What Genes Are Associated With Longevity?

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    To know what genes are associated with longevity, we dive into longevity and genetics. It’s not yet clear, or straight forward to answer, since longevity is associated with lifestyle, epigenetics and genetics. What genes are involved? Some studies suggest that there is no single gene that determines human longevity. However, some specific genes have been identified as being associated with longevity. These genes might be involved in maintaining healthy mitochondria

    Longevity extending life span expectancy

    The average life expectancy in developed countries has increased over time, but it has not kept pace with increases in overall population size. This means that the number of people who live to old age is decreasing. The decline in life expectancy at older ages (above 80 years) has been particularly pronounced in recent decades. This trend is evident for both men and women, and across all ethnic groups. In 1900, life expectancy was about 50 years for a man; today it is approximately 75 years. For a woman, life expectancy in 1900 was around 40 years; now it is nearly 70 years. Over this period, the proportion of elderly persons—those aged 65 or older—has grown dramatically. From 1950 to 2000, the percentage of Americans over the age of 65

    Human longevity genetics or lifestyle?

    Genetics plays an important role in determining how long we will live. However, there is evidence that environmental factors also play a significant role. Studies have shown that certain behaviors such as eating habits, exercise, smoking, drinking alcohol, and even diet can be linked to longer lifespans. These studies suggest that the environment often outshines the genes when it comes to our health. When researchers compare the lifestyles of centenarians to those of younger generations, they find that these centenarians tend to eat healthier diets, drink less alcohol, smoke fewer cigarettes, and engage in more regular physical activity than other people their age.

    Aging and Longevity: A Review of Current Research

    In order to understand the relationship between biology and human longevity, we need to first consider what causes aging. Aging is a process that occurs throughout the body. It results in changes in cells and tissues, which eventually lead to death. As people grow older, their bodies become weaker and more prone to disease. The process of aging begins during fetal development and continues after birth. During this process, cells lose their ability to function properly and repair themselves. Scientists believe that aging is caused by many different things, including poor nutrition, lack of sleep, stress, and exposure to toxins.

    Centenarian Genealogy Study Reveals Genetic Link Between Centenarians and Their Parents

    In a study published in Nature Communications on February 24, 2018, scientists identified a gene mutation shared by centenarians and their parents. The researchers found that mutations in the SLC39A8 gene were present in the DNA of centenarians and their children. People inherit one copy of each chromosome from their mother and father. Each parent passes down half of their chromosomes to their offspring. Therefore, if a person inherits a mutated copy of a particular gene from either parent, then he or she will carry that same mutation. With this information, the researchers could trace back through the family tree and identify specific ancestors carrying the mutation. By comparing the genomes of individuals with extreme longevity, the researchers discovered that the mutation arose within the last 2,000 years. The most likely place for the mutation to have originated was China. The mutation appears to have spread throughout Eurasia, and its presence in modern-day Japan suggests that it may have reached the Far East before spreading into Europe. Researchers speculate that the mutation conferred a selective advantage and allowed ancient humans to survive harsh conditions. The discovery provides new insights into why so few people reach 100 years of age. 

    The genetics of aging

    According to the National Institute on Aging (NIA), about 80 percent of the variability in lifespan among people living today can be explained by genetics. In addition, research has revealed that the genes responsible for aging share common pathways. For example, all of the known aging genes appear to regulate cell metabolism and energy production. This finding suggests that slowing the rate at which cells use up their energy supply might help extend life span. Other genes involved in aging include those that control blood pressure and cholesterol levels.

    Lifestyle choices and longevity

    Some experts claim that increasing the length of your life depends largely on your choice of lifestyle. According to Dr. Michael Roizen, director of the Cleveland Clinic’s Wellness Program, “We know that exercise, healthy eating, not smoking, managing weight, avoiding alcohol abuse, and maintaining a normal level of activity are important to our health and well-being.” However, according to another expert, there is no evidence that any single factor makes a significant difference in how long you live. Instead, the key to longer life spans seems to lie in developing good habits early in life.

    What is the genetics of aging?

    It’s quite simple really. Your body ages because your cells divide more slowly than they die. If you eat less often and don’t get enough calories, your cells won’t grow as quickly. So you’ll stay younger for longer. That doesn’t mean you’re immortal though. Eventually, you’ll die of something else.

    There are some things we can do to slow down the process. We can make sure we eat lots of vegetables, drink lots of water, exercise regularly, etc., but ultimately we just need to accept that our bodies aren’t going to last forever.

    Sometimes, the DNA repair system isn’t working properly. As a result, mistakes happen and the cell begins to mutate. A mutation is like having a tiny change in the code of a computer program.

    Genetics of longevity and aging

    Aging is the gradual decline of an organism over time. It occurs due to the accumulation of damage caused by free radicals produced during metabolic processes. These free radicals cause alterations in macromolecules such as proteins, lipids, nucleic acids, carbohydrates, and other biomolecules. This leads to changes in cellular structure and function. Free radicals also increase oxidative stress leading to chronic inflammation. This results in many diseases including cancer, cardiovascular disease, diabetes mellitus, arthritis, Alzheimer’s disease, Parkinson’s disease, dementia, cataracts, and many others.

    Many studies show that the human genome undergoes progressive deterioration with advancing age. Genomic instability accumulates with age due to various causes such as environmental pollutants, radiation exposure, and increased reactive oxygen species (ROS) levels. ROS are molecules containing oxygen atoms that have unpaired electrons. The number of ROS increases with age. ROS can be generated naturally within the body through metabolism and respiration. In addition, ROS may be formed outside the body through various sources such as air pollution, cigarette smoke, ionizing radiation, pesticides, herbicides, industrial chemicals, and drugs. Aging-related genomic instability eventually leads to mutations which contribute to degenerative disorders.

    Aging is defined as the loss of physiological functions that occur over time. There are two major theories about why this happens. One theory suggests that aging is a consequence of wear and tear on tissues resulting from the accumulation of random molecular errors. The second theory proposes that aging is a programmed event designed to protect organisms against threats to their survival.

    The first theory, known as error catastrophe theory, was proposed by Leonard Hayflick in 1961. He found that normal human fibroblasts can only divide approximately 50 times before they stop dividing. This finding led him to propose that humans live for 60 years. However, he later revised his estimate to 80 years based on data collected from other scientists.

    In 1985, Peter Nowak and colleagues at the University of Michigan discovered that human telomeres shorten each time a cell divides. Telomeres are repetitive sequences of DNA located at the end of chromosomes. When telomeres become too short, the cell stops dividing. This discovery has been widely accepted because it explains why cells stop dividing after a certain amount of time.

    In 1992, Elizabeth Blackburn and Carol Greider showed that telomerase activity protects cells from replicative senescence. Telomerase is a ribonucleoprotein enzyme that synthesizes telomere repeats using its RNA component as a template. This enzyme prevents telomeres from becoming too short. Therefore, it keeps cells from stopping dividing.

    Other researchers have shown that telomerase activity declines significantly with age. This means that telomeres become shorter with increasing age.

    The second theory, known as the disposable soma theory, was proposed by George Williams in 1956. He suggested that individuals must die so that new individuals can replace them. According to this theory, organisms evolve mechanisms to ensure that old cells are eliminated when necessary. For example, young animals shed skin cells and hair follicles every day. These cells are replaced by new ones. This process helps keep an animal’s organs working properly.

    In contrast, older people often experience diseases that cause their organs to deteriorate. As a result, these organs need to be removed and replaced by artificial devices. If a person lives long enough, all of her or his organs will eventually fail. Therefore, death is inevitable.

    According to the disposable soma theory of aging, most of our cells contain a program that instructs them to die once they reach a specific age. However, there is no evidence that supports this hypothesis.

    Genetics and epigenetics of aging and longevity

    According to the free radical theory of aging, oxidative stress causes cellular damage. In turn, damaged cells produce more reactive oxygen species (ROS). ROS gradually accumulate until they overwhelm the body’s antioxidant defenses. Eventually, the body becomes unable to eliminate ROS efficiently. This results in increased levels of ROS inside cells.

    Oxidative stress also damages proteins, lipids, and nucleic acids. It leads to the production of advanced glycation end products (AGE) and lipid peroxides. AGE and lipid peroxides increase with age. They may reduce the ability of insulin to activate glucose transporters in muscle and fat cells. This makes blood sugar levels rise. High blood sugar levels stimulate the release of hormones such as cortisol and adrenaline. The combination of high blood sugar levels and elevated hormone levels increases inflammation. Inflammation accelerates aging and reduces lifespan.

    Oxidative damage to DNA is another source of aging. Damaged DNA accumulates over time. This accumulation contributes to the development of cancer.

    Epigenetic changes contribute to the loss of regenerative capacity during aging. Epigenetic modifications make gene expression less responsive to environmental signals. Thus, epigenetic changes prevent the body from responding appropriately to environmental challenges.

    Epigenetic modifications include DNA methylation, histone acetylation, microRNA expression, non-coding RNAs, and chromatin remodeling.

    DNA methylation occurs on cytosine bases within CpG islands. CpG islands are short sequences of DNA containing many CG sites. Methylated CpG islands suppress transcription.

    Histones are structural proteins that wrap around DNA strands. Histone acetylation affects how tightly DNA coils together. Histone deacetylases remove acetyl groups from histones. Acetylated histones relax DNA and allow for transcription.

    MicroRNAs bind to target mRNA transcripts and inhibit translation into protein. MicroRNA expression decreases with age.

    Non-coding RNAs have been implicated in regulating gene expression. Long non-coding RNAMoRs regulate gene expression by binding to complementary regions of mRNAs. Short non-coding RNANoRs have regulatory functions similar to microRNAs.

    Chromatin remodeling involves changing the structure of chromosomes without altering the sequence of DNA. There are three types of chromatin: heterochromatin, euchromatin, and facultative heterochromatin. Heterochromatin contains condensed, repetitive DNA. Euchromatin has a loose conformation. Facultative heterochromatin consists of both heterochromatin and euchromatin.

    The term “epigenome” refers to the complete set of epigenetic marks present at any given locus in an individual cell. An epigenome is composed of two components: the genome and the epigenome.

    What genes are associated with longevity?

    Mitochondrial function declines with age.

    Aging is characterized by mitochondrial dysfunction. Mitochondria produce energy through oxidative phosphorylation. Oxidative phosphorylation produces ATP, which fuels cellular processes. Mitochondria contain their own DNA. This mitochondrial DNA encodes 13 polypeptide subunits of the electron transport chain complexes. Mutations in these genes cause mitochondrial disorders.

    Aging is characterized by decreased activity of enzymes that repair damaged mitochondria. As a result, mitochondrial mutations accumulate over time.

    Mitochondrial biogenesis is regulated by sirtuins (SIRT1–7). SIRTs are NAD+ dependent class III histone deacetylase enzymes. SIRTs reduce levels of acetylated lysines on histones. This allows for increased transcription of nuclear encoded mitochondrial genes.

    Read more about The Sirtuin Theory of Aging.

    Mitochondrial biogenesis is also regulated by peroxisomes. Peroxisomes are organelles that process fatty acids. Fatty acid oxidation leads to production of reactive oxygen species (ROS) such as superoxide radicals. ROS damage macromolecules including nucleic acids. Peroxisomes play important roles in detoxifying ROS.

    Peroxisomes are required for normal lifespan extension in yeast. Inhibition of peroxisomal beta-oxidation extends lifespan in mice.

    Peroxisomes are essential for proper functioning of the immune system. Mice lacking functional peroxisomes show defects in T lymphocyte development.

    Peroxisomal metabolism may contribute to longevity via its effects on inflammation. Inflammation increases during aging. Inflammatory cytokines stimulate the release of ROS from neutrophils. ROS damage cells and tissues.

    Inflammation contributes to aging by damaging tissue. The inflammatory response includes activation of the innate immune system. Innate immunity is the first line of defense against pathogens. It is activated when pathogen-associated molecular patterns bind to pattern recognition receptors. Pattern recognition receptors include Toll-like receptors (TLRs), NOD-like receptors (NLRs), RIG-I-like receptors (RLRs), C-type lectin receptors (CLRs), and cytosolic DNA sensors. Activation of TLRs induces NFkB signaling. NFkB stimulates expression of proinflammatory cytokines.

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