@GeneticLifehack
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Understand your DNA. Optimize health, diet, & longevity with Genetic Lifehacks. #Biohacking
Small town, MT
Joined February 2015
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Would never have thought that defining the brain as two organs would have implications like
“…for creating ethical brainless clones for transplant.”
GLP-1 drugs get all the headlines for weight loss - and for the contrarian view points.
The real question is why so many people seem to need that signal boosted in the first place.
There are several environmental and lifestyle things that show up in the research as dampening natural GLP-1.
Glyphosate can shift the gut microbiome in ways that reduce GLP-1 production (mouse study, but using realistic exposure levels).
Statins have a similar microbiome story in some data.
Circadian disruption (blue light at night, screens) also lowers GLP-1.
If baseline GLP-1 is getting nudged down by glyphosate, blue light at night, and even some medications -- well, it makes sense and tracks with the obesity epidemic.
geneticlifehacks.com/glp-1-a…
What happens to epigenetic aging in young children when their mothers are given free money?
Well, someone thought to do a study on it.
Mothers were given either $20/month or $333/month, and the kids were tested for epigenetic changes over the first four years of life.
"We found no evidence supporting our hypothesis that higher cash gifts increased children’s Epigenetic-g, although it did correlate with children’s brain activity. There was no evidence that the cash gift had an impact on these epigenetic indices in mothers."
nature.com/articles/s41562-0…
HLA-B27 gets talked about almost only as an autoimmune risk gene. And it does raise relative risk for ankylosing spondylitis a lot (about 20-fold), and most people with ankylosing spondylitis are HLA-B27 positive.
But most carriers never get ankylosing spondylitis. Absolute lifetime risk is still in the ballpark of roughly 6–10%, and other triggers matter. Newer studies show that it is less the old “molecular mimicry” idea and more that HLA-B27 proteins tending to misfold in the ER, which can influence inflammatory pathways like IL-23/IL-17.
There’s also a plus side - HLA-B27 has been linked to better outcomes with HIV and hepatitis C, and a stronger EBV response. The same immune system side that raises autoimmune risk can help against some viruses.
geneticlifehacks.com/hla-b27…
Updating my article on arsenic metabolism and excretion today, and I came across a study that has me wondering why it didn't make the headlines.
Exposure to higher levels of arsenic in the groundwater is associated with a 156% increased relative risk of Alzheimer's.
What has me surprised is that the definition of 'high' that caused that much of an increase was >10 µg/l. They also broke out middle-high and middle-low segments, which also increased the relative risk of Alzheimer's compared to low arsenic (<2 µg/l)
Living in the Rocky Mountain West, there are a lot of people out here drinking well water with arsenic at or above 10 µg/l.
journals.sagepub.com/doi/abs…
This is an interesting new study (mouse study) using a modified form of urolithin A for ALS. The UA-30 compound enhanced FOXO3a, which points to possible positive effects on lifespan. FOXO3A variants are frequently found in centenarians.
Damaged mitochondria drive diseases from ALS to aging itself. Our cells rely on mitophagy to clear them out — and urolithin A (found in pomegranates) boosts this process. Problem: UA is barely absorbed from the gut.
This paper came up with UA-30, a modified UA with far better bioavailability — and in an ALS mouse model, it worked.
Next question: if UA-30 clears damaged mitochondria this well, could it also help extend healthspan/lifespan in aging? jci.org/articles/view/202787
Debbie @ Genetic Lifehacks retweeted
Most genome panels have this SNP checked
Here is mine. Rs1805086. There are others also
I got my raw data and uploaded it to @GeneticLifehack for the analysis
Most of the norepinephrine your brain uses comes from a tiny brainstem cluster called the locus coeruleus. Roughly 30,000 neurons supply the rest of the cortex.
A 2026 CSF study in ME/CFS and long Covid found that the norepinephrine pathway looked low, while dopamine looked normal.
The authors suggest an energy angle.
Turning dopamine into norepinephrine (via DBH inside vesicles) is ATP-intensive, so after exertion, when energy is short, norepinephrine signaling may drop. That lined up with post-exertional malaise severity in their data.
It's an interesting way to think about brain fog and PEM. I don't know that it is the whole story, but definitely an interesting finding.
geneticlifehacks.com/norepin…
1/ Arsenic isn't just a Victorian poison plot -- it's found in well water in some areas, and rice can soak it up from soil and water, especially in growing regions in the southern US.
Why is arsenic important? A 2026 Canadian study showed that women in the top quartile of arsenic exposure were at a 3-fold increased relative risk of breast cancer.
3-fold increase in risk of developing breast cancer for the top 25% of urinary arsenic is huge.
3/ Your body clears arsenic by methylating it (AS3MT) and using glutathione along the way. The bad part is that some intermediates are more toxic than the original arsenic, so the pathway needs to complete so that intermediates aren't lingering.
Genetics AS3MT, methyl groups (MTHFR), and glutathione (GSTs) all matter here.
4/ Practical bits from the research. Test well water if that’s your source. Cooking rice in lots of water and draining (pasta-style), or soaking/parboiling and discarding the water, can cut arsenic. Folate status helps the methylation step.
Full article (genes + lifehacks) geneticlifehacks.com/arsenic…
This is cool. I didn't realize that there were approved drugs now for lifespan and healthspan extension for larger breeds of dogs.
Phase II detox isn’t just one enzyme, it’s a family.
GST enzymes attach glutathione to a bunch of environmental toxicants (PAHs from smoke/exhaust/grilled meat, certain pesticides, aflatoxin metabolites, etc.) so you can excrete them more easily.
GSTM1 is interesting because a lot of people have a full gene deletion (null genotype), meaning no working GSTM1. That doesn’t mean “can’t detox,” because other GSTs overlap and take up the slack. But it can matter more when exposures stack together.
If you’ve ever wondered why the same smoke, pollution, or moldy-food exposure hits people differently, this family of genes is part of that story. geneticlifehacks.com/gst-glu…
1/ Interesting genetics update on APOE4 and Alzheimer’s. Two large studies found rare FN1 variants (fibronectin gene) that reduce fibronectin and look protective in people who carry APOE4. Risk dropped a lot in those analyses (~70% in the reported findings). Only about 1–2% of people have the fibronectin protective variants… but the pathway itself is the big story.
4/ Why should you care even if you don’t have the rare FN1 variant -- the BBB changes show up early in Alzheimer’s, sometimes before tau tangles and excess amyloid-beta plaque. The BBB leakiness allows fibrinogen sneaking into the brain - plus the barrier leaks are another piece of that mess. This also may tie into concussion/TBI research.
5/ One practical angle (not medical advice) here is that excess omega-6 oils raise fibronectin in some studies, while omega-3s don’t. This goes along with some of the research on a healthy diet helping to prevent or slow Alz.
Vitamin A status also ties into the extracellular matrix gene regulation.
Full article with all the details and references:
geneticlifehacks.com/fibrone…
