
Understand your DNA. Optimize health, diet, & longevity with Genetic Lifehacks. #Biohacking
Small town, MT
Joined February 2015
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Psychiatrists are pushing to add an inflammation subtype of depression to the DSM.
The pattern looks a lot like being sick. Sleep problems, low energy, appetite changes, and anhedonia (that "meh, nothing matters" feeling). Researchers see higher TNF-alpha, IL-6 and CRP in some people with depression and anxiety, and anti-inflammatory treatments help some of them but not everyone.
Common sources include gut barrier problems, autoimmune disease and allergies, chronic stress, a high omega-6 to omega-3 ratio, and extra body fat. About 39% of people with rheumatoid arthritis have depression.
Does that cluster sound familiar to anyone?
I'm playing with @bot for creating new videos for an old nutrigenomics course that I've had available for members.
Gotta say that I'm pretty impressed with the speed and quality of what it produces, just from giving it the old videos which were essentially just animated slides.
I've created a free database of measured biogenic amines in food.2,028 measurements from 90 published sources.
Most low-histamine food lists are copies of each other, and there are no sources for the information.
It turns out that recent studies with modern histamine testing methods don't back up some of the commonly listed foods to avoid.
The database shows the studies, the sample counts, the methods, and even the caveats so that you can see where the numbers come from. It also shows studies for tyramine, putrescine, and cadaverine since those biogenic amines can also affect people with DAO genetic variants.
It's 2,028 individual measurements from 90 papers; 1,337 of them are original lab work, and each is traceable to its source.
geneticlifehacks.com/histami…
MTHFR gets blamed for everything online...
The real story is that MTHFR variants change how efficiently you make active folate. This then touches methylation, homocysteine, neurotransmitters, and histamine clearance.
Bad internet lore abounds.
What’s the most confusing MTHFR claim you’ve seen?
1/ One under-discussed root of depression: mitochondria that can’t keep up. When they struggle, ROS rises → inflammatory cytokines rise → mood symptoms follow for some people.
check out the latest Genetic Lifehacks weekly newsletter on histamine, a new tracker, and getting back to homeostasis.
geneticlifehacks.substack.co…
Replying to @AprilSchave
Awesome. Thank you!
Here's what I was going off of as far as the X algo.
Do me a favor if you happen to see this post. Click the share icon and copy the link. I want to see if that boosts this post or not (reading through the newly released X algorithm :-)
Latest Genetic Lifehacks weekly newsletter. Sign up to get it in your inbox!
geneticlifehacks.substack.co…
Latest Genetic Lifehacks weekly newsletter. Sign up to get it in your inbox!
geneticlifehacks.substack.co…
A new study on the pesticide chlorpyrifos shows that higher exposure (e.g. living next to a field that is being sprayed) increases the risk of Parkinson's disease significantly.
Chlorpyrifos is an organophosphate pesticide that is commonly used to control termites, mosquitoes, and roundworms. It is also used on corn and soybeans.
Mice exposed to aerosolized chlorpyrifos developed movement problems and lost dopamine-producing neurons.
link.springer.com/article/10…
Ooohhhh.... This is an interesting study.
Researchers from the University of Arizona have developed a urine test for autism based on gut microbe metabolites. The test has 90% sensitivity and 100% specificity based on the metabolite levels in the urine.
For anyone interested in autism, it is worth reading through the introduction section (and the discussion at the end). The researchers go into the changes in the gut microbiome seen in the majority of people with autism, but then also touch on the ones without gut changes usually having rare genetic mutations that are driving the autistic symptoms.
Here's a few quotes that I thought were interesting:
"In the context of early neurodevelopment, abnormal elevation of certain microbial metabolites—particularly those derived from tryptophan and phenylalanine metabolism—has been associated with adverse effects on gut barrier function, immune signaling, neurotransmitter pathways, and neurobehavioral outcomes"
"Among participants with autism spectrum disorder (ASD), 42% exhibited high levels of one or more tryptophan metabolites, 57% had elevated phenylalanine/tyrosine metabolites, and 26% had high levels of both one tryptophan metabolite and one phenylalanine metabolite. 16% of ASD participants showed increased levels of yeast metabolites." 👇
There's a growing trend (by some pro-keto influencers) of using individual Lp(a) studies to argue the risk from high Lp(a) is overblown.
The latest example: a study showing visceral fat modifies atherosclerosis risk in people with high Lp(a).
It's a real and interesting study showing that high Lp(a) in the presence of a high waist-to-hip ratio (belly fat) increases atherosclerosis risk, while those with high Lp(a) and visceral fat didn't have an increased risk of atherosclerosis.
But cherry-picking one study and saying that Lp(a) doesn't matter if you're thin and healthy misses the broader picture. High Lp(a) is more than just atherosclerosis...
- High Lp(a) raises heart attack risk even without atherosclerosis
- It triples the risk of aortic valve stenosis and calcification of the aortic valves
- Inflammation (hsCRP) is another modifier that changes the equation
The science on Lp(a) is nuanced. That's not a reason to dismiss it — it's a reason to understand it more deeply.
I've updated my Lp(a) article to include the visceral fat research alongside the other modifying factors.👇🔗
Proline is an amino acid that the body uses to make proteins. It is synthesized from the amino acid glutamate in a multistep process. We can also get proline from protein-rich foods, such as gelatin and collagen, which are particularly high in proline.
Proline in mitochondrial aging:
A 2024 study showed that proline is likely very important in healthy aging and may be able to restore mitochondrial function and ameliorate DNA damage in senescent cells. Mitochondrial dysfunction is thought to be one of the driving factors of aging and the decay of health.
Highlights from the study include that increasing proline levels in aging cells:
- induces mitophagy (the recycling of damaged mitochondria), which improves cellular energy production
- reduces senescent mesenchymal stem cells by promoting mitochondrial function
- mitigates DNA damage and inflammatory cytokine expression through its positive effect on mitochondrial function
Read the rest of this article here: longevitylifehacks.substack.…
This is an interesting new study on cognitive health in aging - broken out by APOE status.
The results showed a more than 50% reduction in the risk of dementia in people eating the most red meat. The kicker is that this result was only true for APOE E4 allele carriers.
Standard-dose naltrexone (50–100 mg) blocks mu-opioid receptors to treat alcohol and opioid addiction, but at low doses (LDN) it flips into a micro-immunomodulator.
In this article, I walk through dose-dependent mechanisms (opioid vs TLR4 vs TRPM3), with a table that maps dose → target → clinical use.
geneticlifehacks.com/naltrex…
This is an interesting study on how cardiac output and changes in cerebral blood flow are abnormal in ME/CFS.
Normally, when going from lying down to standing up, there's a compensatory change in cerebral vasodilation -- the body adjusts so that the brain gets enough blood when you stand up.
In 91% of the ME/CFS patients in this study, the brain blood vessels didn't compensate for the change in cardiac outflow in the normal way.
This isn't defined as POTS because heart rate didn't rise. However, the researchers concluded that things like more fluids, salt, compression stockings may help with ME/CFS. Study link below.
(And yes, I'm updating my ME/CFS Genetic Lifehacks article with this today.)














