sábado, 19 de agosto de 2017

This is Health,too.

Brain cells found to control aging


Ana Sandoiu,

Scientists at Albert Einstein College of Medicine have found that stem cells in the brain's hypothalamus govern how fast aging occurs in the body. The finding, made in mice, could lead to new strategies for warding off age-related diseases and extending lifespan. The paper was published online today in Nature.

The hypothalamus was known to regulate important processes including growth, development, reproduction and metabolism. In a 2013 Nature paper, Einstein researchers made the surprising finding that the hypothalamus also regulates aging throughout the body. Now, the scientists have pinpointed the cells in the hypothalamus that control aging: a tiny population of adult neural stem cells, which were known to be responsible for forming new brain neurons.

"Our research shows that the number of hypothalamic neural stem cells naturally declines over the life of the animal, and this decline accelerates aging," says senior author Dongsheng Cai, M.D., Ph.D., (professor of molecular pharmacology at Einstein. "But we also found that the effects of this loss are not irreversible. By replenishing these stem cells or the molecules they produce, it's possible to slow and even reverse various aspects of aging throughout the body."
In studying whether stem cells in the hypothalamus held the key to aging, the researchers first looked at the fate of those cells as healthy mice got older. The number of hypothalamic stem cells began to diminish when the animals reached about 10 months, which is several months before the usual signs of aging start appearing. "By old age -- about two years of age in mice -- most of those cells were gone," says Dr. Cai.

The researchers next wanted to learn whether this progressive loss of stem cells was actually causing aging and was not just associated with it. So they observed what happened when they selectively disrupted the hypothalamic stem cells in middle-aged mice. "This disruption greatly accelerated aging compared with control mice, and those animals with disrupted stem cells died earlier than normal," says Dr. Cai.
Could adding stem cells to the hypothalamus counteract aging? To answer that question, the researchers injected hypothalamic stem cells into the brains of middle-aged mice whose stem cells had been destroyed as well as into the brains of normal old mice. In both groups of animals, the treatment slowed or reversed various measures of aging.

Dr. Cai and his colleagues found that the hypothalamic stem cells appear to exert their anti-aging effects by releasing molecules called microRNAs (miRNAs). They are not involved in protein synthesis but instead play key roles in regulating gene expression. miRNAs are packaged inside tiny particles called exosomes, which hypothalamic stem cells release into the cerebrospinal fluid of mice.

The researchers extracted miRNA-containing exosomes from hypothalamic stem cells and injected them into the cerebrospinal fluid of two groups of mice: middle-aged mice whose hypothalamic stem cells had been destroyed and normal middle-aged mice. This treatment significantly slowed aging in both groups of animals as measured by tissue analysis and behavioral testing that involved assessing changes in the animals' muscle endurance, coordination, social behavior and cognitive ability.

The researchers are now trying to identify the particular populations of microRNAs and perhaps other factors secreted by these stem cells that are responsible for these anti-aging effects -- a first step toward possibly slowing the aging process and treating age-related diseases.
The article is titled, "Hypothalamic stem cells control ageing speed partly through exosomal miRNAs." The other authors are Yalin Zhang. Ph.D., Min Soo Kim, Ph.D., Baosen Jia, Ph.D., Jingqi Yan, Ph.D., Juan Pablo Zuniga-Hertz, Ph.D., and Cheng Han, Ph.D., all at Einstein.
The study was supported by grants from the National Institutes of Health (DK078750, AG031774 , HL113180, and DK099136).

quinta-feira, 17 de agosto de 2017

Are stem cells the link between bacteria and cancer?

Gastric carcinoma is one of the most common causes of cancer-related deaths, primarily because most patients present at an advanced stage of the disease. The main cause of this cancer is the bacterium Helicobacter pylori, which chronically infects around half of all humans. However, unlike tumour viruses, bacteria do not deposit transforming genes in their host cells and how they are able to cause cancer has so far remained a mystery. 

An interdisciplinary research team at the Max Planck Institute in Berlin in collaboration with researchers in Stanford, California, has now discovered that the bacterium sends stem cell renewal in the stomach into overdrive -- and stem cell turnover has been suspected by many scientists to play a role in the development of cancer. By showing that the stomach contains two different stem cell types, which respond differently to the same driver signal, they have uncovered a new mechanism of tissue plasticity. It allows tuning tissue renewal in response to bacterial infection.
While it has long been recognized that certain viruses can cause cancer by inserting oncogenes into the host cell DNA, the fact that some bacteria can also cause cancer has been slower to emerge and much harder to prove. While it is now clear that most cases of stomach cancer are linked to chronic infections with H. pylori, the mechanism remains unknown.
Thomas F. Meyer and his colleagues at the Max Planck Institute for Infection Biology in Berlin have spent many years investigating this bacterium and the changes it induces in the cells of the stomach epithelium. In particular, they were puzzled how malignancy could be induced in an environment in which cells are rapidly replaced. They suspected that the answer might lie in the stem cells found at the bottom of the glands that line the inside of the stomach, which continually replace the remaining cells 'from the bottom up' -- and which are the only long-lived cells in the stomach. Michael Sigal, a clinical scientist of the Charité -- Universitätsmedizin Berlin, who joined the Max Planck team, overturned the established dogma to show that H. pylori not only infects the surface cells, which are about to be sloughed off, but that some of the bacteria manage to invade deep into the glands and reach the stem cell compartment. They have now found that these stem cells do indeed respond to the infection by increasing their division -- producing more cells and leading to the characteristic thickening of the mucosa observed in affected patients.
They used different transgenic mice to trace cells expressing particular genes, as well as all their daughter cells. The results, published in Nature indicate that the stomach glands contain two different stem cell populations. Both respond to a signalling molecule called Wnt, which maintains stem cell turnover in many adult tissues. Crucially, they discovered that myofibroblast cells in the connective tissue layer directly underneath the glands produce a second stem cell driver signal, R-spondin, to which the two stem cell populations responded differently. It is this signal, which turned out to control the response to H. pylori: Following infection, the signal is ramped up, silencing the more slowly cycling stem cell population and putting the faster cycling stem cell population into overdrive.
These findings substantiate the rising awareness that chronic bacterial infections are strong promoters of cancer. 'Our findings show that an infectious bacterium can increase stem cell turnover', says Sigal. 'Since H. pylori causes life-long infections, the constant increase in stem cell divisions may be enough to explain the increased risk of carcinogenesis observed,' and Meyer adds: 'Our new findings shed light on the intriguing ways through which chronic bacterial infections disturb tissue function and provide invaluable clues on how bacteria, in general, may increase the risk of cancer'.
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Materials provided by Max-Planck-Gesellschaft. Note: Content may be edited for style and length.

quarta-feira, 16 de agosto de 2017

Drug-delivering micromotors treat their first bacterial infection in the stomach

Nanoengineers at the University of California San Diego have demonstrated for the first time using micromotors to treat a bacterial infection in the stomach. These tiny vehicles, each about half the width of a human hair, swim rapidly throughout the stomach while neutralizing gastric acid and then release their cargo of antibiotics at the desired pH. Researchers published their findings on Aug. 16 in Nature Communications.

This micromotor-enabled delivery approach is a promising new method for treating stomach and gastrointestinal tract diseases with acid-sensitive drugs, researchers said. The effort is a collaboration between the research groups of nanoengineering professors Joseph Wang and Liangfang Zhang at the UC San Diego Jacobs School of Engineering. Wang and Zhang pioneered research on the in vivo operation of micromotors and this study represents the first example of drug-delivering micromotors for treating bacterial infection.

Gastric acid can be destructive to orally administered drugs such as antibiotics and protein-based pharmaceuticals. Drugs used to treat bacterial infections, ulcers and other diseases in the stomach are normally taken with additional substances, called proton pump inhibitors, to suppress gastric acid production. But when taken over longer periods or in high doses, proton pump inhibitors can cause adverse side effects including headaches, diarrhea and fatigue. In more serious cases, they can cause anxiety or depression.
The micromotors have a built-in mechanism to neutralize gastric acid and effectively deliver their drug payloads in the stomach -- without the use of proton pump inhibitors.

"It's a one-step treatment with these micromotors, combining acid neutralization with therapeutic action," said Berta Esteban-Fernández de Ávila, a postdoctoral scholar in Wang's research group at UC San Diego and a co-first author of the paper.
Each micromotor consists of a spherical magnesium core coated with a protective layer of titanium dioxide, followed by a layer of the antibiotic clarithromycin, and an outer layer of a positively-charged polymer called chitosan that enables the motors to stick to the stomach wall.

This binding is also enhanced by the propulsion of the micromotors, which is fueled by the stomach's own acid. The magnesium cores react with gastric acid, generating a stream of hydrogen microbubbles that propel the motors around inside the stomach. This reaction also temporarily reduces the amount of acid in the stomach, increasing the pH level enough to allow the micromotors to release the drug and perform treatment. The normal stomach pH is restored within 24 hours.

Researchers tested the micromotors in mice with Helicobacter pylori infections. The micromotors -- packed with a clinical dose of the antibiotic clarithromycin -- were administered orally once a day for five consecutive days. Afterwards, researchers evaluated the bacterial count in each mouse stomach and found that treatment with the micromotors was slightly more effective than when the same dose of antibiotic was given in combination with proton pump inhibitors.
The micromotors are mostly made of biodegradable materials. The magnesium cores and polymer layers are dissolved by gastric acid without producing harmful residues.

Researchers say that while the present results are promising, this work is still at an early stage. The team is planning future studies to further evaluate the therapeutic performance of the micromotors in vivo and compare it with other standard therapies against stomach diseases. Researchers also plan to test different drug combinations with the micromotors to treat multiple diseases in the stomach or in different sections of the gastrointestinal tract. Overall, the researchers say that this work opens the door to the use of synthetic motors as active delivery platforms for in vivo treatment of diseases.
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Materials provided by University of California - San Diego. Original written by Liezel Labios. Note: Content may be edited for style and length.

What does music mean? Sign language may offer an answer

How do we detect the meaning of music? We may gain some insights by looking at an unlikely source, sign language, a newly released linguistic analysis concludes.

"Musicians and music lovers intuitively know that music can convey information about an extra-musical reality," explains author Philippe Schlenker, a senior researcher at Institut Jean-Nicod within France's National Center for Scientific Research (CNRS) and a Global Distinguished Professor at New York University. "Music does so by way of abstract musical animations that are reminiscent of iconic, or pictorial-like, components of meaning that are common in sign language, but rare in spoken language."
The analysis, "Outline of Music Semantics," appears in the journal Music Perception; it is available, with sound examples, here: http://ling.auf.net/lingbuzz/002942. A longer piece that discusses the connection with iconic semantics is forthcoming in the Review of Philosophy & Psychology ("Prolegomena to Music Semantics").
Schlenker acknowledges that spoken language also deploys iconic meanings--for example, saying that a lecture was 'loooong' gives a very different impression from just saying that it was 'long.' However, these meanings are relatively marginal in the spoken word; by contrast, he observes, they are pervasive in sign languages, which have the same general grammatical and logical rules as do spoken languages, but also far richer iconic rules.
Drawing inspiration from sign language iconicity, Schlenker proposes that the diverse inferences drawn on musical sources are combined by way of abstract iconic rules. Here, music can mimic a reality, creating a "fictional source" for what is perceived to be real. As an example, he points to composer Camille Saint Saëns's "The Carnival of the Animals" (1886), which aims to capture the physical movement of tortoises.
"When Saint Saëns wanted to evoke tortoises in 'The Carnival of Animals,' he not only used a radically slowed-down version of a high-energy dance, the Can-Can," Schlenker notes. "He also introduced a dissonance to suggest that the hapless animals were tripping, an effect obtained due to the sheer instability of the jarring chord."
In his work, Schlenker broadly considers how we understand music--and, in doing so, how we derive meaning through the fictional sources that it creates.
"We draw all sorts of inferences about fictional sources of the music when we are listening," he explains. "Lower pitch is, for instance, associated with larger sound sources, a standard biological code in nature. So, a double bass will more easily evoke an elephant than a flute would. Or, if the music slows down or becomes softer, we naturally infer that a piece's fictional source is losing energy, just as we would in our daily, real-world experiences. Similarly, a higher pitch may signify greater energy--a physical code--or greater arousal, which is a biological code."
Fictional sources may be animate or inanimate, Schlenker adds, and their behavior may be indicative of emotions, which play a prominent role in musical meaning.
"More generally, it is no accident that one often signals the end of a classical piece by simultaneously playing more slowly, more softly, and with a musical movement toward more consonant chords," he says. "These are natural ways to indicate that the fictional source is gradually losing energy and reaching greater repose."
In his research, Schlenker worked with composer Arthur Bonetto to create minimal modifications of well-known music snippets to understand the source of the meaning effects they produce. This analytical method of 'minimal pairs,' borrowed from linguistics and experimental psychology, Schlenker posits, could be applied to larger musical excerpts in the future.
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Materials provided by New York University. Note: Content may be edited for style and length.

sexta-feira, 28 de abril de 2017

Como funciona o cérebro do adolescente


Rubem Barros

© Fotos: Shutterstock

Desejara que não houvesse idade entre 16 e 23 anos, ou que a mocidade dormisse todo esse tempo.” Na peça Conto de inverno, escrita entre 1610 e 1611 por William Shakespeare, o personagem denomina os jovens de “cérebros ferventes”. Sua reação à rebeldia típica dessa fase da vida revela que nada mudou ao longo do tempo. Os adultos, em geral, sentem muita dificuldade de compreender o comportamento dos adolescentes.

Em tempos modernos, a mesma atitude tem sua melhor tradução em uma expressão bem conhecida de todos nós: “são os hormônios!”, um bode expiatório invisível que explicaria o comportamento dos jovens. Essa afirmação, na verdade, indica pouco conhecimento sobre o assunto.

“Existe apenas um hormônio importante na adolescência, o sexual, e por si só ele não explica outros comportamentos típicos da faixa etária, como a sociabilidade e a propensão ao risco”, diz a neurocientista Suzana Herculano-Houzel, atualmente na Universidade Vanderbilt (EUA), autora de O cérebro em transformação (Objetiva). “Quem comanda as mudanças da adolescência, inclusive a produção do hormônio sexual, é o cérebro”, explica.

É evidente que um adolescente tem o cérebro imaturo, já que, por definição, ele ainda não é um adulto. Mas o corpo desenvolvido, já parecido com o do adulto, acaba gerando nos mais velhos a expectativa de um comportamento mais maduro, o que se torna fonte permanente de frustração. Um dos motivos desse tipo de engano está em informações científicas incorretas. Há duas décadas, a teoria predominante era que o cérebro atingia sua maturidade máxima no final da infância. Mais recentemente, constatou-se que o adolescente, na verdade, não está totalmente maduro fisicamente – inclusive no que diz respeito ao cérebro.

“A maturação do cérebro humano segue pela adolescência e pode continuar até a idade adulta”, diz a neurocientista Sarah-Jayne Blakemore, da Universidade de Londres. “Dez anos atrás, sabíamos pouco sobre o cérebro adolescente. Avançamos muito graças às novas tecnologias de imagem, feitas por ressonância magnética”, acrescenta.

Imagens que dizem muito

Um grande projeto nessa área de pesquisa é conduzido pelo Instituto Nacional de Saúde Mental dos Estados Unidos, que conta com cerca de 8 mil imagens de 2 mil pessoas – entre crianças, adolescentes e adultos –, oferecendo uma nova perspectiva sobre o desenvolvimento do cérebro. Uma das mudanças mais visíveis nessas sequências de imagens ocorre na chamada massa cinzenta, a região mais exterior do órgão, que é constituída pelos corpos celulares dos neurônios. Ao contrário do que se possa imaginar, a massa cinzenta diminui ao longo da adolescência.

Essa diminuição, no entanto, não representa uma perda de neurônios, cujo número, em geral, pouco muda. Ela ocorre devido a uma grande perda de sinapses (conexões entre os neurônios mediadas por substâncias químicas chamadas de neurotransmissores). As sinapses começam a aumentar durante a gestação e atingem o pico aos 6 meses de vida do bebê. Na adolescência, o quadro muda.

“No começo dessa fase, há um grande número de sinapses, mas, quando se inicia a transição para a fase adulta, ocorre uma morte programada de sinapses, que refina as conexões”, diz a neuropsicóloga Cláudia Berlim de Mello, da Universidade Federal de São Paulo (Unifesp) . “Essa perda de algumas sinapses – e consolidação de outras – acontece de acordo com o uso”, explica. Ou seja, sinapses usadas com frequência são reforçadas, enquanto as que deixam de ser usadas são perdidas, de modo que as opções feitas nessa fase da vida ajudarão a formar o cérebro do adulto.

Paralelamente, ocorre outra mudança importante na chamada matéria branca, constituída por axônios (parte do neurônio responsável por conduzir os impulsos elétricos que partem do corpo celular). Ao longo do desenvolvimento, os axônios são cobertos por uma camada de mielina, que forma uma espécie de capa. A mielina é um isolante e aumenta a velocidade de transmissão do sinal entre as células. Assim, enquanto a matéria cinzenta diminui devido ao corte das sinapses, a branca aumenta por causa do aumento na mielina. Entre a perda e o refinamento das sinapses, a massa total do cérebro permanece relativamente constante, mas o funcionamento vai se aprimorando graças às mudanças estruturais e químicas.
Além de ajudar a entender o adolescente, essas descobertas podem levar muitos adultos a questionar a própria maturidade cerebral. Isso porque o corte de sinapses pode avançar até os 30 anos, e o aumento na massa branca, até os 40.

Embates com a família

Há outro dado nesse complexo processo: a maturação do cérebro não se dá de maneira homogênea, mas em ritmos diferentes em cada região. As novas tecnologias de imagem mostram que a última parte do cérebro a amadurecer – o córtex pré-frontal – é justamente a região onde se processam comportamentos tipicamente de adultos, como capacidade de planejamento, concentração, inibição de impulsos e empatia. Ao mesmo tempo que o corte do excesso de sinapses aperfeiçoa o funcionamento dessa importante área, as novas e melhoradas fibras com mielina permitem que diferentes partes dentro do pré-frontal se comuniquem melhor.

“Essa integração resulta em um aperfeiçoamento da linguagem e da coordenação motora, por exemplo”, diz Herculano-Houzel. “Não por acaso, pacientes adultos que sofreram lesões no córtex apresentam comportamentos típicos de adolescentes”, completa.

Com o amadurecimento do córtex pré-frontal, o adolescente vai se aproximando do mundo adulto, embora de maneira não muito suave. “Nessa fase, começam a se desenvolver o comportamento autorreflexivo, a autorregulação e o raciocínio, levando a uma maior consciência crítica de si e dos outros”, diz Berlim de Mello. “Por isso, eles tendem a ver incongruências no mundo dos adultos. Ao contrário da criança, que tende a ser alegre, o adolescente é mais irritadiço e nega ou questiona o que vem antes dele.” Como o cérebro ainda está se consolidando, as oscilações de humor são comuns, assim como o comportamento reativo.

“Eles começam a olhar o mundo de forma mais profunda, mas o lado emocional não está totalmente amadurecido. Daí surgem embates com os adultos e com a família”, explica a neuropsicóloga. “Além disso, eles são mais impulsivos, reativos e intensos. Percebem as incongruências, mas não sabem como lidar com elas.”
Se, por um lado, a maturidade emocional do adolescente oscila, é nessa fase também que ele passa a possuir ferramentas que o preparam para a vida adulta. Surge a capacidade de tomar decisões, julgar e planejar. No córtex pré-frontal, uma região chamada córtex orbitofrontal (localizada atrás dos olhos) é a última a amadurecer e promove as capacidades de usar emoções para nortear decisões e de criar empatia pelos outros – características fundamentais da vida adulta.


Outra mudança fundamental ocorre no sistema de recompensa, “conjunto de estruturas no cérebro responsáveis por premiar com prazer ou bem-estar comportamentos que acabaram de se mostrar úteis ou interessantes”, conforme Herculano-Houzel define em seu livro. Isso significa que o adolescente precisa de muito mais para sentir prazer. É algo difícil de visualizar porque ocorre em nível bioquímico – no cérebro, o prazer é proporcionado pela molécula dopamina, que é um neurotransmissor. Os adolescentes possuem um terço dos receptores para dopamina. Por isso, precisam de experiências mais intensas, que estimulam mais a liberação da substância, para sentir prazer.

Essa mudança, por si só, é a principal responsável pela maioria dos comportamentos típicos do adolescente, como a busca de novidades, os excessos (como ouvir música alta) e o comportamento de risco, que também gera euforia e produção de dopamina. Sem falar na nova e mais importante descoberta: o sexo, cujo prazer só é possível porque o sistema de recompensa se torna sensível aos hormônios que promovem o prazer sexual. E tudo isso não é ruim, pois a procura pelo prazer é o que move o adolescente a descobrir coisas novas e a buscar independência.

Riscos possíveis

As coisas podem se complicar, porém, quando o comportamento de risco e a sociabilidade nascente se combinam. “Na adolescência, a causa principal de morte são os acidentes que, em geral, são causados por comportamento de risco”, diz Blakemore. “Um dos motivos principais do comportamento de risco é a influência do meio social. Os adolescentes são levados a impressionar os amigos, em busca de aprovação, enquanto também vão se tornando mais independentes dos pais.”

O encontro de um cérebro em formação com o comportamento de risco, como consumo de álcool e de drogas, é o ponto de maior vulnerabilidade. Afinal, a especialização das sinapses ocorre tanto para bons quanto para maus hábitos. O risco de dependência é maior porque o jovem está numa fase de experimentação. Dependências adquiridas podem permanecer durante a vida adulta. As descobertas sobre esse período da vida ajudam a lançar um olhar novo sobre o adolescente e a reconhecê-lo como alguém que não está pronto e que, por isso, precisa ser acolhido e orientado. Elas ajudam a pintar com detalhes um quadro que já havia sido delineado pela psicologia, mostrando que a adolescência é uma fase característica e que, também no cérebro, os adolescentes apresentam suas peculiaridades – que precisam ser respeitadas.

Inside the FDA's New Nutrition Facts Labels


FDA food label 

Few people besides federal employees can really appreciate the impact the U.S. Food and Drug Administration has on our daily lives. This public health agency plays a major role in regulating the packaged foods and medicines we consume. That’s a tall order requiring time, personnel and research, which is why—after more than 20 years without a major update—the FDA has finally revamped its labeling system.

“Today, people are eating differently, and science has advanced,” says FDA spokesperson Lauren Kotwicki. The FDA created the new label “to reflect updated scientific information—including the link between diet and chronic diseases such as obesity and heart disease.” Another crucial change: The agency has updated serving-size requirements to more accurately reflect what people eat and drink, Kotwicki says.

Agency of Change

Protecting how and what Americans consume is a huge job. In fact, the FDA, which started with just a single chemist in 1862, has grown to a staff of approximately 15,000 today. It is the oldest comprehensive consumer protection agency in the federal government. With the passage of the Pure Food and Drug Act of 1906, which outlawed interstate commerce of misbranded food and drugs, the agency began its regulatory responsibilities.

Since then, the FDA has evolved to address new medical advances, drug claims and the changing nutritional profile of our food supply, including the influx of additives and preservatives.
And until now, modern food safety legislation had culminated in the Nutrition Labeling and Education Act of 1990, which introduced the Nutrition Facts label we’ve come to know.

What’s New About the Label?

In recent years, federal health officials and consumer advocacy groups called for a change, and the FDA delivered. Kotwicki says the label has been updated in significant ways. Among the changes, the Calories from Fat line item has been removed because research suggests that fat type is more important than the amount alone. And an increased clarity in serving sizes—using dual-column labels for multi-serving food products that can be consumed in one or more sittings (e.g., bread, cereal, many snacks)—should help people better understand what they’re consuming.

A Clearer Health Picture

Shifting FDA policy is a long, labor-intensive process, says Kotwicki. Before Congress can enact new FDA legislation or alter the content of labels, there are many layers of approval involved. For the latest changes, two proposed rules were issued in March 2014, a supplemental proposed rule was issued in July 2015, and the two final rules were published in May 2016.
Amy Gorin, a registered dietitian-nutritionist and owner of Amy Gorin Nutrition, welcomes the result: “You’ll have a faster, clearer picture of what you’re actually eating,” she says.

You’re determined to eat better, so why not commit to these nine additional healthy choices to help you stay fit?
By Danielle Blundell

segunda-feira, 24 de abril de 2017

Combining CoQ10 and Selenium Reduces Cardiovascular Mortality


An important study out of Sweden has surprised researchers who found that combining CoQ10 with selenium can dramatically reduce cardiovascular mortality.
This nutrient combination has also been found to improve heart function, improve quality of life, reduce the number of days a patient stays in the hospital, lower cardiovascular mortality risk by 49%, and even provide protection years after the subjects stopped taking the supplements.

Cardiovascular disease is the leading cause of death both globally and in the US. It kills more than 17 million people worldwide every year—more than all forms of cancer combined.
The exciting news is that supplementing with CoQ10 and selenium could be an important life-saving combination for protecting against cardiovascular mortality.

Slashing Cardiovascular Mortality


Slashing Cardiovascular Mortality

CoQ10 and selenium are both involved in the management of cellular energy. Each compound works to influence energy production and utilization of this energy by organs throughout the body. Studies now show that CoQ10 and selenium have effects that help protect against tissue-damaging oxidative stress.

Researchers from Sweden conducted a double-blind, placebo-controlled study that included 443 healthy adults between 70 and 88 years old. The participants received either a placebo or a combination of 200 mg a day of CoQ10 and 200 mcg a day of selenium tablets.
During an extensive follow up time of 5.2 years, 12.6% of the placebo recipients had died of cardiovascular disease, compared to only 5.9% in the supplement group, which is an impressive and significant difference.

Those taking the combination of CoQ10 and selenium also had significantly better scores on cardiac function compared to those taking the placebo, as determined by an echocardiogram. In addition, levels of a biomarker for heart failure were significantly reduced, which is a favorable finding that indicates reduced cardiovascular disease risk.

This initial study established that supplementing with these two nutrients could cut the cardiovascular death rate by more than 50%, while improving heart function and significantly reducing the risk of further cardiovascular disease in the survivors.
he goal in extending lifespan is to not just live longer, but to live better. In fact, most aging individuals will tell you that their quality of life is more important than simply extending lifespan.CoQ10 and selenium can beneficially impact both.

For this follow-up analysis from the initial Swedish study, when subjects were matched by age, gender, and baseline heart function, the difference was clear. While quality of life scores declined in all subjects (as it does in so many people as they age), the decline was significantly less sharp in the supplemented CoQ10/selenium group than in the placebo group.3

In addition, over the 4-year period, the people in the supplemented group spent 246 fewer days in the hospital than those in the placebo group. Considering the risks posed by being in the hospital—including medical errors, infections, pneumonia, and more—spending fewer days in the hospital could do more than improve quality of life; it could be a potential lifesaving benefit in and of itself.

Long-Term Benefits

A further analysis from the initial Swedish study reveals perhaps the most surprising finding from this major study which was that CoQ10 and selenium were still effective at reducing cardiovascular deaths 10 years after the start of the study. This means that CoQ10 and selenium continued to extend their life-saving benefits years after the participants stopped taking the supplements!

Obesity is top cause of preventable life-years lost, study shows

A team of researchers from Cleveland Clinic and New York University School of Medicine have found that obesity resulted in as much as 47 percent more life-years lost than tobacco, and tobacco caused similar life-years lost as high blood pressure.

Preliminary work presented by Cleveland Clinic at the 2017 Society of General Internal Medicine Annual Meeting analyzed the contribution of modifiable behavioral risk factors to causes-of-death in the U.S. population, using 2014 data.

Based on this preliminary work, the team found the greatest number of preventable life-years lost were due to (in order from greatest to least) obesity, diabetes, tobacco use, high blood pressure and high cholesterol. However, researchers also noted that some individuals may have needs that are very different than those of the broader U.S. population. For an obese and alcoholic patient, for example, alcohol use may be more important to address than obesity, even though obesity has a greater impact on the population.

Results highlight the clinical and public health achievement of smoking cessation efforts because 15 years ago, tobacco would have topped the list.
"Modifiable behavioral risk factors pose a substantial mortality burden in the U.S.," said Glen Taksler, Ph.D., internal medicine researcher from Cleveland Clinic and lead author of the study. "These preliminary results continue to highlight the importance of weight loss, diabetes management and healthy eating in the U.S. population."

A key takeaway is that three (diabetes, hypertension and high cholesterol) of the top five causes of death can be treated, so helping patients understand treatment options and approaches can have a powerful impact on life-years. The results also highlight the importance of preventive care in clinical practice and why it should be a priority for physicians.

To estimate the number of life-years lost to each modifiable risk factor, researchers examined the change in mortality for a series of hypothetical U.S. populations that each eliminated a single risk factor. They compared the results with the change in life-years lost for an "optimal" population that eliminated all modifiable risk factors. Recognizing that some less common factors might place substantial burden on small population subgroups, they also estimated life expectancy gained in individuals with each modifiable risk factor.

"The reality is, while we may know the proximate cause of a patient's death, for example, breast cancer or heart attack, we don't always know the contributing factor(s), such as tobacco use, obesity, alcohol and family history. For each major cause of death, we identified a root cause to understand whether there was a way a person could have lived longer."

Dr. Taksler and colleagues are continuing to conduct research in this area, and analyze and refine results.
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domingo, 23 de abril de 2017

When liver immune cells turn bad

A high-fat diet and obesity turn "hero" virus-fighting liver immune cells "rogue", leading to insulin resistance, a condition that often results in type 2 diabetes, according to research published today in Science Immunology.
Using cells from mice and human livers, Toronto General Hospital Research Institute researchers demonstrated for the first time how under specific conditions, such as obesity, liver CD8+ T cells, white blood cells which play an important role in the control of viral infections, become highly activated and inflammatory, reprogramming themselves into disease-driving cells.

Scientists have been trying for many years to discover why the liver continues to pump out too much glucose in people with diabetes. This paper sheds light on the markers of activation and inflammation in CD8+ T cells and the Interferon-1 pathway which helps stimulate their function.

The research is entitled, "Type 1 Interferon Responses Drive Intrahepatic T cells to Promote Metabolic Syndrome," by first authors Magar Ghazarian, a former graduate student, Dr. Xavier Revelo, a post-doctoral fellow in the lab of Dr. Daniel Winer, and senior authors Dr. Shawn Winer, Laboratory Medicine, St. Michael's Hospital, Laboratory Medicine and Pathobiology, University of Toronto, and Dr. Daniel Winer, Diabetes Research Group and the Department of Pathology, Toronto General Hospital Research Institute and the Departments of Laboratory Medicine and Pathobiology and Immunology, University of Toronto.

"We found that under conditions of obesity and a high-fat diet, the cells that typically strengthen our immune system by killing viruses and pathogens instead increase blood sugar. They become pathogenic and worsen insulin resistance," explains Dr. Dan Winer. In fact, the normal function of the immune cells becomes misdirected. The pathways they would typically use to fight infection create inflammation, unleashing a chemical cascade which impacts insulin and glucose metabolism.

"The immune system in the liver represents a key missing link in our understanding of how the liver malfunctions in obesity to dysregulate sugar levels," adds Dr. Revelo.
In the study, researchers fed mice a high-fat diet, 60% of which was saturated fat, for 16 weeks. Compared with normal chow diet-fed mice, the high-fat diet mice showed worsened blood sugar, increased triglycerides, a type of fat (lipid) in the blood, and a substantial increase in the numbers of CD8+ T cells in the liver.
Instead of responding to viruses or other foreign invaders in the body, the activated CD8+ T cells launch an inflammatory response to fat, and to bacterial components that migrate to the liver from the gut through the blood.
The activated T-cells divide rapidly, pumping out increased numbers of cytokines, proteins that assist them in an active and excessive immune response. This pro-inflammatory response in turn interferes with normal metabolism in the liver, specifically jamming up or blocking insulin signaling to the liver cells.
Since the liver stores and manufactures glucose or sugar depending upon the body's need, the hormone insulin signals whether the liver should store or release glucose. This system keeps circulating blood sugar levels in check. If that signal is disrupted or blocked, the liver continues to make more sugar, pouring it into the bloodstream. If the liver is over-producing glucose, it becomes difficult to regulate blood sugar.

"This response never manifested itself until humans started to eat high-sugar, high-fat, high-calorie diets," says Magar Ghazarian, now a medical student in Ireland.
Adds Dr. Shawn Winer: "We're moving from studying diabetes as a metabolic syndrome - a combination of nutritional and hormonal imbalances - to include the role of the immune system and inflammation. That's the developing link. Inflammation is emerging to be a major mediator of insulin resistance."
Insulin resistance is a pathological condition linked to obesity, in which cells fail to respond normally to the hormone insulin which helps the body metabolize glucose. This results in poor absorption of glucose by cells, causing a buildup of sugar in the blood. Long-term insulin resistance eventually leads to diabetes.
The findings were confirmed in genetically-modified mice, as well as in human liver cells.

The researchers found that in genetically-modified mice lacking Interferon-1, who were also fed a high-fat diet, the CD8+ T cells did not produce an inflammatory response, and the mice had near normal blood sugar levels.
In further investigations of human liver cells from nearly 50 donor tissues of humans with varying degrees of body mass index (BMI) and liver fat, higher levels of CD8+ T cells were linked with higher levels of blood sugar or more advanced fatty liver disease. Donor tissues were obtained from Saint Louis University Hospital, Washington University School of Medicine and Mid-American Transplant Services from St. Louis and University Health Network.

The researchers note that CD8 + T cells could potentially be used as markers for the progression of fatty liver disease, which is expected to become the leading indication for liver transplantation within the next one or two decades.
Type 2 diabetes is one of the fastest growing diseases in Canada with more than 60,000 new cases yearly. Nine out of ten people with diabetes have type 2 diabetes. Being overweight or obese is an important risk factor for diabetes. It is estimated that 3.5 million or about 9% of Canadians have diabetes.