Understand your DNA. Optimize health, diet, & longevity with Genetic Lifehacks. #Biohacking

Small town, MT
Joined February 2015
Debbie @ Genetic Lifehacks retweeted
Replying to @AbudBakri
Started using Genetic Life Hacks based on your rec. It's worth its weight in gold. tyvm
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Debbie @ Genetic Lifehacks retweeted
Protect your tribe One of the best things I did was to run my kids DNA raw data through @GeneticLifehack I can now support their nutritional needs with much more clarity
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Debbie @ Genetic Lifehacks retweeted
A promising new rejuvenation factor discovered by @geochurch et al. 🚀 Using a transcriptomic screen they found SRSF1, an RNA-processing and splicing factor that restores youthful profiles in cells. In a small mouse study, activating SRSF1 extended median lifespan by 14%. nature.com/articles/s43587-0…
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Debbie @ Genetic Lifehacks retweeted
Two bacteria, injected into the bloodstream of mice, wiped out tumors without help from the immune system. A new study shows how they do it, and the mechanism is not what most people would expect. Researchers at the Japan Advanced Institute of Science and Technology, with the University of Tsukuba and Daiichi Sankyo, tested a pair of naturally occurring bacteria called AUN. One is Proteus mirabilis (called A-gyo), isolated from inside a tumor. The other is Rhodopseudomonas palustris (called UN-gyo), a purple photosynthetic bacterium. No genetic engineering was used. The idea of using bacteria against cancer is old. In the 1890s, William Coley noticed that some patients improved after infections and began injecting bacteria on purpose. Most modern versions still depend on the immune system to finish the job. That is a problem. Chemotherapy and radiation suppress immunity, and solid tumors have a low-oxygen core (hypoxia) that immune cells struggle to enter. Checkpoint inhibitors and CAR T cells, the newer immunotherapies, also rely on those immune cells. This study asked whether bacteria could kill tumors on their own. Key findings: • Tumors disappeared completely in the treated mice, and the mice lived longer. This held in mice with normal immune systems, mice with weakened immune systems, and mice carrying human tumors • The mice showed no visible signs of toxicity. There was also no cytokine storm, a dangerous overreaction where the immune system floods the body with inflammation, which is a known risk with some cancer immunotherapies • The two bacteria were mixed at about 3 parts A-gyo to 97 parts UN-gyo. In the lab, they settled back into that same balance within a week, even when researchers started them at very different ratios • Inside tumors, the balance reportedly flips to about 99 parts A-gyo to 1 part UN-gyo, according to the institute's press release • A-gyo was missing the genes for the sticky surface structures bacteria normally use to attach to tissue and cause infection. That likely makes it less harmful than its commercial cousin • Treated tumors were full of blood clots and showed widespread tissue death So this is what seems to be happening from mechanistic angle: First, the bacteria reach the tumor. Tumors are a hospitable place for bacteria. They have low oxygen, leaky blood vessels, and a suppressed local immune response. The bacteria grow there, form biofilms (sticky bacterial communities), and also kill cancer cells directly. Second, they trigger clotting inside the tumor. Cytokines (inflammatory signaling proteins) rise, platelets aggregate, and fibrin (the protein mesh in blood clots) builds up. This is thrombosis, the formation of clots within vessels. Third, the vessels collapse. Think of cutting the water supply to a building. A tumor needs a dense network of new blood vessels to bring in oxygen and nutrients. Clot them off, and the tissue behind them starves and dies. The partnership also appears to act as a safety system. UN-gyo dampens A-gyo's pathogenicity, reduces its ability to rupture red blood cells (hemolysis), and helps push A-gyo into a long, filament-like form in the presence of cancer metabolites. In other words, the second bacterium keeps the first one in check outside the tumor. Big caveats, though. This was all done in mice. Mouse tumors, mouse blood clotting, and mouse immune responses differ from ours, and complete remission in mice has a poor track record of translating to people. Injecting live bacteria into the blood, in people who may already be sick, carries infection risks that mouse studies can't fully capture. The same clotting mechanism that destroys tumors could be dangerous if it occurred outside them. And the study was led by a group that is preparing to launch a startup, which is worth keeping in mind when reading the safety claims. This is, however, a new way to think about cancer, one of the leading causes of death in older adults. The rate of cancer rises steeply after 50, and most current treatments depend on an immune system that also weakens with age and with treatment. A therapy that works without immune cells would matter most for exactly the people who need it most. The broader point is that the tumor itself is an ecosystem, and bacteria that live there may be turned into a tool. Whether that tool is safe enough for people is the question that remains.
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Debbie @ Genetic Lifehacks retweeted
Replying to @bryan_johnson
@GeneticLifehack is a great tool. Completely changed how I supplement with health.
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Debbie @ Genetic Lifehacks retweeted
An invasion of immune cells from skull bone marrow triggers inflammation that drives cognitive and mood decline with age in adults with chronic #TBI, shows work that also identifies fenofibrate as a promising therapy in a pilot trial. @ScienceTM scim.ag/47pMzBt
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Debbie @ Genetic Lifehacks retweeted
Sleep is key to healthy aging. But what if you can’t sleep? Luckily, we may have found a solution for exactly such cases: the repair function of sleep is controlled by circadian changes in chromatin compaction, which in turn are regulated by the DREAM complex🧵 1/7
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Debbie @ Genetic Lifehacks retweeted
Genetics, Circadian Rhythms, and Sunlight Was going through a patient's genetics and found this interesting SNP - rs2675703 5.6x greater risk of seasonal affective disorder. Circadian rhythm rules and optimal sun/light exposure is critical for this genotype The magnitude of the effects is quite large This person noted they were always responded well to sun and felt terrible after long days in the office during winter Sun exposure at critical times during the day and a Chroma Skyportal and he's on his way to success
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Debbie @ Genetic Lifehacks retweeted
NIH-funded researchers identified 36 genes associated with obsessive-compulsive disorder (OCD) and chronic tic disorders, marking an important step forward in understanding the biological mechanisms underlying these conditions. Many of these genes are involved in brain pathways related to impulse control, movement, decision-making, and habit formation. The findings may help guide future research into diagnosis and treatment. Read more: bit.ly/4jwPtvB
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Debbie @ Genetic Lifehacks retweeted
Hear ye, hear ye! We have a Fat Bear Week winner! This year’s Lord of Lard, Earl of Girth and Commander in Beef is... Bear 89 also known as Backpack!
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Debbie @ Genetic Lifehacks retweeted
🔬 NIH’s National Institute of Allergy and Infectious Diseases has launched a clinical trial to help people with alpha-gal syndrome, a condition caused by tick bites that triggers an allergic reaction to a sugar in red meat. ➡️Learn more: bit.ly/4xSiZiS
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Mendelian randomization study found NO association of physical activity, whether self-reported or measured, and sedentary behavior, with heart disease, heart attack, or stroke. Crazy, no? But it just might be true. Causality may be that healthy people exercise, not that exercise makes people healthy. Identical twin studies suggest this, though other Mendelian studies have found differently. link.springer.com/article/10…
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Debbie @ Genetic Lifehacks retweeted
Slow COMT here, this is helpful info 👇
COMT clears dopamine, norepinephrine, and some estrogen metabolites. The common Val158Met variant changes the amount of available enzyme. Slow COMT can mean better working memory and more stress sensitivity. Fast COMT often flips that, and it is sometimes called the warrior gene (dumb name). Slow COMT + a sudden influx of methyl donors (e.g. methylfolate, methyl-B12, SAMe, TMG) can feel like mood whiplash - irritability, anxiety, irrational anger. Quercetin/luteolin can inhibit COMT. Check your genes to know (or ask your spouse AITA...) geneticlifehacks.com/comt-ge…
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Debbie @ Genetic Lifehacks retweeted
When an older heart is transplanted into a younger person, it doesn't stay "old." Vadim Gladyshev's lab shows the heart actually starts aging on the timeline of the body it's now living in — its biological age shifts to match the recipient, not the original donor, at the molecular level. biorxiv.org/content/10.64898…
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Debbie @ Genetic Lifehacks retweeted
Steven Phillips, MD
@StevePhillipsMDSep 23
PANS/PANDAS mechanism just published: (They studied strep but it's not limited to strep, I've seen many cases from bartonella) Strep → IL-17A → microglia → leaky blood-brain barrier → sudden personality changes, OCD, tics, & many more. For 20 years parents were told it was psychosocial. It was inflammation due to an infection. It always was.
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A Mayo Clinic team just built the cleanest causal test I've seen for NAD's role in aging. They engineered mice whose NAD synthesis depends entirely on dietary niacin, then pulled the niacin. Result: kyphosis, muscle and bone loss, cataracts, frailty, cellular senescence, shortened lifespan. Put niacin back and most of it reverses, without fully restoring NAD. That partial-restoration gap matters. It says NAD depletion triggers senescence programs that do not simply snap back when the cofactor returns. We flagged senescence as a load-bearing hallmark in the Biomarkers of Aging Consortium work (Moqri et al., Cell 2023); this is a rare in vivo model that makes the causal chain from cofactor to senescence to phenotype explicit and reversible. Nat Commun, Benitez-Rosendo, Chini et al. doi.org/10.1038/s41467-026-7…
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