most people afraid of raw milk are not afraid to eat parmigiano reggiano cheese

"Insulin resistance" is one of the most used terms in medicine and also one of the least precise When we say "insulin resistance," we're treating it like a single thing. Insulin does dozens of things in your body. In any given tissue, some insulin-signaling pathways can be impaired while others remain intact. In the liver: hyperinsulinemia drives lipogenesis (making fat) while simultaneously failing to suppress gluconeogenesis (making glucose). The same hormone in the same organ creates two dysfunctional outcomes. In skeletal muscle when fat builds up inside the muscle cells this then blocks the signal insulin uses to tell your muscles ", take in this sugar from the blood." This happens before liver dysfunction In your fat tissue, the problem is basically chronic, low-grade inflammation. When fat cells get overloaded, your immune system treats them almost like an injury and prevents insulin from appropriately releasing fat. Fat cells keep storing sugars as fat but slowly leak the fatty acids back out into the blood even when insulin is high. In the brain, when insulin reaches neurons, it helps tell your brain: "You've eaten you can stop feeling hungry now". The hypothalamus controls this and still gets the signal but can't pass it along properly due to PI3K signaling impairment. In all cases, insulin is the messenger molecule and still gets to its destination properly but all other mechanisms that originate from the insulin signal become dysfunctional.

PubMed

Cellular mechanisms of insulin resistance - PubMed

Cellular mechanisms of insulin resistance

PubMed

Insulin signaling, resistance, and the metabolic syndrome: insights from mouse models into disease mechanisms - PubMed

Insulin resistance is a major underlying mechanism responsible for the 'metabolic syndrome', which is also known as insulin resistance syndrome. Th...

PubMed

Mechanisms for insulin resistance: common threads and missing links - PubMed

Insulin resistance is a complex metabolic disorder that defies explanation by a single etiological pathway. Accumulation of ectopic lipid metabolit...

Modern medicine only treats insulin resistance as a way to control blood sugar and ignore all the other organs which are affected due to their chronically inflamed and dysfunctional state.

not sure the audiobook industry has much future. now i just have a llm powered voice system read me epubs.

https://www.weizmann.ac.il/immunology/elinav/sites/immunology.elinav/files/2022-06/Artificial%20sweeteners%20induce%20glucose%20intolerance%20by%20altering%20the%20gut%20microbiota.pdf Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature, 514(7521), 181–186 saccharin, sucralose, aspartame, and acesulfame-K disrupt the gut microbiome by reducing beneficial bacteria such as Lactobacillus and Bifidobacterium

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gut dysbiosis messes with production of short-chain fatty acids, which are critical for healthy lipid and glucose metabolism

our genetics are very stable. we don't produce mutants and evolve into new species rapidly. if you see a disease like cancer incidence increasing it isn't because of genetics. people frequently say they just got unlucky when they get cancer. we give ourselves cancer. cancer grows in metabolic dysfunction. we eat ourselves into cancer. we sit ourselves into cancer. we hide inside the caves of our house into cancer. for most cancers, unfortunately we only have ourselves to blame and that is incredibly uncomfortable to think about and why we spend so much time and money finding molecular markers for malignancy that get turned on during our times of metabolic dysfunction.

you've probably had your HDL cholesterol measured. your doctor told you higher is better. 60, 70, 80 — good numbers. here's the problem: HDL cholesterol concentration is a poor proxy for HDL function. HDL's job is reverse cholesterol transport — pulling cholesterol out of peripheral tissues and delivering it to the liver for excretion. That's the cardioprotective mechanism. But a high HDL-C number doesn't tell you whether your HDL is actually functioning. Oxidation to apolipoprotein A-I (apo A-I), HDL's main protein, impairs its ability to interact with cholesterol transporters (ABCA1, ABCG1). Dysfunctional HDL can actually promote atherosclerosis.

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the studies bear this out: raising HDL-C with drugs doesn't reduce cardiovascular events. torcetrapib raised HDL-C significantly and increased mortality. niacin raises HDL-C but adds no cardiovascular benefit. because the number went up but the function didn't. the emerging measurement is cholesterol efflux capacity (CEC) — how well does your HDL actually pull cholesterol out of cells? that predicts cardiovascular risk better than the raw number. The same thing destroying the body: oxidative stress, chronic inflammation, insulin resistance are the same things impairing HDL function if your HDL is 70 but you're metabolically inflamed, your HDL number is meaningless. more useful is you pCEC score (predicted cholesterol efflux capacity)

Your cells have an energy sensor called AMPK. When it's active, you burn fuel efficiently. When it's suppressed, you store fat and your liver pumps out glucose. Uric acid suppresses AMPK. That means elevated uric acid isn't just a byproduct of metabolic disease — it may be driving it. This is why high fructose corn syrup and fructose added into foods are uniquely damaging. Unlike glucose, which is metabolized in a tightly regulated way, fructose is processed by the liver roughly 10x faster, with no feedback controls slowing it down. That rapid metabolism burns through ATP so quickly that the leftover byproducts get converted into uric acid. Worse, the uric acid then amplifies fructokinase — the very enzyme that processes fructose — creating a vicious cycle where each dose sensitizes your liver to the next one. So the chain is: high fructose corn syrup → ATP depletion → uric acid → AMPK suppressed → insulin resistance, fat storage, and excess glucose production. The problem was never the sugar per se. It's the uric acid it leaves behind.

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the hardest thing to do is shatter your own ego

there are countless reports of people not burning at all or very little when cutting seed oils out of their diet. how could this be? my hypothesis: Linoleic acid (the main fatty acid in seed oils) is bacteriostatic and bactericidal (deadly) to small intestinal lactobacillus

Resilience of small intestinal beneficial bacteria to the toxicity of soybean oil fatty acids | eLife

Lactobacillus johnsonii helps stabilize the skin’s resilience to UV damage

JDDonline - Journal of Drugs in Dermatology

Exploring the Gut Microbiome's Role in Drug-Induced Photosensitivity: A Need for Deeper Investigation - JDDonline - Journal of Drugs in Dermatology

INTRODUCTION Drug-induced photosensitivity is an adverse reaction to ultraviolet (UV) radiation triggered by medications like antibiotics, nonstero...

so if disruption of gut flora by excessive pufa and linoleic acid causes a loss of the gut's protective effects on the skin, then seed oils could very well contribute to ease of sunburning

when you think about biology from first principle and you learn that almost 9% of variants are as a result of in silicon processing of base pairs you begin to wonder if our induction of the sub microscopic world is correct

PubMed

Choice of assemblers has a critical impact on de novo assembly of SARS-CoV-2 genome and characterizing variants - PubMed

Our analyses indicate the critical role of assembly methods for assembling SARS-CoV-2 genome using short reads and their impact on variant characte...

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your body needs cholesterol for cellular health and there is an inverse relationship with cancer and low ldl. more cancer incidence with low ldl

Loom

Join Us for the Inaugural Park Forum: The Case for Bitcoin in Healthcare! 🚀

Hey everyone, I'm excited to invite you to our inaugural Park Forum, 'The Case for Bitcoin in Healthcare,' happening on April 8th in Nashville, coi...

The Case for Bitcoin in Healthcare April 8 in Nashville

imagine there was an environmental thing where intermittent exposure increased cancer risk but continuous exposure was not associated (and maybe inversely associated) with cancer risk. what would you conclude? that you should avoid it or spend as much time around it as possible? that thing is sun

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if you have a ton of data, personal or business there is no reason you don't build your own RAG system. it is very very cheap and gives you universal personal search.

feynman on new ideas: you may feel overwhelmed and just want some peace to sit and come up with something wonderful...but there's a better chance that the stress and chaos is what you need for your good idea to take shape best way to get that chaos and questioning everyday is to just have some kids. soon you will have more ideas than you have time.

ketosis is a survival mechanism, it is not a physiologically normal way to live for weeks on end.

The only problem with peer review is the fact almost all studies keep their raw data private --the peer reviewers rarely see the data and when the study is published, the data remains private. there's no need for peer review if every study just publishes raw data -- then anyone can evaluate whenever they want

mortality trends for classic vaccines

Terry Godier

The Last Quiet Thing

Your possessions came alive. Now they won't stop talking.

tools should be predictable and only draw our attention when they are needed.

definitely a classic influencer post but for some people worth a try. removing the social media apps is probabaly the biggest win for most people. no social media, no need for a phone.