. Food and Drug Administration (FDA) data on acrylamide levels in foods, baked chips may contain more than three times the level of acrylamide as regular chips!

Interestingly, the same trend holds true for other foods, too, which suggests that baking processed potatoes at high temperature may be one of the worst ways to cook them. For instance, according to the FDA’s data, Ore Ida Golden Fries contained 107 ppb of acrylamide in the regular fried version and 1,098 when baked. So remember, ALL potato chips contain acrylamide, regardless of whether they are natural or not; baked or fried. Likewise, they will ALL influence your insulin levels in a very negative way.

Acrylamide is Not the Only Danger

Acrylamide is not the only dangerous genotoxic compound formed when food is heated to high temperatures.

A three-year long EU project, known as Heat-Generated Food Toxicants (HEATOX), whose findings were published at the end of 2007, found there are more than 800 heat-induced compounds, of which 52 are potential carcinogens. In addition to their finding that acrylamide does pose a public health threat, the HEATOX scientists also discovered that you’re far less likely to ingest dangerous levels of the toxin when you eat home-cooked foods compared to industrially or restaurant-prepared foods.

Additionally, the HEATOX findings also suggest that although there are ways to decrease exposure to acrylamide, it cannot be eliminated completely.

According to their calculations, successful application of all presently known methods would reduce the acrylamide intake by 40 percent at the most—which makes me wonder whether chip manufacturers have really succeeded at this point in reducing acrylamide levels to within legal limits… There’s no updated data as of yet, so there’s no telling whether they’ve been able to comply with the 2005 settlement.

For more in-depth information about acrylamide, I recommend reading the online report Heat-generated Food Toxicants, Identification, Characterization and Risk Minimization.  In general however, just remember that cooking food at high temperatures is ill advised. A few of the most well-known toxins created in high-temperature cooking include:

Heterocyclic Amines (HCAs): These form when meat is cooked at high temperatures, and they’re also linked to cancer. In terms of HCA, the worst part of the meat is the blackened section, which is why you should always avoid charring your meat, and never eat blackened sections.

  • Polycyclic Aromatic Hydrocarbons (PAHs): When fat drips onto the heat source, causing excess smoke, and the smoke surrounds your food, it can transfer cancer-causing PAHs to the meat.
  • Advanced Glycation End Products (AGEs): When food is cooked at high temperatures (including when it is pasteurized or sterilized), it increases the formation of AGEs in your food. When you eat the food, it transfers the AGEs into your body. AGEs build up in your body over time leading to oxidative stress, inflammation and an increased risk of heart disease, diabetes and kidney disease.

Sources and References

  • io9 October 21, 2001

This was written by Dr. Joseph Mercola, and published at Mercola

 

’40 year old child’ resembles 8 year old baby: Rare Genetic condition

she is 8-years-old. She has a mysterious condition that has caused her to virtually stop aging

40-Year-Old Child will look into the medical mystery of the rare condition that causes slowed-down aging.  Eight-year-old Gabby Williams weighs only 11 pounds.

A girl from Billings, Mont., looks like an infant and needs full caring as if she is a newborn. Her mother and father change her diapers and feeding her multiple times a day.

Her mother, Mary Margret Williams, told that Gabby hasn’t changed much over the years. In fact, her skin still feels like a baby’s and her hair is still fine-textured.

“She has gotten a little longer and we have jumped into putting her in size 3-6 month clothes instead of 0-3 months for the footies,” she said.

She is one of just a handful of people in the world with a rare condition that slows the aging process. Medical researcher Richard F. Walker has been studying Gabby for two years. His particular interest is investigating the cause of slow aging.

“In some people, something happens to them and the development process is retarded,” he said. “The rate of change in the body slows and is negligible.”

Gabby appears with two others who share her condition: a 29-year-old American with the body of a 10-year-old, and a 31-year-old Brazilian woman who’s two-year-old girl.

Walker suspects that Gabby and the others may have a genetic impairment that interferes with a crucial process called “developmental inertia” that affects growth in humans.