undeather

Hey guys, Few days ago, Robert Lawrence Kuhn (known from: Closer to truth) released a paper which explores all the diverse theories of consciousness and aims to categorize these explanations to understand their broader implications. The paper addresses various perspectives on consciousness, including physicalist, non-physicalist, materialist, quantum, and neurobiological viewpoints. Even though I have a very particular view of conciousness, which was mainly influenced by personal experiences, this is a god-tier piece of literature which gives you a great overview of all the different options on the table. I really enjoyed reading it and I think many of you will feel the same. https://www.sciencedirect.com/science/article/pii/S0079610723001128 https://doi.org/10.1016/j.pbiomolbio.2023.12.003 Enjoy

Check out the youtube-channel of my cherished friend Anoop Kumar, MD. He has his own, conciousness first, framework of what constitutes "healing" and interviews those who apparently cured their chronic and sometimes fatal conditions: Also, check out his interview with Jeff Redeiger, author of the book "CURED".

Why has it been only fear mongering without context from your side lately? Every drug or medical intervention is associated with a whole array of potential side effects - this includes mainstream pharmaceuticals, plant-based "natural" alternatives, as well as acupuncture, chiropractic/osteopathic practices & even homeopathy. Everyone knows that. Going back to "no drugs" is of course inconceivable at this point, since we don't want grandma to drop dead at 60 from a simple pneunomia. The job of good scientific medicine is to approximate risks with benefits. In general, we do a pretty decent job at this - most side effects in commonly used drugs are reversible and subside after stopping treatment. Of course, we don't have a perfect system - so due to the complexity of the human biology, we will always find extreme cases where one treatment leads to life-destroying consquences. That's the game we play and it kinda sucks - but the alternative is way worse. Now, most doctors are of course aware of the unfavorable side effect profile in ciprofloxacin. It's one of the first things you learn about antibiotic drugs in medschool. That's why we don't use it as first line-therapy anymore. Not using ciprofloxacin has been good medical practice since at least 10 years now - and the FDA has even warned about the side effects since the early 2000s. You rarely see this drug anymore, because there are just safer alternatives - the reason we still need it is because if other antibiotics won't work (due to resistance for example) and the patients life is at risk, you always have it as a backup (second/thrid line) option. Of course you will always find a doctors who uses the drug as first line regardless, but that's not because of evdience based medicine, but because they are shitty physicians. So your assertions are wrong. Science has told us about the side effects for a very long time - and we based our decisions to turn away from ciprofloxacin on said scientific data. There are so many good arguments to be had about science being too slow to adapt or financial incentives playing a big role in this game - and I would gadly agree with those. But how about we consider the often complex & nuanced nature of such dynamics instead of falling in those boring "medicine bad"-narratives?

The conversion-rate of ALA to DHA/EPA is highly individual and influenced by a truckload of factors (such as genetic polymorphisms, Omega-6-consumption (esp. lineloic acid), sex, certain diseases, fluctiations in hormone levels (estrogen)..etc.). In general, it's pretty low. I am not aware that there are any strong correlations between ALA and arrythmias - most studies looking into that connection are focused on fish-oil supplements, which are high in EPA/DHA. That said, 50g flaxseed is quite a lot - and this will most likely significantly increase your conversion - as shown in this study. I personally would not worry too much tbh - if you are not supplementing with fish oil as well, then your body will adapt and take what it needs. If you are worried, you can get a omega-3 profile, which will give you a decent approximation.

Would you mind sharing your results please? Did they use "Inductively Coupled Plasma Mass Spectrometry" (ICP-MS) as a measurement-technique? Did you grow up or do you currently live in a war zone? Uranium oxide aerosols from so called "depleted uranium kinetic penetrators" can enter the body through inhalation or through depletion in food products (even though only tiny amounts get absorbed through the GI-tract) There aren't any well developed chelation protocols for uranium (as far is I know) - however, we have many animal studies looking at various potential chelators. DISCLAIMER: This is not medical advice and I do not recommend any of these. Sodium Citrate: Early dog-studies in the 1940s indicate that sodium citrate, administered either intravenously (230 mg/kg) or orally (1.15 g/kg), offer significant protection against uranium poisoning. It enhanced survival rates and mitigated renal damage in animal studies. It might not have a very strong chelation effect, but could counteract some of the negative effects supranormal concentrations might have on your organs. The acid can form stable complexes with uranium and promote excretion. Standard Compounds Tiron and Gallic Acid: Effective in increasing uranium excretion and reducing tissue uranium concentrations when administered shortly after uranium exposure. EDTA: Increases urinary excretion of uranyl ions but is less effective in mobilizing uranium bound to bone. DTPA: Standard chelating agent, though its efficacy is limited for uranium compared to other metals. 5-Aminosalicylic Acid and Ethylene Glycol Tetraacetic Acid (EGTA): Show promise in increasing survival rates and promoting uranium excretion. Newer Compounds: Hydroxypyridonate Compounds: Compounds like 3,4,3-LI(1,2-HOPO) and 5-LIO(Me-3,2-HOPO) show potential for broad-spectrum actinide chelation, demonstrating significant uranium excretion in animal studies. Bisphosphonates: Compounds such as HEDP and other bisphosphonate derivatives have been effective in rerouting uranium from kidneys and bones to the liver, enhancing excretion. My personal recommendations: Don't self-medicate with chelation compounds - only do thos under adequate supervision and with someone who know what they are doing. If you put in some work, you propably will find someone who can help you. First of all, definitely re-do your heavy metal test in the near future. It should use the best avaialble measurement protocol, which is ICP-MS. Until then, I would recommend increasing the levels of citric acid in your food. Also, avoid high amounts of sucrose & fructose (especially added variants) - since there is evidence that those substance might exacerbate the damaging effects of uranium. THis does not mean you should stop eating healthy fruits. Just be more concious about those ingredients and go easy on them. Here is a list of foods high in citric acid: I hope this helps

There is a wide variety of plastic free gum available.

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If you buy a fish oil/algae supplement, look for providers who regularly test the TOTOX-value ("total oxidation") of their products. A fascinating argument I tend to believe is that Omega-3 supplemetns show inconsistent study-results regarding their cardiovascular benefit because they usually don't/or half hazardly control for total-oxidation status. That might counteract some of the potential benefits.

If you stop the medication, your baseline feeling of satiety will return. So if you keep eating those small food-portions, you will experience severe sensations of hunger - and most people won't bare that for long. There are is small subset of patients who seem to keep the weight off, even after stopping the drug. But this usually always coincides with extreme lifestyle-changes. I wouldn't bet on it. Losing weight on Ozempic is different than using weight with changing someones diet-pattern & exercise.

I have seen multiple patients on Ozempic and the results are pretty insane. People who have struggled with their weight for years are suddenly able to lose weight and actually keep it off. Most side effects are mild - from my experinve, mostly slight stomach issues like nausea. Multiple studies have shown a very benign side effect profiles as well. That said, it's a pharmaceutical drug you need to keep talking for results. I think most people working in the medical field would agree that there is a certain group of patients who, for complex biopsychosocial reasons, are just not able to lose weight - and for that group, such drug is literally a miracle-cure. That said, nothing will ever beat the benefits of a persistent lifestyle change - meaning losing weight through diet & exercise. This should always be the #1 goal for every obese patient. However, it's always nice to know that you have the wonder-drug in the background.

Omega 3 from algae is the best way - Fish contain Omega-3 because they eat microalgae and plancton. That said, please don't overconsume Omega-3s - there is more and more evidence that large amounts of omega 3 might actually be pro-arrythmogenic. If you regularly eat fish-products, I would stay under 1,5mg (EPA/DHA)/day

If I had to bet, I would put my money on Bryan developing some sort of aggressively-growing, highly oncogenic form of cancer in the next, let's say 20 years. I would not wish that on him of course - but if you go by complex system principles, then this whole game is doomed to failure at some point. But let's see, maybe I am wrong!

If your symptoms emerge only 20-30 minutes after ingestion, then it has propably nothing to do with fiber, microbiome or caloric intake. My best guess from what I have read so far is propably some sort of intolerance/ IgE-mediated food hypersensitivity. Sometimes this will resolve itself once you cut out the affecetd foodgroups for a longer period of time and then reintroduce them slowly.

How about chickpeas, peas or beans? Same issue or nothing?

How quick? For how long? Does it gradually get worse until a certain point or is it more acute? Is it reproduceable? Do you take any supplements? Do you notice that with any other foods? Have you noticed this in the past?

Fallostatin blocks the effect of "myostatin" - a protein which is an important modulator of muscle-growth in the body. Meaning that you basically let go of one major hypertrophy-breaks, leading to increased muscle-growth in the process. There are actually people who have a (loss of function)-.mutation in these myostatin decoding genes, which lowers their total levels, and they come out as extraordinarily muscular in the process: Those children, as far as I know, do not suffer from any obvious side effect trade-offs. There are hints however, that it might effect the heart in later stages of life. I don't know what to think about this therapy yet - seems like a risky thing to play with such an important regulator - I would defeinitely not recommend it because I dont see the reward for a potentially life changing risk. But let's stay open minded!

It's interesting, but I would be very catious in taking those aspergeresque bay-area-prophecies at face value. If we have learned anything from past predictions, things will usually turn out unpredictably different. I think Hossenfelder made a good video about his claims:

Dave is good at debunking antiscientific nonsense in certain areas - but he does so in his typical arrogant, lecturing and "anyone who disagrees is an idiot"-type attitude. This is particularly painful when he speaks about topics he doesnt really have a deep understanding of - his episode on conciousness is pure cringe. His ideas about religion are just rehearsed New Atheist 101-talking points, which isn't really based on science. He is the most stage orange man on earth.

I feel exactly the same

The book seems to be more an indroductory/overview of Wilber's work - with a pragmatic twist and a focus on practices. If you are already familiar with his concepts, then you will encounter a lot of repetition. That said, I enjoy the audiobook - will keep it and recommend to friends who are not familiar with integral theory.

That's your addiction speaking. Look how you are desperately trying to look for reasons to keep that behaviour alive. Every smoker loves the sensations tabacco gives them, that's why they do it. I work at a Gastrointestinal-clinic, which also includes liver-patients - most of them due to alcohol. While the poison is a different one, the excuses are the same. "What if I just drink at parties?" - "But I like the easiness alcohol gives me in social situations" - "It helps with bearing life" ... I think the right way for you is to stop completely and look for healthier mechanisms to deal with said mental issues. Your future self will thank you for it.

Jason, we already had a lengthy exchange about this topic like 6 months ago - so I will keep it short! 1) The reason the LDL-C targets are constantly lowered is because of the mounting evidence that lower is better. Trial after trial show additional benefits of more aggressive lipid lowering - the feared J-curve or U-curve effect just does not appear. Blood pressure recommendations show a similar pattern, which also makes sense. 2) Smoking, diabetes and hypertension are 3 huge risk factors of atherosclerosis - mainly because of their propensity to cause endothelial activation. Chemical modification (aka oxidation or glycolisation) of lipoproteins is an important part of atherogenesis and especially smoking strongly increases the proportion of ox-LDL - which makes them enter the arterial even easier. There are multiple risks factors that can modify ASCVD-risk through various mechanisms. Of course there are! But one thing that still stands above all of them - if you take away the ApoB-particles - even in presence of smoking or diabetes - then plaque burden reduces DRASTICALLY! - Far more than what quitting the cigarettes would have done on it's own. People with lifelong low ApoB (through genetic mutations) just don't develop the same quantity/quality of atheroclerosis, even in context of other risk factors like diabetes, smoking, hypertension etc. This has been shown again and agian in mendellian randomization studies. Of course, the aim for me as a doctor is to improve all risk factors - first through lifestyle intervention whenever possible - but lipids are just such a major player in this whole game. Observations just fit the model perfectly. 3) I don't know if feeding someone ox-Cholesterol would do something - especially because much of the dietary cholesterol doesn't really get absorbed - not sure how the NPC1L1-transporter in the intestines would deal with ox-Cholesterol. But I get your hypothetical: Of course, if you would increase ox-LDL in the blood, then yeah, you would see an increased tendency of those particles to enter the arterial wall - which would likely end up with more atherogenesis. I am not saying oxidation is not important! If you want to reduce the general oxidative bruden (through diet, movement, stress reduction...)- then Iam with you. But the problem with that hypothesis (the true culprit being oxidation) is that histopathological/biochemical observations (mechanisms of plaque build-up/oxidation happening mainly in the arterial wall), mendellian randomziation data, and many, many intervention trials (increasing antioxidative potentials) just don't show the effect sizes if said hypothesis was true. On the other side we have a SHITTON of evidence - propably one of the most studied areas in the field of medical sciences - that reducing Apo-B particles is causally correlated with a highly reduced ASCVD-risk. 4) Net plaque deposition occurs when the rate of build up exceeds that of removal! Yes! Yes, hypotheically, if we had zero ApoB in our system - atherosclerosis propably wouldn't occur. Without ApoB- there wouldn't be any lipoproteins left, except HDL. Supraphysiolgoical, meaning "more than our body can handle". Our lipid-profile is, to a large degree, genetically determined - someone with a very, very bad lifestyle can improve their Apo-B around 30-40% (on average). Yet if everyone would live a healthy lifestyle, we would still see Apo-B concentrations above the atherogenic-threshhold. Antagonistic pleitropy (in the evolutionary sense) can explain this pretty well imo. Anyway, I will be on vacation for the next week - so not gonna respond any further! Cheers

It's not really "my" position - it's what 170 years of atherosclerosis research and discoveries have led us to conclude about humanities biggest killer, cardiovascular diseases. The lipid model of atherosclerosis fits like a glove onto a wide array of observations. Our understanding is, as almost anything in science, incomplete - but the basics are incredibly consistent with reality. Yes, Apo-B particle number is the best predictor of plaque progression on a population level. For individuals, we look at a complex spectrum of pathophysiological circumstences - meaning that for some people, ApoB is less of a concern than it is for others. 2 patients with the exact same ApoB exposure can develop different degrees of atherosclerosis - one might have a different phenotype for a specific receptor that allows the ApoB to get into the arterial wall even easier, while the other has an inherited enzyme defficiency which leads to lower rates of oxidation. There are thousands of controlling elements, and also other risk factors that would go into that equation. But one thing they all have in common - if you lower ApoB-particles with drugs, lifestyle, genetic mutations (like PCSK9-mutations) or even apheresis, people slow down - stop - or even reverse some of their atherosclerotic progression. This is ultra consistent across various models and also works the other way around (like in people with familial hypercholesterolemia or a progression of plaque when drugs are stopped) No, the oxidation of Apo-B is not inevitable - many factors influence the rate of oxidation. The problem is that most antioxidants mainly deal with oxidative processes in the lumen but not necessarily in the arterial wall. This is a bit of a grey area and more reserach needs to be done - but so far, levels of antioxidants don't correlate with plaque reversal to the degree they should if there was something to the oxidation hypothesis. We know that Reverse Cholesterol Transport happens in every human - HDL particles are able to fish cholesterol particles out of the lesions -however, this is only possible in earlier stages of atherosclerosis. That's why, in general, higher HDL particle numbers are associated with lower cardiovascular risk. No, atherogenesis is not unidirectional - there is a constant build up and removal. But the body can't really keep up with all the supraphysiological levels of Apo-B particles that are present in our blood streams. Once LDL-C (which is a great proxy for ApoB) goes below 70mg/dL (maybe even below 55mg/dL) - we kinda observe a equilibrium where atherosclorosis just doesn't happen in it's usual magnitude.

All ApoB-containing lipoproteins <70 nm in diameter can cross the endothelial barrier, especially in the presence of endothelial dysfunction. In the early stages of atherosclerosis, negatively charged proteoglycans (structural components ) in the arterial wall trap apoB-lipoproteins. This happens because of electrostatic interactions with specific positively charged amino acid residues on the ApoB-proteins. After that happens, the process of atherosclerosis continues as usual! The trapped lipoproteins will go through oxidiation which creates a inflammatory response, macrophages will enter the arterial wall and start sucking up that delicious cholesterol (which came in through the lipoproteins). Since those macrophages are hungry little scamps and can't stop eating, they will turn into foam cells. This is when you can macroscopicly observe so called "fatty streaks" in the artery. From then on, the plaque continues to grow through various mechanisms until it ruptures and creates in infarct. Voilà - that's how plaque formation works!