Research indicates that a lack of dietary fiber may result in accelerated brain aging, potentially contributing to the prevalence of Alzheimer’s disease and dementia. Expert nutritionists, such as Dr. Emily Leeming and Nutritional Psychologist Kimberly Wilson, presented this theory at the Cheltenham Science Festival.
In fact, dementia, a condition characterized by memory loss, is described as a model of accelerated brain aging by Wilson. This highlights the importance of dietary fiber for brain health and overall well-being.
Most adults in the UK are not consuming enough fiber, falling short of the recommended intake of 30g per day for optimal health. This deficiency poses a risk factor for various health conditions, including cognitive decline and neurodegenerative diseases.
According to Leeming and Wilson, consuming fiber-rich foods is essential for brain protection. Fiber is metabolized by gut bacteria, producing short-chain fatty acids that play a crucial role in maintaining the integrity of the blood-brain barrier. These fatty acids help prevent the passage of harmful substances into the brain.
If you are not getting enough fiber in your diet, Leeming suggests incorporating fiber-rich foods like rye bread, beans, nuts, and vegetables. Additionally, consuming dark chocolate and root vegetables with the skin on can help boost your fiber intake.
By increasing fiber consumption, individuals can support their gut health, manage blood sugar levels, and reduce the risk of chronic diseases. Leeming and Wilson emphasize the importance of fiber for overall health and well-being.
Our experts, Kimberly Wilson and Dr. Emily Leeming, have extensive experience in nutrition and psychology, respectively. Wilson is a licensed psychologist and author, while Leeming is a Registered Dietitian and Research Fellow with a focus on the gut microbiome.
Two of the researchers and several study participants with Laron syndrome
Jaime Guevara-Aguirre and Bartel Longo
People with rare genetic mutations that cause short stature and may even live longer are helping to understand the causes of aging.
People with unusual genetic mutations have some characteristics that protect them from heart disease, one of the most common causes of death, and this explains why their life expectancy exceeds that of the general population. You may have.
A signaling molecule called insulin-like growth factor-1 (IGF-1) has long been suspected to be involved in longevity. Several animals, including worms and mice, have been shown to live longer when their levels of this compound are artificially lowered, such as through genetic modification. Centenarians also have slightly lower IGF-1 levels,on average.
In most species, IGF-1 promotes growth when the animal is young and influences how cells use energy later in life. One idea is that there is a trade-off between animals investing energy in further growth and maintaining health.
“As you get older and your body starts to break down, you want to spend your energy on preventing your body from breaking down instead of spending it on growth,” he says. Nir Barzilai from the Albert Einstein College of Medicine in New York was not involved in the new study.
The question of whether this trade-off also occurs in humans is through a rare genetic disease called Laron syndrome, first identified in a group of Ecuadorians whose ancestors left Spain during the Inquisition centuries ago. can be researched.
This mutation causes people to have defective growth hormone receptors, leading to short stature. People with Laron syndrome also have low levels of IGF-1 because the release of IGF-1 is usually triggered by growth hormone.
The researchers found that more people with the disease were surviving longer than expected compared to the general Ecuadorian population. 'We know they are more common in older people' walter longo at the University of Southern California in Los Angeles.
In the latest study, Longo and his colleagues compared 24 people with Laron syndrome from Ecuador or the United States to 27 relatives who did not have the mutation. People with Laron syndrome appeared to be healthier on several heart-related measures, including blood pressure, blood sugar levels, and sensitivity to insulin, a hormone involved in controlling blood sugar levels.
People with this mutation also had higher levels of a compound called low-density lipoprotein. Low-density lipoproteins are also known as “bad cholesterol” because they are thought to make arteries more susceptible to plaque, which can lead to heart attacks. However, only 7 percent of Laron syndrome patients had such plaques, compared with 36 percent of their relatives.
The small number of people in the study means this difference may have arisen by chance, but it does suggest that their arteries appear less unhealthy than those of people without the mutation. suggests, Longo said.
This new finding supports the idea that somehow weakening the IGF-1 signaling pathway in later life can slow the aging process. Alexey Maklakov at the University of East Anglia, Norwich, UK. “It's a matter of timing,” he says. “At critical stages of growth and development, you definitely don't want to do that. But later in life, it can interfere with the function of these pathways.”
Do you notice your muscles becoming more rigid and harder to manage as you age? A new ‘Atlas of Aging’ has been developed to explain why this happens and to provide potential treatments to prevent it. Additionally, it may lead to legal action.
Focusing on the effects of natural aging, this atlas delves into the intricate changes that occur in muscle tissue at the cellular and molecular levels as we grow older. It also highlights how our muscles actively combat the aging process, potentially aiding in the development of new treatments to enhance the aging body.
As we age, our muscles can weaken, making everyday activities like standing and walking more challenging. However, the underlying causes of this decline are not fully understood. Frailty can lead to an increased risk of falls, reduced mobility, and loss of independence.
Lead author, Dr. Sarah Teichman from the Wellcome Sanger Institute, states that these insights into healthy skeletal muscle aging are empowering researchers worldwide to explore various strategies to combat inflammation, promote muscle regeneration, maintain neural connections, and more.
Longevity expert Andrew Steele emphasizes the importance of understanding the cellular changes that contribute to the loss of physical strength as we age. He underscores the potential of this research to develop therapeutic interventions that support healthier aging in future generations.
The creation of the atlas of aging muscle involved utilizing advanced imaging and single-cell sequencing techniques to analyze skeletal muscle samples from 17 adult donors aged between 20 and 75. The findings shed light on gene activity related to protein production and revealed how muscle fibers age at different rates.
Age-related loss of primary fast-twitch muscle fibers is mitigated by the body’s ability to enhance the properties of remaining fibers and rebuild connections between weakened nerves and aging muscles. This understanding can potentially inform strategies to maintain strength and independence as we grow older.
To learn more about the experts involved in this research, Dr. Andrew Steele, a scientist, author, and presenter, has authored “Ageless: The new science of growing older without getting older.” Combining his background in physics with biology, Steele’s work focuses on deciphering human DNA at the Francis Crick Institute in London.
Read more:
What happens to my body as I get older?
9 simple science-backed changes to reverse your biological age
Groundbreaking discovery of anti-aging cells could help people stay young for longer
Protein plaques in the brain may be caused by mitochondrial dysfunction
Sebastian Kauritzky/Alamy
If you own a car, you’ve probably noticed that your engine becomes less efficient over time. The farther you drive, the more fuel it takes to cover the same distance. Eventually, you’ll end up with so little power that you need a physical push to climb a gentle hill.
It is now becoming clear that much the same holds true for the human brain. Microscopic structures called mitochondria, found in all brain cells, are literally the engines of our thoughts and emotions. As we age, we find it increasingly difficult to generate enough energy to power mental activity. Worse, just like an old car leaves behind a cloud of smoke, the power source of our cells begins to produce unnecessary waste products that slowly pollute our brains. This means that mitochondrial dysfunction may underlie some of the most serious brain diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and motor neuron disease.
According to this “grand unified theory” of neurodegeneration, recharging neurons through restoration of their power plants can prolong healthy brain function. This idea has already inspired some exciting new treatments for age-related brain diseases, with multiple drug candidates under investigation. Some researchers are exploring the possibility of transplanting healthy mitochondria into damaged, aging brains to reactivate them. “If you keep replacing the parts in your car, it can last forever,” he says. claudio soto, a neurologist at the University of Texas Health Science Center at Houston. “So what happens if we try to run this…
A study of killifish by the Max Planck Institute revealed that older fish enter a state of starvation due to changes in their adipose tissue. Activating a specific subunit of AMP kinase restores health and longevity in humans, suggesting a new way to promote healthier aging in humans.
Genetic switch rescues aging fish from starvation trap.
Fasting interventions that alternate between fasting and refeeding are generally thought to improve health. However, these interventions do not work well in older animals.
The question is, why?
By studying short-lived killifish, researchers at the Max Planck Institute for the Biology of Aging in Cologne found that older fish deviate from the fasting and refeeding cycles of their youth, and even when they consume food, they permanently It was shown that the body enters a state of fasting. However, the benefits of post-fasting refeeding in old medaka fish can be restored by genetically activating specific subunits of AMP kinase, an important sensor of cellular energy.
These mutant fish experience improved health and longevity and require both fasting and refeeding to provide health benefits, which have been shown to act through AMP kinase. I am.
Medaka ages rapidly. The bright colors of their youth fade in just a few months.Credit: K. Link / Max Planck Institute for the Biology of Aging
It has already been shown in many model organisms that reducing food intake through calorie restriction or periods of fasting has positive effects on health. However, it is difficult for humans to reduce the amount they eat throughout their lifetime. To find the optimal timing for fasting, researchers introduced fasting interventions at different ages, but found that these interventions in older adults did not provide the same benefits as in younger animals.
A research team in Cologne, Germany, now investigated the effects of age-related fasting on medaka fish. Medaka is a rapidly aging fish that grows from young to old in just a few months. The researchers either starved young and old fish for several days or fed them twice a day. They found that the visceral adipose (adipose) tissue of older fish became less responsive to feeding. “Adipose tissue is known to respond most strongly to changes in food intake and plays an important role in metabolism, which is why we looked at it more closely,” said lead author of the study. explains Roberto Ripa.
It is important to alternate between fasting and meals
The researchers found that, unable to respond to the feeding phase, the adipose tissue of old fish enters a permanent state of starvation, where energy metabolism ceases, protein production decreases, and tissue does not renew. “We thought that older fish would be unable to switch to fasting after feeding. Surprisingly, the opposite was true, and older fish would be unable to switch to fasting after feeding. , they were in a state of permanent starvation,” said study leader Adam Antebi, director of the Max Planck Institute for the Biology of Aging.
Permanently fasted adipose tissue
When the researchers looked more closely at how the fat tissue of old fish differs from that of young fish, they discovered a specific protein called AMP kinase. This kinase is a cellular energy sensor and is composed of various subunits, among which the activity of the γ1 subunit decreases with age. When scientists genetically engineered this subunit to increase its activity, the starvation-like state was overcome, and the old fish became healthier and lived longer.
human aging
Interestingly, an association was also found between the γ1 subunit and human aging. Significantly lower levels of certain subunits were measured in samples from older patients. Additionally, in human samples, we were able to show that people who are less frail at older ages have higher levels of the γ1 subunit.
“Of course, we still don’t know whether the human γ1 subunit is actually involved in healthy aging. The next step is to find a molecule that precisely activates this subunit and use it to “We investigate whether this can have a positive impact on aging,” explains Adam Antebi.
Reference: “Refeeding related AMPK”γ1 Complex activity is a hallmark of health and longevity.” Roberto Ripa, Eugen Barrissa, Joachim D. Steiner, Raymond Lavoie, Andrea Annibal, Nadine Hocher, Christian Razza, Luca Dolfi, Chiara Calabrese, By Anna M. Meyer, Maria Cristina Polidori, and Roman – Ulrich Müller and Adam Antebi, November 13, 2023, natural aging. DOI: 10.1038/s43587-023-00521-y
Researchers used computer models to investigate the evolutionary role of aging. They challenge the notion that aging has no positive effects and suggest that aging may promote evolution in a changing environment, thereby benefiting subsequent generations. I am. Their findings indicate that aging may be an advantageous trait selected by natural evolution. Credit: SciTechDaily.com
The mysteries of aging have fascinated people for thousands of years. Because aging is usually associated with a gradual decline in most bodily functions, many people are willing to do anything to stop or reverse this process. Aging is a natural part of life, but biologists understand surprisingly little about the evolutionary emergence of this process. It’s not clear whether aging is inevitable. That’s because there are some organisms that never seem to age at all, and there is also a phenomenon known as negative aging or rejuvenation. In some turtles, vital functions improve with age.
Studying the evolutionary role of aging
Researchers at the Institute for Evolution, led by scholar Airs Zatmary, have sought to debunk previously proposed but unproven theories of aging. This theory suggests that, under the right circumstances, evolution can encourage the proliferation of genes that control aging.
To test their hypothesis, the researchers used a computer model they developed. This model is an algorithm that allows scientists to simulate long-term processes in populations of organisms and genes in a controlled environment. Essentially, such models allow you to run evolutionary scenarios and get results in hours instead of millions of years. Modern evolutionary research is unthinkable without computer modeling.
Exploring the purpose of aging
The basic research question was simple. The question was, “Is there any meaning to aging?” Does it serve some evolutionary function or is it truly a bitter and deadly byproduct of life? “If there is selection for aging, then aging may have an evolutionary function. Our study aimed to reveal this selection,” he says Eörs Szathmáry. “According to the classical explanation, aging occurs in a population even without selection. It is because individuals die sooner or later without aging (as a result of disease or accidents), This creates an opportunity for genes to accumulate that have a negative effect on older individuals (thus causing aging), meaning that aging is only a side effect of evolution. It means that there is no adaptive function.”
Challenging common sense
During the last century, several evolutionary theories have been formulated to explain inevitable aging without active functions using different biological mechanisms. Although some scientists accepted this assumption as fact, the discovery of organisms that do not age led more and more researchers to question the inevitability of aging and to suggest that perhaps aging has benefits as well. I suggested that it might be.
“The evolutionary biology community has accepted that classical non-adaptive theories of aging cannot explain all aging patterns in nature, meaning that the explanation of aging has once again become an open question. “I mean,” Zatomary said. “Alternative adaptation theories provide a solution to this problem by suggesting positive effects of aging. For example, aging and death may be more advantageous for individuals in a changing environment. This is because doing so reduces competition that prevents the survival and reproduction of more fit offspring with a better genetic makeup.
However, this scenario is only true if the individual is surrounded primarily by relatives. Otherwise, during sexual reproduction, non-senescent individuals would “steal” better (better adapted to environmental changes) genes from aging population members, thus erasing significant senescence.
Aging as a catalyst for evolution
Hungarian biologists ran a model and found that aging can actually accelerate evolution. This is an advantage in a changing world. Faster adaptation allows us to find suitable traits faster, which supports the survival and spread of offspring genes. This means that aging can become a highly advantageous trait and be favored by natural selection.
Reference: András Siraj, Tamash Charan, Mauro Santos, Airs Zatmary, “Directional selection combined with kin selection favors the establishment of senescence”, October 23, 2023. BMC biology. DOI: 10.1186/s12915-023-01716-w
Funding: National Agency for Research, Development and Innovation (Hungary), Bolyai János Research Fellowship of the Hungarian Academy of Sciences, New National Excellence Program of the Ministry of Culture and Innovation, Ministry of Science and Innovation, Autonomous Region of Catalonia 2021 Special Guest Scientist Volkswagen Foundation, Hungary Fellowship Program of the Academy of Sciences (Initiative “Leben?
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