Humanity+ is the world’s largest transhumanist organization that advocates ethical use of technology and evidence-based science for radical life extension.
Category: life extension – Page 411
Aging is the biggest risk factor for cancer, but the mechanisms linking these two processes remain unclear. Using GTEx and TCGA data, we compared genes differentially expressed with age and genes differentially expressed in cancer among nine human tissues. In most tissues, aging and cancer gene expression pattern changed in the opposite direction. The exception was thyroid and uterus, where we found transcriptomic changes in the same direction in aging and in their corresponding cancers. The overlapping sets between genes differentially expressed with age and genes differentially expressed in cancer across tissues were enriched for several processes, mainly cell cycle and the immune system. Moreover, cellular senescence signatures, derived from a meta‐analysis, changed in the same direction as aging in human tissues and in the opposite direction of cancer signatures. Therefore, transcriptomic changes in aging and in cellular senescence might relate to a decrease in cell proliferation, while cancer transcriptomic changes shift toward enhanced cell division. Our results highlight the complex relationship between aging and cancer and suggest that, while in general aging processes might be opposite to cancer, the transcriptomic links between human aging and cancer are tissue‐specific.
Great Diet Information: #Longevity
Inflammation is also called the silent killer. It is silent because as your body struggles with inflammation, it also does all it can to maintain balance. This means that symptoms are sometimes hard to decipher and can even be hidden for some time.
Inflammation can be a good thing
A little bit of inflammation is a good thing, a lot can be extremely dangerous. When we are injured or sick, the immune system jump into gear and brings an army of white blood cells to the area of concern by increasing blood flow. For instance, when you get a cut or a scrape it generally becomes puffy, red and hot. This is inflammation – more white blood cells have arrived to handle the situation. Acute inflammation is how the body responds to foreign pathogens – it protects us from harm.
Researchers at the Buck Institute, including Dr. Judy Campisi, have published a new study that shows, for the first time, that senescent cells are associated with age-related blood clots [1].
As we get older, increasing numbers of our cells enter into a state known as cellular senescence. Senescent cells do not divide or support the tissues of which they are part; instead, they emit a range of potentially harmful chemical signals known as the senescence-associated secretory phenotype (SASP), which encourages nearby healthy cells to enter the same senescent state.
The presence of high levels of SASP reduces tissue repair, increases chronic inflammation, and can even raise the risk of cancer and other age-related diseases.
A new study shows that scientists might be able to not only slow the process of aging but actually reverse it, Benjamin Button-style.
Volunteers in a California study were given a cocktail of three common drugs for one year— a growth hormone and two diabetes medications. Scientists had been testing the drugs in the hope of regenerating the thymus gland.
But upon further analysis, they found that participants had lost an average of 2.5 years on their “epigenetic clock,” measured by analyzing marks on a person’s genomes, according to the journal Nature. Participants’ immune systems also showed signs of rejuvenation.
Discussions like this one are among the major reasons for my involvement in the transhumanist movement. Steele Archer of the Debt Nation show has hosted an excellent panel on life-extension advocacy – its history, motivations, and future prospects, as well as the societal implications and relationship to technological advancement more broadly. Watch it here for interdisciplinary insights from Ira Pastor, Johannon Ben Zion, and myself: .
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Telomeres are the protective caps of our chromosomes and play a central role in the aging process. Shorter telomeres are associated with chronic diseases and high stress levels can contribute to their shortening. A new study now shows that if telomeres change in their length, that change is also reflected in our brain structure. This association was identified by a team of scientists including Lara Puhlmann and Pascal Vrtička from the Max Planck Institute for Cognitive Brain Sciences in Leipzig together with Elissa Epel from the University of California and Tania Singer from the Social Neuroscience Lab in Berlin as part of Singer’s ReSource Project.
Telomeres are protective caps at the ends of chromosomes that become shorter with each cell division. If they become so short that the genes they protect could be damaged, the cell stops dividing and renewing. Consequently, the cell is increasingly unable to perform its functions. This mechanism is one of the ways in which we age.
Telomere length is therefore regarded as a marker for the biological age of a person—in contrast to their chronological age. For two people of the same chronological age, the person with shorter telomeres has an increased risk of developing age-related diseases such as Alzheimer’s or cancer, and even a shorter life expectancy.
A recent review shows the current state of the industry with regards to using human pluripotent stem cells (hPSCs) to create cells that are useful for the study of, and therapies for, the human heart.
Pluripotent Stem Cells
Stem cells are the cells that form every other cell in the body, and adult humans naturally have native populations of stem cells to replace losses; the depletion of these reserves is stem cell exhaustion, which is one of the hallmarks of aging. To create stem cells from regular (somatic) cells, researchers use a technique called induced pluripotency, which creates induced pluripotent stem cells (iPSCs). However, purely naive, dedifferentiated pluripotent cells, which could create any cell in the body, are only of limited use and are not effective as a therapy. To form specific somatic cell lines, stem cells must first be differentiated into specific types.
Cells that become senescent irrevocably stop dividing under stress, spewing out a mix of inflammatory proteins that lead to chronic inflammation as more and more of the cells accumulate over time. Publishing in the September 24 edition of Cell Reports, researchers at the Buck Institute identified 44 specific senescence-associated proteins that are involved in blood clotting, marking the first time that cellular senescence has been associated with age-related blood clots.
“The incidence of venous thrombosis, which includes deep vein thrombosis and pulmonary embolism is extremely low until the age of 45, when it begins to rise rapidly. Over time it becomes a major risk factor for death. By 80, the condition affects five to six people per thousand individuals,” said Judith Campisi, PhD, Buck professor and senior co-author of the study. “Blood clots are also a serious side effect of chemotherapy, which sets off a cascade of senescence in those undergoing treatment. That’s why blood thinners, which carry their own risks, are often included in treatment protocols.”
Scientists in the Campisi lab and other labs around the world are working to develop senolytics, drugs which would clear senescent cells from the body, potentially providing treatment options for many age-related diseases that are either caused or linked to senescence. They include Alzheimer’s and Parkinson’s diseases, cardiovascular disease, osteoarthritis, macular degeneration, age-related cancers and sarcopenia, among others.