Elders with negative attitude about aging may be less resilient to stress
Older adults with a positive attitude about aging may be more resilient to stress, according to a new study.
“Previous research has generally found the same thing, a more positive attitude is beneficial,” said coauthor Jennifer Bellingtier, of North Carolina State University in Raleigh.
“People with positive attitudes are less likely to be hospitalized and tend to live longer,” she told Reuters Health.
The researchers had 43 adults, ages 60 to 96, answer questions about their experience with aging in general, like feeling more or less useful now than when they were younger, or more or less happy.
Then, on a daily basis for eight days, participants completed questionnaires that asked about stressful events and negative emotions like fear, irritability or distress.
As reported in The Journals of Gerontology: Series B, people with more positive attitudes about aging generally tended to report consistent emotional states across the eight-day period, regardless of stressors.
For older adults, stress often centers on relations with family or friends, while for younger people it may more often be related to work, Bellingtier said.
Almost all cardiovascular functions tend to be worse in people with more negative reactions to stress, she said.
“The media presents a distorted view of aging, making jokes about mental and physical incompetence,” Bellingtier said. “The more you’re exposed to it the more you’re picking up those stereotypes.”
In fact, she said, older adults are often happier with their lives than people in their 20s or 30s, given their real world life experience and time to develop meaningful relationships.
She and her coauthors tried to account for personality in general as well, since people who are generally positive may have more positive attitudes about aging.
Becca Levy of the Yale School of Public Health in New Haven, Connecticut, has also studied this question, although she wasn’t part of this new study. She told Reuters Health by email that negative age stereotypes can exacerbate older individuals’ stress experience, while positive age stereotypes can buffer their experience of stress.
“In a recent intervention study with older individuals, we found that it is possible to bolster positive age stereotypes and reduce negative age stereotypes,” Levy said.
Are certain cultures or races more or less prone to Alzheimer’s or other dementias?
My answer to Are certain cultures or races more or less prone to Alzheimer's or other dementias?
Answer by Connie b. Dellobuono:
Less prone to disease are people in blue zones (exercise more, believe in God, whole foods, genes): http://www.worldlifeexpectancy.com/longevity-hot-spots
Alzheimer's disease is more in places where there is less sunshine, western lifestyle (stress filled, exercise less) and following a western diet.
Are certain cultures or races more or less prone to Alzheimer's or other dementias?
Love and tolerance and not hate and bigotry
Such bigotry isn’t limited to any specific part of the country. In a recent incident in Williamsburg, Brooklyn — a neighborhood that is held up as the archetype of the gentrification of New York City — two Muslim women were the targets of anti-Muslim sentiment.
Amani Alkhat and Eman Bare say they were on their way to lunch, and waiting at a stoplight when an employee of a bar said to them, over his shoulder: “ISIS.”
According to a Facebook post she wrote following the incident, Alkhat turned around and said, “Excuse me?” to the man, who grinned and responded, “Are you a part of ISIS? I’m just asking!”
She continued:
He had some bad luck in the Muslim women he chose to harass today, right? We immediately turned around and confronted him. I asked, “Well, are you a part of the KKK? Are you a Nazi? Actually, are you a mass shooter? Are you going to light us up right now?” I guess these two so-called oppressed girls in headscarves scared him off, because he quickly gathered his things to run back into his store. I guess he didn’t believe #MuslimWomenTalkBack!
Should Filipinas follow Venezuelan women on opting for sterilization due to food shortages
Venezuela’s food shortages, inflation and crumbling medical sector have become such a source of anguish that a growing number of young women are reluctantly opting for sterilizations rather t…
Source: Should Filipinas follow Venezuelan women on opting for sterilization due to food shortages
Should Filipinas follow Venezuelan women on opting for sterilization due to food shortages
Venezuela’s food shortages, inflation and crumbling medical sector have become such a source of anguish that a growing number of young women are reluctantly opting for sterilizations rather t…
Source: Should Filipinas follow Venezuelan women on opting for sterilization due to food shortages
Should Filipinas follow Venezuelan women on opting for sterilization due to food shortages
Venezuela’s food shortages, inflation and crumbling medical sector have become such a source of anguish that a growing number of young women are reluctantly opting for sterilizations rather than face the hardship of pregnancy and child-rearing.
Traditional contraceptives like condoms or birth control pills have virtually vanished from store shelves, pushing women towards the hard-to-reverse surgery.
“Having a child now means making him suffer,” said Milagros Martinez, waiting on a park bench on a recent morning ahead of her sterilization at a nearby Caracas municipal health center.
The 28-year-old butcher from the poor outskirts of Caracas decided on the operation after having an unplanned second child because she could not find birth control pills.
In the Philippines, the average number of children per household is 6 where the father has no job and the mother takes more than 3 odd jobs: laundry woman, street vendor and more. Young children coming from a big family are forced to work at a young age to support a whole family.
Other factors affecting the increasing poverty level in the Philippines are:
- low wages of teachers and nurses and rest of workforce
- poor educational system in elementary and high school, families have to opt for expensive private schools
- traffic and poor transportation making it hard for hard working college students who are also taking on odd jobs to send themselves to college in the absence of student loan system
- expensive food items, crowded homes, poor living situation, lack of government funding in health care and social welfare and more
- absence of condoms/family planning support, air pollution from cars/factories/smoking
Microbes manipulate behavior and mood, obesity and cancer
It sounds like science fiction, but it seems that bacteria within us – which greatly outnumber our own cells – may very well be affecting both our cravings and moods to get us to eat what they want…
Source: Microbes manipulate behavior and mood, obesity and cancer
Microbes manipulate behavior and mood, obesity and cancer
It sounds like science fiction, but it seems that bacteria within us – which greatly outnumber our own cells – may very well be affecting both our cravings and moods to get us to eat what they want…
Source: Microbes manipulate behavior and mood, obesity and cancer
Microbes manipulate behavior and mood, obesity and cancer
It sounds like science fiction, but it seems that bacteria within us – which greatly outnumber our own cells – may very well be affecting both our cravings and moods to get us to eat what they want, and often are driving us toward obesity.
In an article published this week in the journal BioEssays, researchers from UC San Francisco, Arizona State University and University of New Mexico concluded from a review of the recent scientific literature that microbes influence human eating behavior and dietary choices to favor consumption of the particular nutrients they grow best on, rather than simply passively living off whatever nutrients we choose to send their way.
A Power Struggle Inside the Gut
Bacterial species vary in the nutrients they need. Some prefer fat, and others sugar, for instance. But they not only vie with each other for food and to retain a niche within their ecosystem – our digestive tracts – they also often have different aims than we do when it comes to our own actions, according to senior author Athena Aktipis, PhD, co-founder of the Center for Evolution and Cancer with the Helen Diller Family Comprehensive Cancer Center at UCSF.
Are we at the mercy of our gut bacteria? The above image illustrates how microbes can “pull our strings,” driving us to crave foods that give them the nutrients they need, including fat and sugar.
While it is unclear exactly how this occurs, the authors believe this diverse community of microbes, collectively known as the gut microbiome, may influence our decisions by releasing signaling molecules into our gut. Because the gut is linked to the immune system, the endocrine system and the nervous system, those signals could influence our physiologic and behavioral responses.
“Bacteria within the gut are manipulative,” said Carlo Maley, PhD, director of the UCSF Center for Evolution and Cancer and corresponding author on the paper. “There is a diversity of interests represented in the microbiome, some aligned with our own dietary goals, and others not.”
Fortunately, it’s a two-way street. We can influence the compatibility of these microscopic, single-celled houseguests by deliberating altering what we ingest, Maley said, with measurable changes in the microbiome within 24 hours of diet change.
“Our diets have a huge impact on microbial populations in the gut,” Maley said. “It’s a whole ecosystem, and it’s evolving on the time scale of minutes.”
There are even specialized bacteria that digest seaweed, found in humans in Japan, where seaweed is popular in the diet.
The Connection Between Digestive Tract and Brain
Research suggests that gut bacteria may be affecting our eating decisions in part by acting through the vagus nerve, which connects 100 million nerve cells from the digestive tract to the base of the brain.
Microbes have the capacity to manipulate behavior and mood through altering the neural signals in the vagus nerve, changing taste receptors, producing toxins to make us feel bad, and releasing chemical rewards to make us feel good,” said Aktipis, who is currently in the Arizona State University Department of Psychology.
In mice, certain strains of bacteria increase anxious behavior. In humans, one clinical trial found that drinking a probiotic containing Lactobacillus casei improved mood in those who were feeling the lowest.
Maley, Aktipis and first author Joe Alcock, MD, from the Department of Emergency Medicine at the University of New Mexico, proposed further research to test the sway microbes hold over us. For example, would transplantation into the gut of the bacteria requiring a nutrient from seaweed lead the human host to eat more seaweed?
The speed with which the microbiome can change may be encouraging to those who seek to improve health by altering microbial populations. This may be accomplished through food and supplement choices, by ingesting specific bacterial species in the form of probiotics, or by killing targeted species with antibiotics. Optimizing the balance of power among bacterial species in our gut might allow us to lead less obese and healthier lives, according to the authors.
“Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating,” the authors wrote.
Implications for Obesity, Diabetes and even Cancer
The authors met and first discussed the ideas in the BioEssays paper at a summer school conference on evolutionary medicine two years ago.
Aktipis, who is an evolutionary biologist and a psychologist, was drawn to the opportunity to investigate the complex interaction of the different fitness interests of microbes and their hosts and how those play out in our daily lives. Maley, a computer scientist and evolutionary biologist, had established a career studying how tumor cells arise from normal cells and evolve over time through natural selection within the body as cancer progresses.
In fact, the evolution of tumors and of bacterial communities are linked, points out Aktipis, who said some of the bacteria that normally live within us cause stomach cancer and perhaps other cancers.
“Targeting the microbiome could open up possibilities for preventing a variety of disease from obesity and diabetes to cancers of the gastro-intestinal tract. We are only beginning to scratch the surface of the importance of the microbiome for human health,” she said.
The co-authors’ BioEssays study was funded by the National Institutes of Health, the American Cancer Society, the Bonnie D. Addario Lung Cancer Foundation and the Institute for Advanced Study, in Berlin.
UC San Francisco (UCSF), now celebrating the 150th anniversary of its founding, is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy, a graduate division with nationally renowned programs in basic, biomedical, translational and population sciences, as well as a preeminent biomedical research enterprise and two top-ranked hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital San Francisco.
Para-inflammation can drive the formation of tumors, aspirin stops it
A previously unidentifiable type of low-grade inflammation may explain why common anti-inflammatory drugs such as aspirin have shown promise against some types of cancer – even when patients don’t …
Source: Para-inflammation can drive the formation of tumors, aspirin stops it
Para-inflammation can drive the formation of tumors, aspirin stops it
A previously unidentifiable type of low-grade inflammation may explain why common anti-inflammatory drugs such as aspirin have shown promise against some types of cancer – even when patients don’t display typical signs of inflammation.
A team led by researchers in the labs of Atul Butte, MD, PhD, director of the Institute for Computational Health Sciences and a professor of pediatrics at UC San Francisco, and Yinon Ben-Neriah, MD, PhD, a professor of immunology and cancer research at the Lautenberg Center of Immunology of Hebrew University Medical School in Jerusalem, identified the role of a subtle form of inflammation in human and mouse cancer cells. According to the authors, this so-called “parainflammation” may explain how a number of different forms of cancer begin.
“Understanding the initial triggers of tumor formation is one of the main challenges in cancer research,” said Dvir Aran, PhD, a postdoctoral scholar in the Butte lab who was co-lead author of the new paper with Audrey Lasry, a PhD student in Ben-Neriah’s lab. “We think parainflammation could be a big part of this puzzle.”
The research was published online on July 8 in the open-access journal Genome Biology.
Common Cancer Gene Mutations ‘Turn Off the Brakes’
Growing evidence over the past decade suggests that people who take a regular dose of aspirin or other non-steroidal anti-inflammatory drug (NSAID) are significantly less susceptible to colorectal cancer, breast cancer and a number of other malignancies. This relationship is mysterious, because most of the cancers that aspirin appears to prevent typically show no overt signs of inflammation.
Aran and colleagues hypothesized that there must be some sort of low-level of inflammation, undetectable with standard methods, that could interact with gene mutations to trigger cancer.
In a previous study, Ben-Neriah’s lab showed that they could induce just such a state of low-level tissue inflammation in mice, which they categorized as parainflammation. They found that non-immune cells, including cells known to give rise to cancer, were able to activate some of the same genetic pathways typically used by the immune system. These pathways then interacted with p53, a regulator of cellular division, to prevent the cells from continuing to grow and divide, driving them toward a state known as cellular senescence.
But when p53 becomes mutated, as it does in many different forms of cancer, the researchers found that parainflammation loses its protective role and becomes dangerous for the tissue.
“Without p53, the brakes are off, and the previously protective energy of parainflammation can drive the formation of tumors,” Ben-Neriah said.
The new study identified a specific pattern of gene expression characteristic of carcinogenic parainflammation in mice with both experimentally induced intestinal parainflammation and mutated p53. This newly identified gene-expression signature, which gave the researchers a way to detect the previously invisible phenomenon, allowed them to detect parainflammation in an array of mouse organoid tumors, human cancer cell lines, and human tumor samples.
The new work is an important advance in understanding the link between inflammation and cancer, said Yale School of Medicine immunobiologist Ruslan Medzhitov, PhD, who coined the term parainflammation in 2008 to describe a theoretical state of low-level inflammation, which he hypothesizes could play a beneficial role in helping cells respond to tissue stress or damage. “The ability to molecularly detect parainflammation should help devise cancer treatments that are tailored to these stereotypic paths the tumors follow,” he said.
Linking Parainflammation to Human Cancer Mortality
To determine the role of parainflammation in human cancers, the researchers mined The Cancer Genome Atlas (TCGA), a National Institutes of Health electronic database, and retroactively examined 6523 primary tumors of 18 different cancer types for the molecular signature of parainflammation. They found that more than a quarter of all tumor samples exhibited parainflammation, and that it was much greater in some cancer types than others: for example, more than three-quarters of pancreatic adenocarcinomas exhibited parainflammation, while no kidney cancers showed significant signs of parainflammation.
The researchers found that tumor samples with the highest levels of p53 mutations also had the highest levels of parainflammation, corresponding with their hypothesis that parainflammation is permissive of p53-driven cancers. High parainflammation was particularly apparent in fast-growing cancers, such as pancreatic and bladder cancers. Within cancer types, higher rates of parainflammation were linked to increased mortality.
In line with their initial hypothesis, the researchers also showed that NSAIDs dampened parainflammation in both cancerous mouse intestinal tumors and cancer cell lines of oral, pancreatic and colorectal origin. These results suggest that the newly developed genetic signature of parainflammation could also be used to better predict which patients would benefit from an aspirin regimen following cancer surgery.
Though the results suggest aspirin may have great promise in fighting cancer, the researchers also cautioned that it is not without side effects. Aran envisions a genetic test for parainflammation, similar to existing tests for predicting breast cancer recurrence, to identify patients who would be most likely to benefit from a course of NSAIDs.
Connecting the Dots of Public Genome Data
Identification of the parainflammation signature is the result of a multi-year collaboration. The work began when Aran, whose background is in bioinformatics, was a PhD student in the lab of co-author Asaf Hellman, PhD, a researcher at Hebrew University Medical School. While Lasry led the animal and cell-line experiments from Ben-Neriah’s lab at Hebrew University, Aran joined Butte’s lab at UCSF to take advantage of the lab’s techniques for computationally analyzing public biomedical data sets.
“The public genomic data allowed us to connect the dots and draw significance from mouse models to humans,” Aran said.
Butte cited the new paper as a key example of what can be done when research data is shared broadly across the research community. “This paper shows how years of research data can be reused to study cancer immunology, one of the newest areas of cancer therapeutics,” he said. “More importantly, it shows the benefits of our efforts to connect research models of cancer, like cell lines and mouse models, with actual cancer therapy in humans, which remains a major challenge in cancer immunology, and one we have been specifically funded to address.”
The research was supported by a Gruss Lipper Postdoctoral Fellowship; the National Cancer Institute of the National Institutes of Health; the Israel Science Foundation (ISF) Centers of Excellence, and the I-CORE program of ISF; the European Research Council; the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation (AMRF); and the Rosetrees Trust. The authors declare no competing financial interests. See the online version of the paper for a full list of authors.
UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy; a graduate division with nationally renowned programs in basic, biomedical, translational and population sciences; and a preeminent biomedical research enterprise. It also includes UCSF Health, which comprises two top-ranked hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital San Francisco, and other partner and affiliated hospitals and healthcare providers throughout the Bay Area.
Neurons ‘Predict’ Drinking’s Restorative Effects Well Before They Unfold
By Leigh Beeson A new UC San Francisco study shows that specialized brain cells in mice “predict” the hydrating effects of drinking, deactivating long before the liquids imbibed can actually change…
Source: Neurons ‘Predict’ Drinking’s Restorative Effects Well Before They Unfold
Neurons ‘Predict’ Drinking’s Restorative Effects Well Before They Unfold
By Leigh Beeson
A new UC San Francisco study shows that specialized brain cells in mice “predict” the hydrating effects of drinking, deactivating long before the liquids imbibed can actually change the composition of the bloodstream. The results stand in stark contrast to current views of thirst regulation, which hold that the brain signals for drinking to stop when it detects liquid-induced changes in blood concentration or volume.
Thirst neurons, located in the subfornical organ (SFO) of the brain, do make us thirsty when they sense that blood volume has dipped or when blood becomes too concentrated. But the same signaling mechanism can’t operate in reverse to alert us to stop drinking because thirst is satiated too soon after a person begins to drink, said UCSF’s Zachary Knight, PhD, senior author of the study, which appears in the August 3, 2016 issue of Nature. Nor can current theories explain why we usually like to drink something while we eat.
“You drink a glass of water and you instantly feel like your thirst is quenched, but it actually takes tens of minutes for that water to reach your blood,” said Knight, assistant professor of physiology. “You eat something salty and you instantly beginning to feel thirsty even though that food is just in your mouth. The dominant model that thirst is a response to changes in the blood didn’t explain that.”
After employing a technique that causes specific, targeted populations of neurons in the mouse brain to fluoresce brightly when active, they used fiber optic probes to measure the activity of SFO neurons when mice drank water. They found that SFO neuron activity shut off almost immediately after the mice started to drink and that the mice stopped drinking shortly thereafter. The brief time scale of these events suggests that, rather than acting only as monitors of blood composition, the SFO must also be linked to sensors in the mouth and throat that rapidly detect food and water consumption.
To confirm the relationship between oral-cavity sensors and SFO neurons, the research group deprived the mice of water overnight and used optogenetic methods – in which particular cells are genetically altered so light delivered via fiber optics can activate or inhibit those cells — to shut down SFO neuron activity when they were again given access to water. Despite the water deprivation, and the presumed changes in the blood that would cause, the mice didn’t drink. But as soon as the researchers stopped silencing the SFO neurons, the mice drank copiously.
The researchers used similar methods to explore why eating often prompts people to drink and why a drink’s temperature affects how refreshing we find it.
“When you sit down at a meal, it’s such a universal experience to have a beverage with you, and we’ve never understood why that is — why you take a bite of food and then take a drink of water,” said Christopher Zimmerman, lead author of the study and a UCSF Discovery Fellow in the Knight laboratory. “And almost everyone has had the experience of exercising or doing some sort of activity and becoming really thirsty, and almost viscerally feeling better after drinking a cold glass of water. But why does cold water seem to quench your thirst so much more rapidly?”
To answer the first question, mice that went without food for a night were given food the following morning but no water. SFO neurons lit up almost immediately as the mice began to eat. Mice who were allowed both food and water also experienced the increase in thirst neuron activity, and when the researchers tamped down the neurons’ activity, the mice reduced their water consumption (though they continued to eat).
When mice were given access to water bottles of varied temperatures, the researchers found that although all the mice drank enough water to turn off their SFO neurons, it required significantly fewer licks to deactivate SFO neurons if the water the mice drank was cold. The scientists zeroed in on temperature as a crucial factor in SFO activity by applying cold metal, similar to that found on animal water-bottle droppers, to the mice’s mouths. This proved as effective as cold water in shutting down the activity of SFO cells.
The new study is an extension of Knight’s previous work on hunger neurons in mice, for which he was awarded a National Institutes of Health New Innovator Award in 2015. In that research his team used similar techniques to record the activity of hunger neurons in mice for the first time and showed that these neurons shut off in response to the sight and smell of food well before the mice actually consumed anything — a surprising finding that parallels those in the new Nature study — just as thirst neurons “anticipate” the bodily changes that drinking will produce, hunger neurons shut down long before mice are actually satiated by eating.
The study was co-authored by Yen-Chu Lin, Erica Huey, and Gwendolyn Daly, research specialists in the Knight Lab, as well as David Leib, Ling Guo and Yiming Chen, students in the UCSF Neuroscience Graduate Program. The study was funded by a UCSF Discovery Fellowship, the New York Stem Cell Foundation, the the American Diabetes Association, Rita Allen Foundation, the McKnight Foundation, the Alfred P. Sloan Foundation, the Brain and Behavior Research Foundation, the Esther A. and Joseph Klingenstein Foundation, the Program for Breakthrough Biomedical Research, an NIH New Innovator Award, the UCSF Diabetes and Obesity Centers, and grants from the National Science Foundation and the National Institutes of Health.
UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy; a graduate division with nationally renowned programs in basic, biomedical, translational and population sciences; and a preeminent biomedical research enterprise. It also includes UCSF Health, which comprises two top-ranked hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital San Francisco, and other partner and affiliated hospitals and healthcare providers throughout the Bay Area.