Debbie @ Genetic Lifehacks

@GeneticLifehack

Oct 23

Max Marchione

@maxmarchione

Oct 23

BREAKING: Scientists have used a powerful new form of CRISPR called prime editing directly inside the human body for the first time.

They aim to rewrite faulty DNA responsible for Wilson disease that can cause severe liver and brain damage.

A major milestone in gene editing.

Debbie @ Genetic Lifehacks

@GeneticLifehack

Oct 23

Ric Flair®

@RicFlairNatrBoy

Oct 23

I Want To Sincerely Apologize To My Agent, Steve Solomon, Washington State Horror Con @wahorrorcon, @bigeventny, And Especially All My Fans In Seattle For Having To Cancel My Scheduled Appearance.

Unfortunately, I Am Dealing With A Blood Clot In My Leg, And My Doctors Have Limited My Travel To 3–4 Hours. Seattle Falls Outside That Range, And As Disappointed As I Am, I Have To Put My Health And Recovery First.

Blood Clots Are Extremely Serious And Can Be Life-Threatening. We Have Seen This Recently With Jalen Hurts And The Complications Involving Blood Clots In His Lungs. It Is A Reminder That This Is Not Something To Take Lightly, And I Must Follow Medical Advice.

I’m Scheduled To Have A Procedure To Strip The Affected Vein, Which My Doctors Expect Will Allow Me To Be Cleared For More Travel Afterward.

Please Know This Decision Was Not Made Lightly. I Am Truly Sorry For The Inconvenience And Disappointment, And I Am Incredibly Grateful For Your Patience, Understanding, And Continued Support.

I Look Forward To Getting Healthy And Seeing You All Down The Road. Thank You For The Love And Support.

Much Love,
Ric Flair

Debbie @ Genetic Lifehacks

@GeneticLifehack

Oct 23

Superman

@thesupermannx

Oct 22

Scientists found a way to flush Alzheimer’s plaque out of the brain in minutes.

Without any surgery and drugs.

Your brain has a waste-clearance network called the glymphatic system. It flushes out toxic proteins and dead cells.

But it only really activates during deep, u don't sleep, the trash piles up. Over time, that buildup leads to cognitive decline and Alzheimer's.

Until today.

Researchers just published a paper proving they can manually trigger this cleaning cycle.

Without you ever going to sleep.

They used 40.68 MHz ultrashort waves (USW) beamed non-invasively into the brain.

Within 10 minutes, the brain's fluid flow rapidly accelerated.

The waves artificially synchronized the neurons into a Delta state, the exact frequency of deep sleep. This forced the brain's water channels to open and start flushing out the system.

They tested it on mice with traumatic brain injuries and Alzheimer's pathology.

The brain swelling dropped. The toxic proteins were cleared out. Cognitive deficits actually improved.

No surgery. No massive chemical interventions. Just a frequency.

Debbie @ Genetic Lifehacks

@GeneticLifehack

Oct 23

NIH

@NIH

Oct 22

NIH researchers have discovered a natural defense mechanism that may help the body prevent plaque from building up inside arteries, opening new possibilities for treating atherosclerotic cardiovascular disease, a leading cause of death in the U.S. x.com/i/article/2113…

Debbie @ Genetic Lifehacks

@GeneticLifehack

Oct 23

On3

@On3

Oct 22

Southern head coach and NFL Hall of Famer Marshall Faulk has been diagnosed with Parkinson’s disease, he announced🙏

on3.com/news/marshall-…

Debbie @ Genetic Lifehacks

@GeneticLifehack

Oct 22

S Blitshteyn MD, FAAN, FANA, Dysautonomia Clinic

@dysclinic

Oct 22

🚨 My new paper on small fiber #neuropathy in NONPAINFUL conditions is published. Neuropathy is traditionally defined by neuropathic (tingling, numbness, burning, shooting) pain, but there are neurologic and non-neurologic conditions where objective findings of small fiber revalent despite the pain being absent or minimal. I outline comprehensive treatment options for small fiber neuropathy with both evidence-based and emerging therapies in the Table. 🧠
clinmedres.org/content/24/3/97

Debbie @ Genetic Lifehacks

@GeneticLifehack

Oct 22

Dr. Rhonda Patrick

@foundmyfitness

Oct 22

Low omega-3 intake has been identified as a leading dietary contributor to preventable death.

It's estimated that low seafood omega-3 intake accounted for 84,000 deaths in one Harvard-led U.S. analysis, compared with 82,000 attributed to trans fats. That’s a substantial omething missing in the diet.

And the intake gap is substantial. Nearly 90% of Americans aren't meeting seafood recommendations.

We pay a lot of attention to ingredients we should avoid, but we should also ask whether we’re getting enough of the nutrients we need.

For omega-3s, that means paying attention to EPA and DHA (the forms found in seafood). Fatty fish like salmon is a direct source. Omega-3 supplementation can also help fill any gap not being met through whole-food sources.

Debbie @ Genetic Lifehacks

@GeneticLifehack

Oct 22

Daniel Tawfik

@dantawfik

Oct 22

Adults with mitochondrial disease burned about 195 more calories a day than healthy controls in a metabolic chamber, while moving 26% less. Yet over 10 days of normal life, their total energy expenditure looked the same as everyone else's.

A new study in Cell Press Blue, led by n Picard @MitoPsychoBio at Columbia University, suggests the extra cost is real. It just gets hidden because people with these defects move less.

The study compared 10 adults with mitochondrial disease to 10 healthy controls of similar age, sex, height, and BMI.

Mitochondria carry their own small set of DNA, separate from the DNA in your cell nucleus. All 10 patients had a confirmed mutation in that mitochondrial DNA. Five had a single letter change in the genetic code (the m.3243A>G mutation). Five were missing a large chunk of the DNA entirely (a single large deletion).

Different mutations, same problem. Both damage oxidative phosphorylation, or OxPhos, the final stage of energy production where mitochondria use oxygen to make most of your ATP.

The question was simple. If the cell's energy machinery is damaged, does the whole body burn less energy, more, or the same?

Answering it is harder than it sounds, because a single measurement can mislead. So the researchers measured each person three different ways:

1. Resting energy expenditure for one hour, fasted, lying still.
2. A 23 hour stay in a whole-room calorimeter (an airtight room that measures oxygen use and CO2 output) with fixed meals, fixed lights-out, and hourly blood draws.
3. Ten days of free living, using doubly labeled water (you drink water tagged with two isotopes, and how fast they leave your body reveals total energy burned).

The findings were fairly insightful:

• Resting energy expenditure did not differ between groups (+19 kcal/day, p = 0.989), after adjusting for fat-free mass (everything in the body that isn't fat).
• In the chamber, 24 hour expenditure was higher in mitochondrial disease by 195.5 kcal/day (p = 0.016). The gap held across day and night.
• Wrist acceleration was 26% lower in patients, yet energy spent per unit of movement was 58% higher.
• During sleep, patients burned 116.7% of their resting rate versus 102.3% in controls. Heart rate variability (a marker of how well your nervous system shifts into recovery mode) was 58% lower.
• In free living, total daily expenditure was similar (p = 0.48), but patients moved 39% less.
• Plasma GDF15, a stress hormone made by cells under mitochondrial strain, was about 4.6 times higher in patients (1,840 vs 404 pg/mL). C-reactive protein, an inflammation marker, was 301% higher.

So what's happening here?

Think of a car with a worn engine. It burns more fuel per mile. If the driver cuts back on trips, the monthly gas bill looks normal, but the engine is still inefficient.

Mitochondrial defects seem to be raising the energetic cost of living, and the body appears to balance the budget by lowering voluntary activity.

This fits the constrained energy model, which holds that total daily expenditure stays within a narrow range because activity and other costs trade off against each other.

GDF15 is the candidate messenger. It acts on a receptor called GFRAL, found only in the brainstem, and in other settings it causes malaise, suppresses appetite, and reduces activity. In this study, higher GDF15 tracked with disease severity, fatigue ratings, higher energy cost per unit of movement, higher sleep expenditure, and lower free-living activity.

Some things to take into consideration:

The sample is 10 per group, with two different mutation types pooled together.

Wrist accelerometers capture movement poorly, and the energy measure includes non-movement costs like inflammation, so the study can't say how much of the extra cost is muscle inefficiency.

The chamber was a strange place to sleep, with an IV line and sensors, and both groups burned more than expected at night.

Patients also ate only 95% of their measured expenditure versus 107.5% in controls, so their lower fat burning in the chamber could reflect a calorie deficit and not the mutation.

The GDF15 data are correlations across a case-control gradient. They can't show whether GDF15 causes the inactivity, or whether inactivity, symptoms, and GDF15 all follow from the disease. Proving that would take trials that block the pathway, and the team recommends caution because GDF15 may be a useful energy-sensing signal.

For patients, the findings point to managing the downstream costs: sleep problems, anemia, heart and lung dysfunction, and psychological stress. They also suggest exercise may help partly by lowering the energy cost of everyday movement. That is an interpretation, supported by earlier training studies in this population.

There is a broader question for the rest of us. This was a rare disease, and these patients carried mutations in most of their mitochondrial DNA copies. Healthy aging looks nothing like that. But some of the same pieces show up as we get older, and what follows here is my extrapolation, not something the study tested.

• Mitochondrial DNA damage accumulates with age, though at much lower levels than in disease.
• GDF15 rises steadily with age, and in large cohorts it is one of the strongest blood predictors of mortality and age-related disease.
• Older adults tend to spend more energy per step when walking, and fatigue and falling activity are among the earliest signs of functional decline.

If mitochondrial strain raises the cost of living even modestly, and the body responds by quietly cutting activity through a signal like GDF15, that could be one route by which aging becomes self-reinforcing. Less movement means less muscle and fewer mitochondria, which raises the cost of the next trip. A hidden energy tax would be hard to see in a resting test, and most people would just call it getting older.

Training is the best-supported way to improve mitochondrial function and lower the cost of movement, and the case for staying active gets stronger if the brake is partly biological and not just motivational. Any drug aimed at GDF15 or its receptor is years from clinical use, and blocking an energy-sensing signal could carry risks.

The broader lesson is about measurement. A one hour resting test missed the problem entirely. Only the full day in the chamber exposed it, and only the free-living data showed how behavior hides it. Fatigue may be less a failure of motivation than a response to an energy bill the body can't afford.

Debbie @ Genetic Lifehacks

@GeneticLifehack

Oct 22

Bryan Johnson

@bryan_johnson

Oct 21

> T cells trigger severe gut lining damage

> GLP agonists directly protect against intestinal destruction

> I'm going to test this on myself

Debbie @ Genetic Lifehacks

@GeneticLifehack

Oct 22

Owen Gregorian

@OwenGregorian

Oct 22

Scientists Say a Simple Blood Test Could Reveal Depression | New York University, SciTechDaily

Scientists have discovered that aging immune cells may hold a hidden blood-based clue to detecting depression.

Scientists have discovered that the biological aging of certain white an important clue to depression, potentially opening the door to a blood test that could help identify the condition.

The study found that measuring how quickly these immune cells age can help predict emotional and cognitive symptoms of depression, including hopelessness and loss of pleasure. Interestingly, the same biological markers were not associated with physical symptoms such as fatigue or changes in appetite.

Published in The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences, the findings could bring scientists closer to developing an objective biological marker for depression, a mental health condition that affects nearly one in five US adults.

Why Depression Is So Difficult to Detect

Doctors currently diagnose depression primarily by evaluating symptoms reported by patients. Although blood tests may help eliminate other possible medical explanations, there is still no established biological test that can reliably identify depression or detect its earliest signs.

Part of the challenge is that depression does not affect everyone in the same way. Some people develop physical (or somatic) symptoms, including exhaustion, reduced appetite, or agitation. Others experience changes in thinking and mood, such as persistent hopelessness or anhedonia, a condition characterized by an inability to experience pleasure or maintain interest in activities that were once enjoyable.

“Depression is not a one-size-fits-all disorder—it can look really different from person to person, which is why it’s so important to consider varied presentations and not just a clinical label,” said study author Nicole Beaulieu Perez, assistant professor at NYU Rory Meyers College of Nursing. “Our study reveals unique biological underpinnings of mental health that are often obscured by broad diagnostic categories.”

Why Researchers Studied Women With HIV

Depression occurs more frequently among people living with certain conditions that affect the immune system, including HIV. Several overlapping factors may contribute to this increased risk, such as ongoing inflammation, social stigma, and socioeconomic challenges.

Women living with HIV face particularly high rates of depression. When depression goes untreated or unrecognized, it can interfere with their ability to participate in medical care and consistently take antiretroviral medications, which are essential for managing HIV.

“For women with HIV who may be experiencing depression, we want to better understand what’s going on and catch it earlier so that it doesn’t harm their whole overall health,” said Perez.

To investigate possible biological connections between depression and HIV, the research team focused on accelerated biological aging. Previous studies have linked this process to both conditions.

Unlike chronological age, which simply counts the years since a person was born, biological age reflects changes occurring within the body over time. Researchers can estimate biological age using tools known as “epigenetic clocks,” which analyze chemical changes to DNA. These modifications can influence how genes function without altering the underlying genetic code.

Blood Samples Reveal a Surprising Depression Link

The researchers examined information from 440 participants in the Women’s Interagency HIV Study, including 261 women living with HIV and 179 women without the infection.

To evaluate depression, they used the Center for Epidemiologic Studies Depression Scale (CES-D), a standardized 20-item questionnaire designed to assess both physical and nonphysical symptoms.

Blood samples were then analyzed using two different epigenetic clocks. One estimated biological aging across multiple types of cells and tissues, while the other focused specifically on monocytes, a type of white blood cell involved in the body’s immune defenses.

Monocytes help the immune system respond to infections and other threats. They are especially important in HIV infection, and previous research has found elevated monocyte levels in people experiencing depression.

The results revealed a notable difference between the two aging measures.

Biological aging in monocytes was associated with nonphysical depression symptoms, particularly anhedonia, hopelessness, and feelings of failure. This relationship appeared in women both with and without HIV.

However, the same aging measure was not associated with physical symptoms of depression.

“This is particularly interesting because people with HIV often have physical symptoms like fatigue that are attributed to their chronic illness rather than a depression diagnosis. But this flips that on its head because we found that these measures are associated with mood and cognitive symptoms, not somatic symptoms,” said Perez.

The broader epigenetic clock, which measured aging across multiple cell and tissue types, showed no association with depression symptoms.

These differences suggest that examining biological aging in specific immune cells may reveal connections to mental health that are missed when researchers measure aging more generally.

Could a Blood Test Transform Depression Diagnosis?

Although the findings are promising, Perez emphasized that additional research is necessary before measurements of immune cell aging can become part of routine depression diagnosis or treatment.

The study identifies a potential biomarker, but it does not establish a clinically validated blood test for depression. Researchers will need to investigate the relationship further and determine how reliably these biological signals can identify depression across different populations.

Eventually, such a test could complement traditional mental health assessments, potentially helping clinicians recognize depression sooner and tailor treatment to individual patients.

One possible application would be using a person’s biological profile to help predict which antidepressant medication is most likely to be effective. This could reduce some of the uncertainty involved in finding appropriate treatment.

“I think about the adage, ‘What gets measured gets managed.’ An aspirational goal in mental health would be to combine subjective experience with objective biological testing,” said Perez. “Our findings bring us a step closer to this goal of precision mental health care, especially for high-risk populations, by providing a biological framework that could guide future diagnosis and treatment.”

Read more:

scitechdaily.com/scientists-say…