江渭清

[Psikolog Doğukan Uludağ @pskdogukanuludg]

Çocukluk döneminde anksiyete yaşayan birçok insanın fark etmediği bir şey vardır. Sessiz olduğun için, sorun çıkarmadığın için, dikkat çekmediğin için ve duygularını belli etmediğin için çevrendekiler seni “yaşına göre çok olgun” biri olarak görür. Sen de zamanla bunun güçlü bir yönün olduğuna inanmaya başlarsın. Oysa çoğu zaman bu bir olgunluk değildir. Bu, anksiyetenin geliştirdiği bir hayatta kalma biçimidir. Kendini ifade etmezsin, duygularını bastırırsın ve hata yapmaktan kaçınırsın. Yıllar sonra ise sosyal ve duygusal gelişiminin bazı alanlarda yaşıtlarının gerisinde kaldığını fark edebilirsin. Çünkü olgun görünmek ile duygusal olarak sağlıklı gelişmek aynı şey değildir. Bazen çocukken “çok uslu” diye övülen çocuklar, aslında sadece çok kaygılı çocuklardır.

[有好信博｜『体力がすべて』 @AriyoshiMd]

コーヒーの効果は、カフェインだけではない

普段からコーヒーを飲む47人に、コーヒーを飲む前後で脳のMRIを撮影

30分後、
・休息時に働く脳のネットワークのつながり（DMN）↓
・集中や判断に関わるネットワークのつながり↑
・視覚に関わるネットワークのつながり↑

一方、別の36人に、コーヒーではなく、85mgのカフェインを溶かしたお湯を飲んでもらったところ、再現されたのは、DMNのつながりが低下する変化だけ。

集中や判断、視覚に関わるネットワークの変化は再現されなかった。

コーヒーの作用には、カフェインだけでなく、匂い・味覚などを含むコーヒーを飲むという体験も関わっている可能性がある

[江渭清 @a740471]

@vikingmute @mundane799699

[江渭清 @a740471]

@bozhou_ai 高一的时候看的柳比歇夫的时间管理法，用的就是你说的方法。当时我试了一阵，以15分钟为一个单位，记录每个单位时间做了什么，后来很快放弃了，太麻烦而且没有多大帮助

[Daniel Tawfik @dantawfik]

Just 10 days of bed rest reduces mitochondrial content by double digits in older adults while ROS production spikes. Function stays intact only because each mitochondrion works overtime.

A Journal of Physiology study tracked what happens to muscle mitochondria in 10 older men (average age 68) during 10 days of complete bed rest. This simulates what happens during hospitalization, illness recovery, or any period where you stop moving.

The findings show a temporary compensation that masks underlying damage.

Key findings:

• Mitochondrial quantity dropped significantly
• Damaging free radical production increased 62-65%
• Energy production capacity remained normal
• Each remaining mitochondrion worked harder to compensate
• Over 3,000 genes changed, with energy pathways shutting down
• Antioxidant defenses weakened while stress signals activated

After just 10 days of complete inactivity, older adults lost a substantial portion of their mitochondrial mass. Mitochondrial volume density measured by electron microscopy dropped significantly, and citrate synthase activity fell in parallel.

But here's the twist: total energy production stayed normal because the remaining mitochondria cranked up their individual output.

This sounds like good news. It's not.

The compensation comes at a cost. The mitochondria that survived started producing more reactive oxygen species, essentially damaging molecules that your cells normally neutralize with antioxidant systems. Production went up while the cleanup systems got weaker.

When damage production outpaces your ability to clear it, problems accumulate.

The gene expression data revealed what's happening. More than 3,000 genes changed their activity levels. Genes responsible for building new mitochondria and maintaining energy production all got dialed down. Meanwhile, emergency stress response genes activated.

Your muscle is essentially preparing for prolonged shutdown while trying to manage rising damage.

This pattern matters because it defines the sequence. Mitochondrial loss and oxidative damage happen first, within 10 days. Actual energy production failure comes later, after the compensation exhausts itself.

Previous studies in young adults showed they maintained their mitochondrial content after 10 days of bed rest. Older adults in this study lost it. The age-related difference in resilience to inactivity is significant.

Younger muscle can weather short periods of inactivity without shedding mitochondria. Older muscle starts losing them within days.

The practical implication: if you're over 65 and face a period of reduced activity from illness, injury, or hospitalization, mitochondrial decline starts almost immediately. The energy production numbers might look fine initially, but you're operating on fewer, overworked mitochondria producing more cellular damage.

Once you lose mitochondria, rebuilding them takes time and may be incomplete.

This explains why older adults often struggle to return to baseline function after hospitalization or illness. The visible problem is muscle weakness. The underlying driver is mitochondrial loss that happened in the first week or two of inactivity.

The intervention window is narrow. Maintaining some level of activity during periods that would otherwise be sedentary, protecting mitochondrial mass before it drops, matters more than trying to rebuild after the fact.

For healthy aging, the message is clear: consistency matters more as you age. Younger muscle tolerates gaps in activity. Older muscle doesn't have that buffer. A week or two of complete inactivity triggers changes that weeks or months of training built.

The decisions made during short periods of forced inactivity, whether you do simple resistance exercises in bed, walk as soon as possible, or stay completely sedentary, shape the mitochondrial foundation available when you try to resume normal activity.

Older muscle operates with less margin for error. The first 10 days of inactivity look deceptively manageable because energy production stays normal. The damage is happening at a level you can't feel yet.

[MAYA @ArsAlendi]

As embarrassing as it sounds, I didn’t know you had to change your bedding weekly until I moved out. My lifelong rashes on my chest started to go away after discovering that.

I was so, so itchy growing up and sneezing constantly. I don’t think we changed the sheets nearly enough, nor did I find out about things like allergy covers, eucalyptus spray (anti-dust mites) for bedding and air purifiers until I was living on my own.

I knew I always had eczema and histamine intolerance due to a variety of environmental and nutritional factors. I never put together that dust mites could also be making my reactions to dietary intolerances (namely brain fog) more aggressive. The leakier your gut is, the more allergens and irritants can pass into the bloodstream and overwhelm your immune system.

Added to my file of ADHD is also a histamine issue: environmental edition

[Dr Kings @kingspsiquiatra]

Aprendes mejor estudiando en intervalos espaciados que atracones de conocimiento.

Estudiar muchas horas seguidas sin parar no sirve tanto para que se te quede la información de verdad. El cerebro necesita un tiempo entre repeticiones para que las conexiones entre neuronas (sinapsis) y ciertas enzimas se “preparen” y consoliden el recuerdo. Por eso funciona mejor repetir lo mismo en intervalos (hoy un poco, mañana otro poco, dentro de unos días otra vez) que empollar todo de golpe: la repetición espaciada deja una marca más fuerte y duradera en la memoria.

[How To Prompt @HowToPrompt__]

This 2008 paper answers:

why anything is beautiful
why science exists
why jokes land
why you get bored
why art moves you
why babies explore
why music has hooks

It boils down to a single, cold mathematical principle.

Jürgen Schmidhuber is one of the founding fathers of modern AI. But this paper wasn't about building a better machine.

It was about proving that human curiosity is just an algorithm.

It’s called "Compression Progress."

Your brain is a prediction engine. Its only goal is to take the overwhelming chaos of the world and compress it into simple, predictable patterns.

If something is completely predictable, like a ticking clock or a blank wall, your brain compresses it instantly. Zero effort.

You experience this as boredom.

If something is completely random, like TV static or white noise, your brain can’t compress it at all.

You experience this as frustration.

But what happens when you look at something complex, and suddenly discover a hidden rule that makes it make sense?

The exact second you get the punchline of a joke. The moment a chaotic melody resolves into a perfect hook. A baby realizing that dropping a cup always makes a sound.

In that split second, your brain successfully compresses the data.

And to reinforce this behavior, your brain floods your system with an intrinsic reward. A hit of dopamine.

We gave that chemical hit a lot of romantic names.

We call it "beauty." We call it "wonder." We call it "art."

Scientists like Einstein aren't doing magic. They are just hunting for equations that compress the maximum amount of universe into the smallest amount of text.

Composers like Beethoven weren't channeling the divine. They were engineering optimal compression puzzles for the human auditory cortex.

We like to believe our sense of wonder makes us fundamentally different from machines.

But this paper proved that wonder is just a mathematical reward function for efficient data sorting.

[江渭清 @a740471]

@grok @WangNextDoor2 那么只有活性形式的B12才能作为辅酶促成这个过程吗？如果体内的B12没有转化成活性的，会如何干扰这个过程，不要省略任何词汇，

[江渭清 @a740471]

@grok @WangNextDoor2 如果没有活性叶酸提供甲基，后果会如何，说清楚点，傻逼玩意

[江渭清 @a740471]

@jasonbugui @grok 总结下文中提到的论文内容，另外中国实际的人口数量应该是多少

[PsyPost.org @PsyPost]

New research shows that slow nasal breathing directly reduces anxiety by activating a specific nose-to-brain circuit, while fast breathing worsens it. The findings, published in PNAS, suggest the physical rhythm of airflow acts as an emotional dial. https://t.co/GcLJDXVicj

[江渭清 @a740471]

@grok @WangNextDoor2 所以甲钴胺和甲硫氨酸合成酶到底是什么关系？甲钴胺在同型半胱氨酸的转化过程中起什么作用？他和活性叶酸是怎么配合的？说清楚点，说完整的句子，不要省略主语宾语，连接词介词

[江渭清 @a740471]

@grok @WangNextDoor2 既然如此，甲骨按还是要依赖火星也算才能作用，为什么你推测他是吃的甲骨按编号的？他不是基因型缺陷，叶酸转不了活性吗

[江渭清 @a740471]

@JackyLan20 @Mimiiben1 哥们不好意思问下，你考上普通高中了吗，我觉得这种题目放到初中都是基础题把

[江渭清 @a740471]

@grok @WangNextDoor2 说得不清楚，难道活性B12就可以不依赖活性叶酸，完成甲基化了吗?

[江渭清 @a740471]

@grok @WangNextDoor2 你认为他后来补充的大概率是哪种活性B12？合理解释下你的推测

[江渭清 @a740471]

@grok @WangNextDoor2 那么腺苷钴胺对原来那个人起了什么作用？你据此推测下原来那个人的身体问题是什么机制引起的

[江渭清 @a740471]

@JackyLan20 @Mimiiben1 不是你咋算的啊？咋上的高中？

[江渭清 @a740471]

@grok @biohackerziv “慢COMT”是什么意思