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Continue reading “23 Younger Biological Age: Supplements, Diet (Blood Test #6 in 2023)” »

One of the most popular dog breeds is the Golden Retriever. Unfortunately, these dogs are also at high risk for developing cancer. New research has investigated genetic factors that may be able to extend the lives of these beloved dogs. This work focused on longevity genes instead of those that have been associated with cancer, and led to the identification of gene variants that could extend the dogs’ lifespan by as much as two years. The findings have been reported in GeroScience.

While most golden retrievers are predisposed to cancer, some of these dogs can live to be as old as 15 or 16 years. So the researchers thought that there might be genetic factors that were mitigating the effect of the cancer-related genes, noted co-corresponding study author Robert Rebhun, Maxine Adler Endowed Chair in oncology at the UC Davis School of Veterinary Medicine. The gene that had this effect was HER4.

A study published today by scientists from Harvard University and epigenetic research company TruDiagnostic has shed light on the reasons why our bodies are aging on a cellular level, laying the foundations for medical based treatment options to reduce the risk of age-related death and disease in highly targeted ways.

Longevity. Technology: Age is the number one risk factor for most chronic diseases and death across the world. Epigenetics (or the way our genes are put to use throughout our bodies) has emerged as a crucial method of evaluating health, and while previous DNA methylation clocks could determine how advanced one’s body has aged, they have not yet been able to provide information to the reasons why someone might have accelerated or decelerated aging outcomes.

“In our research, we set out to create the best method to quantify the biological aging process. However, aging is extremely complex,” explains Harvard Medical School Associate Professor Dr Jessica Lasky-Su. “To solve this issue of complexity, our approach was to gather data across multiple sources of information. We chose to do this by building one of the most robust aging datasets in the world by quantifying patients’ proteomics, metabolomics, clinical histories and DNA methylation.”

Here’s my latest Opinion piece just out for Newsweek…focusing on cyborg rights.

Over the past half-century, the microprocessor’s capacity has doubled approximately every 18–24 months, and some experts predict that by 2030, machine intelligence could surpass human capabilities. The question then arises: When machines reach human-level intelligence, should they be granted protection and rights? Will they desire and perhaps even demand such rights?

Beyond advancements in microprocessors, we’re witnessing breakthroughs in genetic editing, stem cells, and 3D bioprinting, all which also hold the potential to help create cyborg entities displaying consciousness and intelligence. Notably, Yale University’s experiments stimulating dead pig brains have ignited debates in the animal rights realm, raising questions about the ethical implications of reviving consciousness.

Continue reading “Creating Sapient Technology and Cyborg Rights Should Happen Soon” »

Scientists have successfully gene-edited chickens to make them partially resistant to the bird flu and believe full immunity may be within reach.

Half a century after its foundation, the neutral theory of molecular evolution continues to attract controversy. The debate has been hampered by the coexistence of different interpretations of the core proposition of the neutral theory, the ‘neutral mutation–random drift’ hypothesis. In this review, we trace the origins of these ambiguities and suggest potential solutions. We highlight the difference between the original, the revised and the nearly neutral hypothesis, and re-emphasise that none of them equates to the null hypothesis of strict neutrality. We distinguish the neutral hypothesis of protein evolution, the main focus of the ongoing debate, from the neutral hypotheses of genomic and functional DNA evolution, which for many species are generally accepted. We advocate a further distinction between a narrow and an extended neutral hypothesis (of which the latter posits that random non-conservative amino acid substitutions can cause non-ecological phenotypic divergence), and we discuss the implications for evolutionary biology beyond the domain of molecular evolution. We furthermore point out that the debate has widened from its initial focus on point mutations, and also concerns the fitness effects of large-scale mutations, which can alter the dosage of genes and regulatory sequences. We evaluate the validity of neutralist and selectionist arguments and find that the tested predictions, apart from being sensitive to violation of underlying assumptions, are often derived from the null hypothesis of strict neutrality, or equally consistent with the opposing selectionist hypothesis, except when assuming molecular panselectionism. Our review aims to facilitate a constructive neutralist–selectionist debate, and thereby to contribute to answering a key question of evolutionary biology: what proportions of amino acid and nucleotide substitutions and polymorphisms are adaptive?

Half a century after its foundation, the neutral theory of molecular evolution continues to attract controversy. The debate has been hampered by the coexistence of different interpretations of the core proposition of the neutral theory, the ‘neutral mutation–random drift’ hypothesis. In this review, we trace the origins of these ambiguities and suggest potential solutions. We highlight the difference between the original, the revised and the nearly neutral hypothesis, and re-emphasise that none of them equates to the null hypothesis of strict neutrality. We distinguish the neutral hypothesis of protein evolution, the main focus of the ongoing debate, from the neutral hypotheses of genomic and functional DNA evolution, which for many species are generally accepted. We advocate a further distinction between a narrow and an extended neutral hypothesis (of which the latter posits that random non-conservative amino acid substitutions can cause non-ecological phenotypic divergence), and we discuss the implications for evolutionary biology beyond the domain of molecular evolution. We furthermore point out that the debate has widened from its initial focus on point mutations, and also concerns the fitness effects of large-scale mutations, which can alter the dosage of genes and regulatory sequences. We evaluate the validity of neutralist and selectionist arguments and find that the tested predictions, apart from being sensitive to violation of underlying assumptions, are often derived from the null hypothesis of strict neutrality, or equally consistent with the opposing selectionist hypothesis, except when assuming molecular panselectionism. Our review aims to facilitate a constructive neutralist–selectionist debate, and thereby to contribute to answering a key question of evolutionary biology: what proportions of amino acid and nucleotide substitutions and polymorphisms are adaptive?

COVER STORY: The epigenetic clock uses DNA methylation to calculate the metric of “epigenetic age”. Epigenetic age acceleration (epigenetic > chronological age) has been repeatedly linked to pediatric asthma and allergic disease, demonstrating its potential as a diagnostic biomarker. However, questions remain about the accuracy and utility of epigenetic clocks in children.

This review by researchers at University of British Columbia examines the most used current epigenetic clocks and details the associations between epigenetic age acceleration and asthma/allergic disease. They explore the potential of the epigenetic clock as a biomarker for asthma and discuss the need for a pediatric epigenetic clock that is accurate in blood samples in order to maximize the utility of this powerful tool.

In a new study, Abudayyeh and Gootenberg led a team of scientists on a quest to identify and characterize Fanzor enyzmes in large-scale genetic databases. Their genetic mining venture, published in Science Advances, outlines the discovery of over 3,600 Fanzors in eukaryotes, including algae, snails, amoebas and the viruses that infect them.

Fanzors evolved new features to survive and thrive in eukaryotes

Five distinct families of Fanzors could be identified from the study data. By comparing the biological makeup of these families, Abudayyeh and colleagues could track their evolutionary history. Fanzors most likely evolved from proteins called TnpB, which are encoded in transposons – mobile genetic elements often nicknamed “jumping genes”. In Nature, the McGovern team hypothesized that the TnpB gene may have “jumped” from bacteria to eukaryotes in a genetic “shuffling” many years ago. Abudayyeh and Gootenburg’s new study and genetic tracing implies that this event likely occurred several times, with Fanzors “jumping” from viruses and symbiotic bacteria. Their analyses also suggest that once these genes had made their way into eukaryotes, they evolved new features that promoted their survival, including the ability to enter a cell’s nucleus and access its DNA.