Tag: Health & Medicine

Brain’s reaction to the taste of beer helps explain why it’s hard to stop at one

Beer gets into our heads, even before the alcohol has time to kick in.
Image credit: 123RF Stock Photo

I remember quite vividly the first time I tried beer — I almost spit it out. Bitter, bubbly and generally bad, I didn’t get why everyone seemed to be so enamored with it. Yet I, like so many people in the world, continued to drink it. Have you ever wondered why we, as a species, consume alcoholic beverages even though they taste terrible at first?

A new study suggests that despite the bitter taste, the chemicals in beer trigger the brain’s reward system. This pleasurable effect might just explain why we’re so willing to keep drinking past the first sip — until intoxication takes over, and we’ll drink just about anything. But more importantly, this new research, published today in the journal Neuropsychopharmacology,  may explain why some people can drink casually while others slip into alcoholism.  Continue reading “Brain’s reaction to the taste of beer helps explain why it’s hard to stop at one”

Conservation is important – for the sake of our health

Growing up, I was one of those lucky kids who wasn’t allergic to anything. I felt like I was invincible – while my friends were pestered by pollen or peanuts, I was able to eat and play with reckless abandon. Childhoods like mine, however, are becoming more and more scarce. A recent study found that in 2008, peanut allergies in kids were three and a half times higher than a decade before, with similar trends occurring in a number of food allergies. Similarly, the prevalence of hay fever in developed countries has increased about 100 percent in each of the last three decades. It’s not just allergies – other chronic inflammatory diseases, from arthritis to asthma, continue to rise in our populations. A new paper in the Proceedings of the National Academy of Sciences suggests that perhaps the problem isn’t what we’re putting into our environment, but what we’re removing from it: that the loss of biodiversity is negatively impacting our health.

One of the most popular hypotheses to explain the rise in inflammatory conditions is known as the Hygiene Hypothesis, which says that our increasingly sterile lifestyle is to blame for our allergic reactions. We now live in a world of antibacterial soaps, instant hand sanitizer, vaccines, and antibiotics, all of which have taken over the job of protecting our children from dirt and germs. Left with nothing to do, kid’s immune systems get a little stir crazy, and start attacking even minor invaders like pollen with increased zeal. But Ilkka Hanski and his colleagues from the University of Helsinki in Finland suggest the Hygiene Hypothesis extends beyond how clean we keep our house. They put forward a Biodiversity Hypothesis, which suggests that less contact with the nature and biodiversity is adversely affecting the microbes on and in our bodies, leading to increased susceptibility to immune disorders.

To test this hypothesis, the research team investigated the relationship between biodiversity, allergen susceptibility, and skin microbial communities in a little over 100 randomly chosen teenagers in Finland. The kids grew up in a variety of settings, from tightly-packed villages to rural farmlands. For each participant, they measured how sensitive their skin was to allergens and what kind of microbes were living on there. Based on their skin’s immune reaction, they classified the students as allergen-sensitive (a condition known as atopy) or not. The researchers also roughly calculated the level of environmental biodiversity where the participants lived by looking at the amount of plant cover of their yards and the major land use types within 3 km of their homes, allowing comparisons between it and the participant’s allergy sensitivity and skin microorganisms.

The team found a strong, significant correlation between the diversity of a particular class of skin bacteria, called gammaproteobacteria, and allergen sensitivity. Though they only represented 3% of the skin bacterial community, gammaproteobacteria were the only class that showed a significant decrease in diversity in the atopic individuals. So, to get a closer look at this phenomenon, directly comparing the presence of different gammaproteobacteria with levels of an anti-inflamatory marker, IL-10, in the subjects’ blood. The presence of one gammaproteobacterial genus, Acinetobacter, was strongly linked to higher levels of IL-10 in healthy individuals but not in the allergen-sensitive ones. As the authors explain, this suggests that these microbes may help teach the immune system to ignore pesky allergens.

“The positive association between the abundance of the gammaproteobacterial genus Acinetobacter and IL-10 expression… in healthy individuals, but not in atopic individuals, is consistent with IL-10’s central role in maintaining immunologic tolerance to harmless substances.” Thus, the authors say, “the lack of association between Acinetobacter and IL-10 expression in atopic individuals in the present study might re?ect a breakdown of the regulatory mechanisms.”

How, exactly, Actinetobacter and other gammaproteobacteria influence our immune system has yet to be determined. What the authors did show is that environment a person grows up in has a strong effect on the presence and diversity of this group of bacteria. Since gammaproteobacteria are are commonly found in soil and on plants (including ?owering plants and their pollen), it may not seem that surprising to the researchers that the environmental diversity around a subject was strongly correlated to increased diversity of their skin gammaproteobacteria. But what is astounding is that this relationship held even when the researchers stepped back and looked at the overall connection between allergen sensitivity and the surrounding environment; the more natural biodiversity where the kid grew up, the less likely he or she was to be sensitive to allergens.

“The present results demonstrate that biodiversity can be surprisingly strongly associated with atopy.”

This suggests that the urban-dwelling nature of developed countries may be to blame for their increasing problem with inflammatory diseases. If so, conservation of natural spaces, including parks and other green initiatives, may be key to protecting the health of future generations. “Interactions with natural environmental features not only may increase general human well being in urban areas, but also may enrich the commensal microbiota and enhance its interaction with the immune system, with far-reaching consequences for public health.”

Since allergies cost us almost $14.5 billion annually including medical expenses, missed school and work, and over the counter drugs, there may be a strong monetary incentive to conserve our natural areas – if only for the sake of our health. That’s not even considering the other economic incentives for conservation, including water filtration and storm protection, which have been estimated at over $4.4 trillion dollars per year.

What all these studies tell us is that the cost of conservation is strongly outweighed by its benefits. Period.

 

Reference: Hanski, I., von Hertzen, L., Fyhrquist, N., Koskinen, K., Torppa, K., Laatikainen, T., Karisola, P., Auvinen, P., Paulin, L., Makela, M.J. & Environmental biodiversity, human microbiota, and allergy are interrelated, Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.1205624109

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Reversing a heart attack: scientists reprogram scar tissue into working muscle

Cardiovascular disease is the world’s leading cause of death. Approximately every 25 seconds, an American has a heart attack. One of the vessels to the heart gets blocked, cutting off blood flow to part of the heart. Then, the starving tissue begins to die, causing pain in the chest and difficulty breathing and, eventually, death. Every minute, someone in America dies from one of these coronary events. Those that survive the attack are still at risk for future problems as dead heart muscle leads to scar tissue that weakens the heart and increases the chance of heart failure. Until now, there was little that could be done for them, other than to encourage healthy lifestyle practices.

Just this week, Gladstone researchers announced a major breakthrough in heart disease research: they successfully reprogrammed scar tissue in live mice back into functional heart muscle.

A mouse heart a month after a heart attack - scar tissue appears white

The researchers were able to use a virus-based system to deliver three key genes that guide embryonic heart development—Gata4, Mef2c and Tbx5 (GMT)—to areas of mouse hearts that were damaged in a heart attack. Within a month, cells that normally became scar tissue were beating away again as if they were not knocking on death’s door just 30 days before. By the three month mark, treated mice showed marked improvements in cardiac functioning.

“The damage from a heart attack is typically permanent because heart-muscle cells—deprived of oxygen during the attack—die and scar tissue forms,” said Dr. Deepak Srivastava, director of cardiovascular and stem cell research at Gladstone. “But our experiments in mice are a proof of concept that we can reprogram non-beating cells directly into fully functional, beating heart cells—offering an innovative and less invasive way to restore heart function after a heart attack.”

“This research may result in a much-needed alternative to heart transplants—for which donors are extremely limited,” said lead author Dr. Li Qian, a post doc at the California Institute for Regenerative Medicine. But the best part is that this method would use the person’s own cells, removing the need for stem cells or donor hearts. “Because we are reprogramming cells directly in the heart, we eliminate the need to surgically implant cells that were created in a petri dish.”

“We hope that our research will lay the foundation for initiating cardiac repair soon after a heart attack—perhaps even when the patient arrives in the emergency room,” said Srivastava. The ability to regenerate adult heart tissue from its own cells is a promising approach to treating cardiac disease because it may face fewer obstacles to clinical approval than other approaches. However, there is much to be done before this breakthrough becomes a treatment. “Our next goal is to replicate these experiments and test their safety in larger mammals, such as pigs, before considering clinical trials in humans.”

Previous work has been able to do this kind of cellular reprogramming in cultured cells, but clinically it is much more efficient if a treatment can work directly on live hearts. In 2010, coronary heart disease was projected to cost the United States $108.9 billion, including the cost of health care services, medications, and lost productivity. If research such as this can lead to improved functioning after a heart attack, it could save millions in health care costs, not to mention potentially save lives by preventing heart failure down the line. While this research’s implications for heart disease treatment is clear, this kind of in vivo reprogramming may be also useful in a variety of other diseases where tissue damage is a major cause of symptoms, including Alzheimer’s and Parkinson’s disease.

A normal and reprogrammed heart cell beating eight weeks after a heart attackReference: Qian, L. et al. 2012. In vivo reprogramming of murine cardiac fibroblasts into induced cardiomyocytesNature DOI:10.1038/nature11044