Category Archives: Human Genetics

Prehistoric people in Europe were consuming milk thousands of years before humans evolved the genetic trait allowing us to digest the milk sugar lactose as adults, finds a new study. The research, published in Nature, mapped pre-historic patterns of milk use over the last 9,000 years, offering new insights into milk consumption and the evolution of lactose tolerance.

Until now, it was widely assumed that lactose tolerance emerged because it allowed people to consume more milk and dairy products. But this new research, led by scientists from the University of Bristol and University College London (UCL) alongside collaborators from 20 other countries, shows that famine and exposure to infectious disease best explains the evolution of our ability to consume milk and other non-fermented dairy products.

While most European adults today can drink milk without discomfort, two thirds of adults in the world today, and almost all adults 5,000 years ago, can face problems if they drink too much milk. This is because milk contains lactose, and if we dont digest this unique sugar, it will travel to our large intestine where it can cause cramps, diarrhoea, and flatulence; known as lactose intolerance. However, this new research suggests that in the UK today these effects are rare.

Professor George Davey Smith, Director of the MRC Integrative Epidemiology Unit at the University of Bristol and a co-author of the study, said: To digest lactose we need to produce the enzyme lactase in our gut. Almost all babies produce lactase, but in the majority of people globally that production declines rapidly between weaning and adolescence. However, a genetic trait called lactase persistence has evolved multiple times over the last 10,000 years and spread in various milk-drinking populations in Europe, central and southern Asia, the Middle East and Africa. Today, around one third of adults in the world are lactase persistent.

By mapping patterns of milk use over the last 9,000 years, probing the UK Biobank, and combining ancient DNA, radiocarbon, and archaeological data using new computer modelling techniques, the team were able to show that lactase persistence genetic trait was not common until around1,000BC, nearly4,000years after it was first detected around 4,7004,600 BC.

The lactase persistence genetic variant was pushed to high frequency by some sort of turbocharged natural selection. The problem is, such strong natural selection is hard to explain, added Professor Mark Thomas, Professor of Evolutionary Geneticsand study co-author from University College London.

In order to establish how lactose persistence evolved, Professor Richard Evershed, the studys lead from Bristols School of Chemistry, assembled an unprecedented database of nearly 7,000 organic animal fat residues from 13,181 fragments of pottery from 554 archaeological sites to find out where and when people were consuming milk. His findings showed milk was used extensively in European prehistory, dating from the earliest farming nearly 9,000 years ago, but increased and decreased in different regions at different times.

To understand how this relates to the evolution of lactase persistence, the UCL team, led by Professor Mark Thomas, assembled a database of the presence or absence of the lactase persistence genetic variant using published ancient DNA sequences from more than 1,700 prehistoric European and Asian individuals. They first saw it after around 5,000 years ago. By 3,000 years ago it was at appreciable frequencies and is very common today. Next, his team developed a new statistical approach to examine how well changes in milk use through time explain the natural selection for lactase persistence. Surprisingly, they found no relationship, even though they were able to show they could detect that relationship if it existed, challenging the long-held view the extent of milk use drove lactase persistence evolution.

Professor George Davey Smiths team had been probing the UK Biobank data, comprising genetic and medical data for more than 300,000 living individuals, found only minimal differences in milk drinking behaviour between genetically lactase persistent and non-persistent people. Critically, the large majority of people who were genetically lactase non-persistent experienced no short or long-term negative health effects when they consume milk.

Professor Davey Smith added: Our findings show milk use was widespread in Europe for at least 9,000 years, and healthy humans, even those who are not lactase persistent, could happily consume milk without getting ill. However, drinking milk in lactase non-persistent individuals does lead to a high concentration of lactose in the intestine, which can draw fluid into the colon, and dehydration can result when this is combined with diarrhoeal disease.

Meanwhile, Thomas had been thinking along related lines, but with more of an emphasis on prehistoric famines. He commented: If you are healthy and lactase non-persistent, and you drink lots of milk, you may experience some discomfort, but you not going to die of it. However, if you are severely malnourished and have diarrhoea, then youve got life-threatening problems. When their crops failed, prehistoric people would have been more likely to consume unfermented high-lactose milk exactly when they shouldnt.

To test these ideas, Professor Thomas team applied indicators of past famine and pathogen exposure into their statistical models. Their results clearly supported both explanations the lactase persistence gene variant was under stronger natural selection when there were indications of more famine and more pathogens.

The authors concluded: Our study demonstrates how, in later prehistory, as populations and settlement sizes grew, human health would have been increasingly impacted by poor sanitation and increasing diarrhoeal diseases, especially those of animal origin. Under these conditions consuming milk would have resulted in increasing death rates, with individuals lacking lactase persistence being especially vulnerable. This situation would have been further exacerbated under famine conditions, when disease and malnutrition rates are increased. This would lead to individuals who did not carry a copy of the lactase persistence gene variant being more likely to die before or during their reproductive years, which would push the population prevalence of lactase persistence up.

It seems the same factors that influence human mortality today drove the evolution of this amazing gene through prehistory.

The study was supported by funding from theRoyal Society, theRCUK-Medical Research Council (MRC)andNatural Environment Research Council (NERC), and theEuropean Research Council.

Paper

Dairying, diseases and the evolution of lactase persistence in Europe by R Evershed et al in Nature.

See original here:
July: genetic-dairystudy | News and features - University of Bristol

Summary: The discovery of new genetic signatures associated with age-related macular degeneration may lead to better diagnosis and treatment of the currently incurable vision disorder.

Source: Garvan Institute

Better diagnosis and treatment of the incurable eye disease age-related macular degeneration is a step closer, thanks to the discovery of new genetic signatures of the disease.

Scientists from the Garvan Institute of Medical Research, the University of Melbourne, the Menzies Institute for Medical Research at the University of Tasmania and the Center for Eye Research Australia, reprogrammedstem cellsto create models of diseased eye cells, and then analyzed DNA, RNA and proteins to pinpoint thegenetic clues.

Weve tested the way that differences in peoples genes impact the cells involved inage-related macular degeneration. At the smallest scale weve narrowed down specific types of cells to pinpoint the genetic markers of this disease, says joint lead author Professor Joseph Powell, Pillar Director of Cellular Science at Garvan.

This is the basis of precision medicine, where we can then look at what therapeutics might be most effective for a persons genetic profile of disease.

Age-relatedmacular degeneration, or AMD is the progressive deterioration of the maculara region in the center of the retina and towards the back of the eyeleading to possible impairment or loss of central vision. Around one in seven Australians over the age of 50 is affected, and about 15 percent of those aged over 80 havevision lossor blindness.

The underlying causes of the deterioration remain elusive, but genetic andenvironmental factorscontribute. Risk factors include age,family historyand smoking.

The research is published today in the journalNature Communications.

The researchers took skin samples from 79 participants with and without the late stage of AMD, called geographic atrophy. Their skin cells were reprogrammed to revert to stem cells called inducedpluripotent stem cells, and then guided withmolecular signalsto become retinal pigment epithelium cells, which are the cells affected in AMD.

Retinal pigment epithelium cells line the back of the retina and are essential to the health and functioning of the retina. Their degeneration is associated with the death of photoreceptors, which are light-sensing neurons in the retina that transmit visual signals to the brain and are responsible for the loss of vision in AMD.

Analysis of 127,600 cells revealed 439 molecular signatures associated with AMD, with 43 of those being potential new gene variants. Key pathways that were identified were subsequently tested within the cells and revealed differences in the energy-making mitochondria between healthy and AMD cells, rendering mitochondrial proteins as potential targets to prevent or alter the course of AMD.

Further, the molecular signatures can now be used for screening of treatments using patient-specific cells in a dish.

Ultimately, we are interested in matching the genetic profile of a patient to the best drug for that patient. We need to test how they work in cells relevant to the disease, says co-lead of the study Professor Alice Pbay, from the University of Melbourne.

Professor Powell and co-lead authors Professor Pbay, and Professor Alex Hewitt from the Menzies Institute for Medical Research in Tasmania and the Center for Eye Research Australia, have a long-running collaboration to investigate the underlying genetic causes of complex human diseases.

We have been building a program of research where were interested in stem cell studies to model disease at very large scale to do screening for future clinical trials, says Professor Hewitt.

In another recent study, the researchers uncovered genetic signatures of glaucomaa degenerative eye disease causing blindnessusing stem cell models of the retina and optic nerve.

The researchers are also turning their attention to the genetic causes of Parkinsons and cardiovascular diseases.

Author: Press OfficeSource: Garvan InstituteContact: Press Office Garvan InstituteImage: The image is credited to Grace Lidgerwood

Original Research: Open access.Transcriptomic and proteomic retinal pigment epithelium signatures of age-related macular degeneration by Joseph Powell et al. Nature Communications

Abstract

Transcriptomic and proteomic retinal pigment epithelium signatures of age-related macular degeneration

There are currently no treatments for geographic atrophy, the advanced form of age-related macular degeneration. Hence, innovative studies are needed to model this condition and prevent or delay its progression.

Induced pluripotent stem cells generated from patients with geographic atrophy and healthy individuals were differentiated to retinal pigment epithelium. Integrating transcriptional profiles of 127,659 retinal pigment epithelium cells generated from 43 individuals with geographic atrophy and 36 controls with genotype data, we identify 445 expression quantitative trait loci in cis that are asssociated with disease status and specific to retinal pigment epithelium subpopulations.

Transcriptomics and proteomics approaches identify molecular pathways significantly upregulated in geographic atrophy, including in mitochondrial functions, metabolic pathways and extracellular cellular matrix reorganization.

Five significant protein quantitative trait loci that regulate protein expression in the retinal pigment epithelium and in geographic atrophy are identified two of which share variants with cis- expression quantitative trait loci, including proteins involved in mitochondrial biology and neurodegeneration. Investigation of mitochondrial metabolism confirms mitochondrial dysfunction as a core constitutive difference of the retinal pigment epithelium from patients with geographic atrophy.

This study uncovers important differences in retinal pigment epithelium homeostasis associated with geographic atrophy.

Here is the original post:
Genetic Clues to Age-Related Macular Degeneration Revealed - Neuroscience News

The video shows a discussion on genome-editing technique rather than an mRNA procedure. mRNA isnt even mentioned once in the entire video.

Context:

While the world continues to deal with the impact of COVID-19, misleading posts accompanying a 2.17 minutes-long video are doing the rounds over social media spreading misinformation about mRNA COVID-19 vaccines by linking them to a genome-editing technology. One such Facebook post is titled WEF video from 2015 discussing the ability of an mRNA medical procedure to permanently change the genetics of the subject and its offspring. Similar posts include a screengrab of the video and make references to COVID-19 vaccines. What do you think they were really doing with all these covid shots? further asked the post. Such posts aim to instill suspicion and fear in the viewers minds about the technology used in COVID-19 vaccines.

In fact:

The 2.17 minutes-long video being circulated on social media begins with the speaker stating, So this is a precision tool that now allows us to take this protein RNA complex and introduce it into cells or tissues.

It appears that the term RNA has been erroneously misinterpreted as mRNA. In addition, we found an extended version of the video,which is 5.25 minutes-long, on the World Economic Forums official YouTube channel, and the video does not mention mRNA even once.

In the video, University of California professor Jennifer Doudna discusses RNA therapies and DNA editing breakthroughs in 2015 at a World Economic Forum(WEF) event. The CRISPR-Cas9 co-discoverer Doudna describes how the technology can alter DNA and offers the possibility of curing human genetic disorders. Professor Doudna has won the 2020 Nobel Prize in Chemistry along with Professor Emmanuelle Charpentier for discovering the gene-editing technique (CRISPRCas9).In the video, she says that compared to what a word processor does for writing, the technique allows for modifying genomic code in living organisms. Doudna claims that they discovered Cas9, a protein that can be designed to split double-stranded DNA, repair breaks, and correct genetic mutations.

According to Medline Plus, CRISPR-Cas9 is an acronym for clustered regularly interspaced short palindromic repeats and CRISPR-associated protein 9. According to the National Human Genome Research Institute, the genome is the entire set of DNA instructions found in a cell. An individuals genome contains all the information needed for growth and function.

National Cancer Institute defines an mRNA as a particular form of RNA. mRNA molecules transfer the data from the DNA in the cells nucleus to the cytoplasm, where proteins are made. However, the CRISPR-Cas9 system involves guide RNA (gRNA). Furthermore, mRNA is not even mentioned in the original paper published on the subject in Science in 2012.

Medline Plus notes that ethical concerns are often raised when human genomes are edited using tools like CRISPR-Cas9. This DNA editing technology is being investigated for several diseases, including single-gene disorders, in research and clinical trials. Contrary to claims on social media, only particular tissues are affected by the modifications, which are not transferred from generation to generation unless the gene alterations are in the egg, sperm, or embryonic cells. Only in such cases, may the changes be passed on to succeeding generations.

Thus, it is evident that there is no relation between COVID-19 vaccines and genome editing technology as these two technologies are entirely different. Conspiracy theorists have constantly claimed that COVID-19 vaccines were meant to alter human DNA among other bogus claims. These false claims have been repeatedly debunked by Logically and other independent fact-checkers in the past.

The verdict:

The video is about DNA editing techniques and not an mRNA procedure. Some fallacious social media posts linking this technology to COVID-19 vaccines merely show a small portion of the entire video. The authorized mRNA COVID-19 vaccines do not use the gene editing method being explained in the video. Thus, we mark this claim misleading.

Here is the original post:
Fact Check: A video from 2015 discusses the ability of an mRNA medical procedure to change the genetics of - The Paradise News

According to a new study, a blood test could predict the risk of developing leukemia years in advance.

By identifying changes in blood cell production, a blood test could predict the risk of developing leukemia in the elderly population years in advance, according to new research.

Experts say that identifying those most at risk should make it possible to provide preventive or early treatment in the future to improve patient outcomes.

Leukemia is often caused by the disruption of the delicate balance in blood cell production where new cells are manufactured and old blood cells die.

Mutations in blood stem cells as we age can mean that the altered cells can have a growth benefit over other blood cells and outnumber them in what is referred to as fitness advantage.

Scientists from the Universities of Edinburgh and Glasgow investigated how changes in fitness advantage that occur in blood production might provide clues to the risk of developing leukemia depending on the type of mutation that occurs.

We measured changes in the blood samples of 83 older individuals of the Lothian Birth Cohorts, taken every three years over a 12-year period. Using the combined knowledge of mathematicians, biologists, and genome scientists, we set out to understand what these changes mean for our risk of developing leukemia as we grow older, said Dr. Tamir Chandra, a chancellors fellow at the MRC Human Genetics Unit in Edinburgh.

The Lothian Birth Cohorts 1921 and 1936 are longitudinal studies of brain, cognitive and general aging which have followed up individuals every 3 years between the ages of 70 and 82 for the 1921 cohort and the ages of 79 to 92 for 1936.

The research team then combined these complex genomic data with a machine-learning algorithm to link different mutations with different growth speeds of blood stem cells carrying these mutations.

They discovered that specific mutations give distinct fitness advantages to stem cells measured in people without leukemia, which can then be used to forecast how quickly the mutated cells will grow, and therefore determine leukemia risk.

According to the scientists, further research is needed to validate these results in a larger population due to the limited sample size in the current study.

Dr. Kristina Kirschner, co-lead author and Senior Lecturer at the University of Glasgows Institute of Cancer Sciences, said: In knowing an individual patients risk of developing leukemia, clinicians can schedule shorter gaps between appointments in those most likely to develop the disease and provide early treatment, which is more likely to be successful.

Dr. Linus Schumacher, co-lead author and Chancellors Fellow at the Centre for Regenerative Medicine of the University of Edinburgh, said: To understand leukemia risk, we need to consider the balance between the different cells involved in blood cell production and how this balance changes as we grow older. By linking genomic data with machine learning we have been able to predict the future behavior of blood cells based on the mutations they develop.

Reference: Longitudinal dynamics of clonal hematopoiesis identifies gene-specific fitness effects by Neil A. Robertson, Eric Latorre-Crespo, Maria Terradas-Terradas, Jorge Lemos-Portela, Alison C. Purcell, Benjamin J. Livesey, Robert F. Hillary, Lee Murphy, Angie Fawkes, Louise MacGillivray, Mhairi Copland, Riccardo E. Marioni, Joseph A. Marsh, Sarah E. Harris, Simon R. Cox, Ian J. Deary, Linus J. Schumacher, Kristina Kirschner and Tamir Chandra, 4 July 2022, Nature Medicine.DOI: 10.1038/s41591-022-01883-3

These findings have been published in the journal Nature Medicine. This research was funded by the Medical Research Council, Leukemia UK, and Cancer Research UK.

The Lothian Birth Cohort receives funding from Biotechnology and Biological Sciences Research Council, the Economic and Social Research Council, Age UK, Wellcome, the Royal Society, the Medical Research Council and the University of Edinburgh.

Visit link:
Blood Test Could Predict Risk of Leukemia Years in Advance - SciTechDaily

A new British study found that the original SARS-CoV-2 virus (i.e. Wuhan strain) can impair cognitive ability in a way equivalent to making the brain age by two decades. Currently, 67 percent of the worlds population has been vaccinated against the COVID-19 pandemic. Is it possible that the vaccines themselves can also cause aging damage?

Nevertheless, theres no need to worry, aging is proven to be a process, and there is a way to help reverse the aging process.

The study was published in the journal EClinicalMedicine. Experts from the University of Cambridge and Imperial College London Medical School evaluated the cognitive effects of the COVID-19 infection in humans.

The research subjects consisted of COVID-19 patients who were hospitalized for severe illness between March and July 2020.

After these patients recovery from acute infection, the researchers conducted follow-up visits for an average of six months to analyze and evaluate their anxiety, depression, and post-traumatic stress. The researchers discovered a significant decline in the patients attention, complex problem solving skills, and memory, along with reduced accuracy, and prolonged reaction time.

These cognitive deficits are similar to the cognitive decline a person would experience between the ages of 50 to 70, which is equivalent to aging by two decades and losing 10 IQ points.

In addition, the recovery of cognitive ability is very slow in patients with COVID-19 infections.

Why does COVID-19 infection cause abnormal aging? Lets first take a look at one concept.

The relationship between genes and epigenetics are like seeds and soil. Genes are like seeds, while epigenetics is like soil. Genes in the human body do not usually change after birth. They are like seeds that lie dormant in the soil, and some will grow, and some will not. What determines whether these seeds will grow or not are the genetic switches, or epigenetics.

Epigenetics is the study of these factors that affect genes being turned on or off. Specifically, one common type of gene switchDNA methylationcan change the expression of genes, shutting them down and making them non-functional. Methylation is a somewhat complex biochemical process in the body, the important thing to remember is that it is one of the ways epigenetic takes place and a process by which genes get turned on and off.

As a result of DNA methylation, there are variations in whether the same genes can be expressed in different organs and at different ages, and the amount of expression.

Cells become senescent as we age. That means they stop dividing and enter a kind of stasis. Instead of dying off as they normally would, they persist, but change shape and size andsecrete inflammatory molecules that cause other nearby cells to become senescent.

In an article published in Nature Reviews Genetics, Steve Horvath, a professor of human genetics and biostatistician at the University of California Los Angeles, concluded that as people age and have more senescent cells, there are characteristic changes in the methylation status of human DNA.

Human beings experience birth, aging, illness, and death, which is now discovered by our scientists to be controlled by our internal epigenetic clock. This is similar to the observations that everything in our universe has its cycle of formation, stasis, degeneration, and destruction.

Professor Horvath summarized the DNA methylation profiles associated with aging in an epigenetic clock of aging. While our years on Earth are are chronological age, how we live and inherent factors affect how long we will actually live, which is our biological age, or the age of our body. Biological ages can be estimated by using the methylation profiles of aging-related genes. In other words, scientists can focus in on genes linked to aging and then look at how those genes are methylating and from this gauge how far along the person is in that process of degeneration and death. These genetic focal points were carefully selected by scientists, independent of gender, body part, comorbidities, and other factors. And the results have been highly accurate, with a precision of over 95 percent in gauging a persons biological age.

Humans have a normal aging methylation curve. If a persons DNA methylation is above the curve, he or she will age faster than his or her peers; if it is below the curve, he or she will appear younger than his or her peers.

So, what factors can accelerate aging, i.e. epigenetic clock of aging?

A study conducted in Belgium was published in 2018 in the journal Aging. It found that the following factors accelerate epigenetic aging in humans:

This makes us wonder if COVID-19 infection can accelerate the epigenetic aging clock.

A study published in the journal Nature Communications answers this question. The study collected blood samples from 232 healthy individuals, 194 non-severe COVID-19 patients and 213 severe COVID-19 patients for DNA methylation analysis and found that the epigenetic age of COVID-19 patients was significantly accelerated.

In addition, the epigenetic age acceleration in COVID-19 patients is related to the stage of the disease. The age acceleration is fastest during the acute inflammatory phase, when the body and the virus are in intense combat; and it is slightly reversed during the recovery phase.

Even after the infection is over, many people still have symptoms of long COVID. Is this related to the aging caused by COVID-19?

Epigenetic aging is seen in the graying of hair and loosening of teeth. However, on a cellular level, cells in the human body also gradually age.

Cellular senescence refers to a state of cell cycle arrest when cells are stressed, as well as the secretion of various inflammatory cytokines at the same time. In a paper published in Nature Aging, a Japanese research team stated that senescent cells do not die immediately, but instead, they spread inflammatory cytokines to nearby uninfected cells, causing more cells to senesce as well.

So, what are the effects of cellular senescence on our health?

Cellular senescence plays an important role in many age-related diseases, such as degenerative diseases of the nerves, eyes, lungs, and heart.

The aforementioned study was conducted prior to the Omicron variant outbreak, and the Omicron variant is clearly less pathogenic than the old strain. In fact, some of the mutation sites of the Omicron variant counteracted the factors that caused cellular senescence. It is estimated that Omicron causes significantly less accelerated senescence or sequelae than the old strain.

However, the vaccines we are currently administering are still developed using the spike proteins of the old strain of early 2020, so is there a risk of accelerated aging?

The COVID-19 vaccines mainly express spike proteins in the human body. In a study published in the Journal of Virology in 2021, researchers from Saint Louis University in Missouri transfected spike proteins of the old strain into cells in vitro. It was later discovered that a large number of cellular senescence markers (including specific cytokines, interleukins, and specific enzymes, etc) were found in the spike-transfected cells, compared to the control group.

In addition, the spike proteins increase inflammatory factors, cause mitochondrial damage, produce misfolded proteins, and cause genomic instability, all of which accelerate cellular aging.

Reversing aging sounds like a dream come true for everyone. We have already understood so many mechanisms related to aging, so is it possible to find a way to slow down or even reverse aging?

In fact, our daily diet, work habits, and lifestyle all affect the epigenetic aging clock. For instance, during high-temperature cooking, red meat produces glycosylated end products, which are associated with cellular aging; poultry and fish are relatively healthy; and the vitamins in fruits and vegetables help keep cells young, which can help slow down or reverse the aging clock.

In addition, an article published in 2017 in the journal Psychoneuroendocrinology, American and French scholars investigated whether or not sitting in meditation affects the epigenetic aging clock.

The studys subjects were 18 individuals who had been meditating for at least 10 years and meditated for at least 30 minutes a day, and 20 non-meditators. They were divided into two groups: under and over 52 years of age, respectively. The researchers measured the DNA methylation in their blood cells for estimation of their epigenetic aging acceleration.

The results showed that the epigenetic aging acceleration increased in elderly non-meditators, while the acceleration in elderly meditators was more similar to that of younger people and was not affected by the epigenetic aging effect.

Gene expression is also associated with changes in our appearance, so meditators appear younger than their actual age. Furthermore, meditators also have younger brains.

The University of California Los Angeles and the Australian National University jointly published a study in 2016 in the journal NeuroImage. The studys subjects were 250 meditators and 50 non-meditators, both groups with an average age of 51.4 years.

The researchers analyzed and compared the brain ages of the two groups and found that the brain age of the meditators was younger than their actual age. For instance, 50-year-old meditators had the same brain age as a 42.5-year-old non-meditator, while 60-year-old meditators had the same brain age as the 51-year-old non-meditators in the control group.

Interestingly, for the meditators over 50, each additional year of their actual age would make their brain age one month and 22 days younger than their actual age.

In summary, damage caused by SARS-CoV-2 to the human body speeds up the human epigenetic clock of aging and dumbs down the brain. Vaccines based on the old strains in 2020 may also harm the human body in this regard.

At least 67 percent of the worlds people have now been vaccinated; will people in the future get older more quickly? No. It is too early to conclude anything based on cellular data alone rather than human studies. However, the cellular data is a clear reminder for us to take precautions to prevent this.

Meanwhile, it is quite worrisome that when we discussed this topic during a Health 1+1 live broadcast on July 12 2022, quite a few audience members had commented that they themselves or their friends or relatives had become obviously older after receiving the jabs.

The good news is that aging is a long process. During this process, for example, we can develop the habits of healthy living, including eating well, exercising,and daily meditation, which can help slow down or even reverse the aging process, and furthermore bring us various positive health benefits, which will be detailed in future articles.

Views expressed in this article are the opinions of the author and do not necessarily reflect the views of The Epoch Times. Epoch Health welcomes professional discussion and friendly debate. To submit an opinion piece, please follow these guidelines and submit through our form here.

Visit link:
COVID-19 Can Make the Brain Age by 2 Decades; Here's 1 Way to Reverse Aging - The Epoch Times

Pontzer, H., Wood, B. M. & Raichlen, D. A. Hunter-gatherers as models in public health. Obes. Rev. 19, 2435 (2018).

PubMed Article Google Scholar

Sonnenburg, J. L. & Sonnenburg, E. D. Vulnerability of the industrialized microbiota. Science 366, eaaw9255 (2019).

CAS PubMed Article Google Scholar

Kenyon, C. J. The genetics of ageing. Nature 464, 504512 (2010).

CAS PubMed Article Google Scholar

Lpez-Otn, C., Blasco, M. A., Partridge, L., Serrano, M. & Kroemer, G. The hallmarks of aging. Cell 153, 11941217 (2013).

PubMed PubMed Central Article CAS Google Scholar

Wilson, K. A. et al. Evaluating the beneficial effects of dietary restrictions: a framework for precision nutrigeroscience. Cell Metab. 33, 21422173 (2021).

CAS PubMed PubMed Central Article Google Scholar

Rodgers, G. P. & Collins, F. S. Precision nutrition-the answer to what to eat to stay healthy. JAMA 324, 735736 (2020).

PubMed Article Google Scholar

Liu, G. Y. & Sabatini, D. M. mTOR at the nexus of nutrition, growth, ageing and disease. Nat. Rev. Mol. Cell Biol. 21, 183203 (2020).

CAS PubMed PubMed Central Article Google Scholar

Szwed, A., Kim, E. & Jacinto, E. Regulation and metabolic functions of mTORC1 and mTORC2. Physiol. Rev. 101, 13711426 (2021).

CAS PubMed PubMed Central Article Google Scholar

Harrison, D. E. et al. Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature 460, 392395 (2009).

CAS PubMed PubMed Central Article Google Scholar

Dorling, J. L., Martin, C. K. & Redman, L. M. Calorie restriction for enhanced longevity: the role of novel dietary strategies in the present obesogenic environment. Ageing Res. Rev. 64, 101038 (2020).

PubMed PubMed Central Article Google Scholar

Sowah, S. A. et al. Calorie restriction improves metabolic state independently of gut microbiome composition: a randomized dietary intervention trial. Genome Med. 14, 30 (2022).

CAS PubMed PubMed Central Article Google Scholar

O'Flanagan, C. H., Smith, L. A., McDonell, S. B. & Hursting, S. D. When less may be more: calorie restriction and response to cancer therapy. BMC Med. 15, 106 (2017).

PubMed PubMed Central Article CAS Google Scholar

Madeo, F., Carmona-Gutierrez, D., Hofer, S. J. & Kroemer, G. Caloric restriction mimetics against age-associated disease: targets, mechanisms, and therapeutic potential. Cell Metab. 29, 592610 (2019).

CAS PubMed Article Google Scholar

Chong, C. R., Sallustio, B. & Horowitz, J. D. Drugs that affect cardiac metabolism: focus on perhexiline. Cardiovasc Drugs Ther. 30, 399405 (2016).

CAS PubMed Article Google Scholar

Schreiber, K. H. et al. A novel rapamycin analog is highly selective for mTORC1 in vivo. Nat. Commun. 10, 3194 (2019).

PubMed PubMed Central Article CAS Google Scholar

Lamming, D. W. et al. Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity. Science 335, 16381643 (2012).

CAS PubMed PubMed Central Article Google Scholar

Sarbassov, D. D. et al. Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB. Mol. Cell 22, 159168 (2006).

CAS PubMed Article Google Scholar

Gonzlez, A., Hall, M. N., Lin, S. C. & Hardie, D. G. AMPK and TOR: the yin and yang of cellular nutrient sensing and growth control. Cell Metab. 31, 472492 (2020).

PubMed Article CAS Google Scholar

Lin, S. C. & Hardie, D. G. AMPK: sensing glucose as well as cellular energy status. Cell Metab. 27, 299313 (2018).

CAS PubMed Article Google Scholar

Fontana, L. & Partridge, L. Promoting health and longevity through diet: from model organisms to humans. Cell 161, 106118 (2015).

CAS PubMed PubMed Central Article Google Scholar

Kapahi, P., Kaeberlein, M. & Hansen, M. Dietary restriction and lifespan: lessons from invertebrate models. Ageing Res. Rev. 39, 314 (2017).

PubMed Article Google Scholar

Schulz, T. J. et al. Glucose restriction extends Caenorhabditis elegans life span by inducing mitochondrial respiration and increasing oxidative stress. Cell Metab. 6, 280293 (2007).

CAS PubMed Article Google Scholar

Ristow, M. & Zarse, K. How increased oxidative stress promotes longevity and metabolic health: the concept of mitochondrial hormesis (mitohormesis). Exp. Gerontol. 45, 410418 (2010).

CAS PubMed Article Google Scholar

Weir, H. J. et al. Dietary restriction and AMPK increase lifespan via mitochondrial network and peroxisome remodeling. Cell Metab. 26, 884896.e5 (2017).

CAS PubMed PubMed Central Article Google Scholar

Boccardi, V., Murasecco, I. & Mecocci, P. Diabetes drugs in the fight against Alzheimer's disease. Ageing Res. Rev. 54, 100936 (2019).

CAS PubMed Article Google Scholar

Calissi, G., Lam, E. W. & Link, W. Therapeutic strategies targeting FOXO transcription factors. Nat. Rev. Drug Disco. 20, 2138 (2021).

CAS Article Google Scholar

Greer, E. L. & Brunet, A. Different dietary restriction regimens extend lifespan by both independent and overlapping genetic pathways in C. elegans. Aging Cell 8, 113127 (2009).

CAS PubMed Article Google Scholar

Giannakou, M. E., Goss, M. & Partridge, L. Role of dFOXO in lifespan extension by dietary restriction in Drosophila melanogaster: not required, but its activity modulates the response. Aging Cell 7, 187198 (2008).

CAS PubMed Article Google Scholar

Miyauchi, T. et al. Up-regulation of FOXO1 and reduced inflammation by -hydroxybutyric acid are essential diet restriction benefits against liver injury. Proc. Natl Acad. Sci. USA 116, 1353313542 (2019).

CAS PubMed PubMed Central Article Google Scholar

Furuyama, T. et al. Effects of aging and caloric restriction on the gene expression of Foxo1, 3, and 4 (FKHR, FKHRL1, and AFX) in the rat skeletal muscles. Microsc. Res. Tech. 59, 331334 (2002).

CAS PubMed Article Google Scholar

Shimokawa, I. et al. The life-extending effect of dietary restriction requires Foxo3 in mice. Aging Cell 14, 707709 (2015).

CAS PubMed PubMed Central Article Google Scholar

Xia, Y. et al. Neuronal C/EBP/AEP pathway shortens life span via selective GABAnergic neuronal degeneration by FOXO repression. Sci. Adv. 8, eabj8658 (2022).

CAS PubMed PubMed Central Article Google Scholar

Zhu, S. et al. The roles of sirtuins family in cell metabolism during tumor development. Semin. Cancer Biol. 57, 5971 (2019).

CAS PubMed Article Google Scholar

Xie, N. et al. NAD(+) metabolism: pathophysiologic mechanisms and therapeutic potential. Signal Transduct. Target Ther. 5, 227 (2020).

CAS PubMed PubMed Central Article Google Scholar

Covarrubias, A. J., Perrone, R., Grozio, A. & Verdin, E. NAD(+) metabolism and its roles in cellular processes during ageing. Nat. Rev. Mol. Cell Biol. 22, 119141 (2021).

CAS PubMed Article Google Scholar

Lin, S. J., Defossez, P. A. & Guarente, L. Requirement of NAD and SIR2 for life-span extension by calorie restriction in Saccharomyces cerevisiae. Science 289, 21262128 (2000).

CAS PubMed Article Google Scholar

Houtkooper, R. H., Pirinen, E. & Auwerx, J. Sirtuins as regulators of metabolism and healthspan. Nat. Rev. Mol. Cell Biol. 13, 225238 (2012).

CAS PubMed PubMed Central Article Google Scholar

Cohen, H. Y. et al. Calorie restriction promotes mammalian cell survival by inducing the SIRT1 deacetylase. Science 305, 390392 (2004).

CAS PubMed Article Google Scholar

Han, X. et al. Targeting Sirtuin1 to treat aging-related tissue fibrosis: From prevention to therapy. Pharm. Ther. 229, 107983 (2022).

CAS Article Google Scholar

Civitarese, A. E. et al. Calorie restriction increases muscle mitochondrial biogenesis in healthy humans. PLoS Med. 4, e76 (2007).

PubMed PubMed Central Article CAS Google Scholar

Gomes, P. et al. The yin and yang faces of the mitochondrial deacetylase sirtuin 3 in age-related disorders. Ageing Res. Rev. 57, 100983 (2020).

CAS PubMed Article Google Scholar

Nakagawa, T., Lomb, D. J., Haigis, M. C. & Guarente, L. SIRT5 Deacetylates carbamoyl phosphate synthetase 1 and regulates the urea cycle. Cell 137, 560570 (2009).

CAS PubMed PubMed Central Article Google Scholar

Bordone, L. et al. SIRT1 transgenic mice show phenotypes resembling calorie restriction. Aging Cell 6, 759767 (2007).

CAS PubMed Article Google Scholar

Herranz, D. et al. Sirt1 improves healthy ageing and protects from metabolic syndrome-associated cancer. Nat. Commun. 1, 3 (2010).

PubMed Article CAS Google Scholar

North, B. J. et al. SIRT2 induces the checkpoint kinase BubR1 to increase lifespan. EMBO J. 33, 14381453 (2014).

CAS PubMed PubMed Central Article Google Scholar

Benigni, A. et al. Sirt3 deficiency shortens life span and impairs cardiac mitochondrial function rescued by Opa1 gene transfer. Antioxid. Redox Signal 31, 12551271 (2019).

CAS PubMed Article Google Scholar

Brown, K. et al. SIRT3 reverses aging-associated degeneration. Cell Rep. 3, 319327 (2013).

CAS PubMed PubMed Central Article Google Scholar

Kawahara, T. L. et al. SIRT6 links histone H3 lysine 9 deacetylation to NF-kappaB-dependent gene expression and organismal life span. Cell 136, 6274 (2009).

CAS PubMed PubMed Central Article Google Scholar

Vakhrusheva, O. et al. Sirt7 increases stress resistance of cardiomyocytes and prevents apoptosis and inflammatory cardiomyopathy in mice. Circ. Res. 102, 703710 (2008).

CAS PubMed Article Google Scholar

Korotkov, A., Seluanov, A. & Gorbunova, V. Sirtuin 6: linking longevity with genome and epigenome stability. Trends Cell Biol. 31, 9941006 (2021).

CAS PubMed Article Google Scholar

Read the original here:
Dietary regulation in health and disease | Signal Transduction and Targeted Therapy - Nature.com

NEW YORK & SAN FRANCISCO--(BUSINESS WIRE)--Kallyope, a leading biotechnology company focused on identifying and developing therapeutics targeting the gut-brain axis, and Brightseed, creators of Forager, a pioneering artificial intelligence platform that illuminates the connections between nature and human health, have entered a strategic research collaboration to screen plant compounds to identify and validate active agents that can be further derived into potential therapeutics targeting weight loss management and glucose control.

Brightseeds Forager is building the worlds largest library of small molecule bioactive compounds mapped to human biological targets. The research collaboration will leverage Brightseeds novel insights on bioactives and the Kallyope Klarity platform, comprising the worlds broadest set of integrated end-to-end capabilities to further unlock gut and brain biology and the gut-brain axis. Should early-stage research result in the identification of any lead compounds candidates, Kallyope has rights to derivatize and develop therapeutics in humans while Kallyope and Brightseed will share rights to consumer applications of identified compounds.

This collaboration brings together two leading, diverse technological platforms and teams for the discovery of novel consumer products that may have therapeutic benefits for Type 2 diabetes and obesity, said Jay Galeota, president and CEO, Kallyope. We are excited to have the opportunity to work with Brightseed, whose capabilities are highly synergistic with our lead metabolism therapeutics program and deep drug discovery and development expertise. This partnership is also consistent with our strategy to leverage our platform via collaborations in non-core areas that broaden our impact on public health.

Kallyope and Brightseed scientists will initially collaborate to leverage validated biology for the discovery of lead plant-derived compounds that may modulate body weight and glucose control. The teams will then iterate on the lead and determine optimal plant sources of compounds using their sophisticated computational platform.

Seventy-five percent of our current healthcare spending in the U.S. goes towards treating chronic health conditions that severely impair the quality of life of millions of people. We need to reimagine more scalable approaches to combat the scourge of diet-induced chronic conditions, said Jim Flatt, co-founder and CEO, Brightseed. Kallyope is one of the visionary pharmaceutical companies that recognize the need to develop health products that can prevent or reduce the risk of certain chronic diseases. Historically, nature has provided the majority of small molecules that are used to inform our medicines. In partnership with Kallyopes high value gut-brain axis biological targets and technology platform, we will discover the next generation of natural bioactives to improve health and reduce the incidence of diet-related chronic disease.

About Bioactives

Bioactives are small molecule compounds produced by plants, fungi, and microbes that grow in and adapt to environments that present a wide range of challenges to their survival. Bioactives also benefit the health of humans they are the enlivening caffeine in tea, the powerful antioxidant lycopene in tomatoes, and they inform active ingredients in medicines like Taxol, Aspirin, and Metformin, a first-line treatment for Type 2 diabetes, derived from the French lilac flower. Science has long known that bioactives are critical to human health, yet the vast majority remain unknown and uncharted. Brightseeds A.I., Forager, discovers bioactives in nature and maps them to human health outcomes at a rate and accuracy that was previously impossible.

About Kallyope

Kallyope, headquartered at the Alexandria Center for Life Science in New York City, is a biotechnology company dedicated to unlocking the therapeutic potential of the gut-brain axis. The companys cross-disciplinary team integrates advanced technologies in sequencing, bioinformatics, neural imaging, cellular and molecular biology, and human genetics to provide an understanding of gut-brain biology that leads to transformational therapeutics to improve human health. The companys founders are Charles Zuker, Ph.D., Lasker Award winner Tom Maniatis, Ph.D., and Nobel laureate Richard Axel, M.D. For more information visit http://www.kallyope.com.

About Brightseed

Brightseed illuminates nature to restore human health. Brightseeds Forager is a pioneering computational platform and A.I. that discovers and maps the bioactive compounds in nature and understands which of them have the greatest impact on human health. Discoveries undergo safety and regulatory review, clinical evaluation, and commercial development to deliver powerful, natural health solutions. To date, Forager has mapped more than 2 million plant compounds, and Brightseed is working with brands and organizations that impact the health of millions of people every day. Interested organizations can contact Brightseed by visiting https://brightseedbio.com/partner.

More:
Kallyope and Brightseed Enter Collaboration to Identify and Validate Novel Plant-Based Bioactives - Business Wire

Like most aspects of biology, early human development involves many complex processes. Despite the rhetoric around these issues, clear lines between having a heart and not having a heart or being able to survive outside of the uterus are scarce, or nonexistent.

There arent these set black-and-white points for much of this, says obstetrician-gynecologist Nisha Verma, a fellow with the American College of Obstetricians and Gynecologists in Washington, D.C.

Heres whats known about five key aspects of pregnancy biology that often come up in abortion debates.

Thats because how dates are determined is supremely confusing. The standard pregnancy clock actually starts ticking before a sperm cell encounters an egg, two weeks before, on average.

Follow the latest news and policy debates on agricultural biotech and biomedicine? Subscribe to our newsletter.

A Texas law bans abortions after detection of an unborn childs heartbeat. But the rhythmic sounds heard on an ultrasound early in pregnancy arent caused by the opening and closing of heart valves as they move blood through the hearts chambers, the motion that produces a typicallub dubsound. Thats because those chambers havent yet developed. On early ultrasounds, the heartbeat-like sounds are created by the ultrasound machine itself.

The word viability is often used as a sharp cut-off point to mark the age at which a fetus could survive outside of the uterus. The problem is that one clear cut-off does not exist.

This is an excerpt. Read the original post here

The rest is here:
When does life begin? Here are five critical points in a pregnancy and the misconceptions surrounding them - Genetic Literacy Project

After Hunts unusual flight home, Shanidar Z made it safely to the University of Cambridge for digital scanning and will eventually be transferred back to northern Iraq to feature as the centerpiece of a new museum. The skeleton could be up to 90,000 years old, but its DNA will be used to further understanding of modern human historyby analyzing and statistically comparing the ancient DNA against the genomes of modern populations, to demonstrate when different population groups parted company, Hunt says.

Once a population splits into two or more reproductively isolated groups, the genes in each new population will evolve gradually in new directions as a result of random gene mutations as well as exposure to various environmental factors that prevent successful reproductioncoming into contact with new diseases, for instance.

Its through work like this that scientists have been able to chart the migration of different populations of humans and Neanderthal groups around the planet over the last 70,000 years, and also bust some myths about their habits and migration patterns. We now know that humans and Neanderthals interbred quite commonly, and that Neanderthal communities were likely more caring and intelligent than weve previously given them credit for. According to Hunt, evidence of burial rituals at the Shanidar Cave suggests memory, and that they looked after their injured and sick members.

Separately, analysis of ancient DNA against the modern human genome has revealed that we still carry some genetic sequences that were present in people living millennia ago. Such analysis even helped to identify a new subspecies of humans 12 years agothis discovery of Denisovans, believed to have existed across Asia around 400,000 years ago, demonstrates how much is still unknown about our human origins.

At the Francis Crick Institute in London, a major project is underway to create a reliable biobank of ancient human DNA to help build on such discoveries. Population geneticist Pontus Skoglund is leading the 1.7 million ($2.1 million) project, which will sequence 1,000 ancient British genomes by gathering data from skeletal samples from the past 5,000 years, with help from around 100 other UK institutions. From the database he hopes to determine how human genetics have changed over millennia in response to factors such as infectious diseases and changes in climate, diet, and migration.

Part of that is looking for genetic traits that may have been advantageous for past humans during earlier epidemics, he says. There is no doubt we can learn something from this in our understanding of how we manage contemporary disease and other outbreaks.

Skoglunds team sources their samples from archaeological digs around the country or from museums with existing collections. His favorite bones to sequence are the ones found in our inner ear: These are particularly good at preserving DNA, since they are the least susceptible to microbial invasion and other factors that could cause DNA to deteriorate, he explains.

The bones are ground down to be run through a sequencing machine in much the same way as any DNA sample. But the ancient DNA requires specialist protocolsmodern DNA has very long fragments that are basically intact, whereas with ancient DNA we only get on average around 35 percent of the total base pairs.

Read more:
What the DNA of Ancient Humans Reveals About Pandemics - WIRED

Do you remember your science lessons from school? Do you remember learning about chromosomes? We were taught that there are two chromosomes X and Y and that each of us has a set of chromosomes. Individuals with XX (or two X chromosomes) are female, while those with XY (or one X and one Y chromosome) are male. A recently published study has now revealed that many men can actually carry an extra chromosome.The study was published in the journal Genetics in Medicine. It included data on more than 207,000 men. It was discovered that of the participants, over 350 had an extra chromosome, either X or Y.Very few of these men knew about this abnormality or had it mentioned in their medical records.

Talking to the Guardian Dr Ken Ong, co-senior author of the study who is a pediatric endocrinologist in the Medical Research Council (MRC) Epidemiology Unit at the University of Cambridge says that they were surprised at how common this abnormality is.

Watch |Robots to solve ocean's pollution menace: 15mm long robo-fish to hunt for plastic

The National Human Genome Research Institute reported that previous estimations indicated that approximately 100 to 200 men out of every 100,000 are XXY. An estimated 18 to 100 out of every 100,000 were believed to be XYY.

Having an extra chromosome can raise the risk of certain health conditions. Those having Klinefelter syndrome (KS) or an extra X chromosome are linked to reproductive problems like infertility and delayed puberty. According to the National Human Genome Research Institute, XXY men are four times more likely than XY men to have late puberty.

Also read |A beer a day might keep your gut flora healthy: Study

On the other hand, with an extra Y chromosome or 47,XYY syndrome does not come with reproductive problems but was linked to learning disabilities, including delay in acquiring speech and motor skills. According to the Genetic and Rare Diseases Information Center, they also have unusually low muscle tone.

Additionally, both XXY and XYY men have a higher rate of type 2 diabetes, atherosclerosis (plaque buildup in the artery walls), pulmonary embolism (blood clots in the veins and lung arteries), and chronic obstructive pulmonary disease (which obstructs airflow to the lungs).

Also read |The tiny mites that have sex on our faces may go extinct

In their report, the authors questioned: "why both KS and 47,XYY should show striking similarities in conferring substantially higher risks for many diseases in common." As per them, future research is needed to examine the reasons causing this elevated risk.

(With inputs from agencies)

Watch WION LIVE HERE:

You can now write for wionews.com and be a part of the community. Share your stories and opinions with us here.

See more here:
For the men out there: Do you fall sick often? This might be why - WION