Neil Johnson

763 posts

Neil Johnson

@NeilXJohnson

Katılım Ağustos 2023

528 Takip Edilen100 Takipçiler

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Neil Johnson@NeilXJohnson·18 Nis

@jimiuorio @CaryKelly11 Seed oils and the so-called "whole grains" full of rancid grain oils. But don't just go by what I say, here you go! Oil Crop Science journal "Lipid oxidation in food science and nutritional health: A comprehensive review". sciencedirect.com/science/articl…

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Neil Johnson@NeilXJohnson·8h

@LiveAncestral Commercial "whole grains" are a lie. All commercial whole grains have been subjected to 20 minutes of steaming for enzyme inactivation followed by kiln drying for water activity control and deodorization. Devoid of vitamins, the only nutritional claim remaining is "fiber".

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Maxine Pye@LiveAncestral·9h

Everything the guidelines told me to do made me sicker. Eat less saturated fat. Eat more wholegrains. Limit red meat. Choose low fat dairy. Use vegetable oils. Base every meal on starchy carbohydrates. Eat five portions of fruit and vegetables a day. Snack between meals to keep blood sugar stable. Count your calories. Limit eggs. Be afraid of cholesterol. I followed every single one. If you have done everything right and still feel wrong, this is why. 3 years ago I stopped doing all of it. Not because I found willpower or followed a stricter plan. Because I stopped confusing my body with food it was never designed to run on and started giving it what it actually needs. Real animal protein. Real fat. Meals that actually satisfy. When you eat this way your hunger signals work. Your body stops asking for food every two hours because it has what it needs to function. That is not discipline. That is biology. The hardest part was unlearning decades of advice that was wrong.

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Neil Johnson@NeilXJohnson·15h

@chokatsu_life It's the seed oil causing the damage to our digestive system. Refined oils rich in linoleic fatty acid. It's best to stick with animal fat and especially animals not fed corn and soy. Ruminant, wild caught fish, raw coconut fat, plus cocoa butter.

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もちまる@腸活美容@chokatsu_life·1d

これ、実は腸からのSOSです。ウンチが便器にベッタリ張りついて何回流しても落ちないあの現象。水圧の問題でもなく、トイレの寿命でもなく、あなたの掃除不足でもなく。実はそれ、

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Sama Hoole@SamaHoole·2d

The Black Death arrived in England in 1348. Within two years, somewhere between a third and a half of the population was dead. The peasants who survived noticed something within a generation. There was nobody left to work the fields. The labour shortage was so severe that landlords, for the first time in English history, had to bid for workers. The peasants, suddenly possessed of leverage, demanded payment partly in meat. Beef, mutton, and bacon began appearing in the manorial accounts of agricultural labourers' wages. Skeletal records from English burials in the late 1300s and 1400s, set against pre-plague remains, show measurable increases in average adult height. Bone density improves. Dental health improves. Iron-deficiency markers decline. The peasants got taller. The peasants got stronger. The peasants started causing political problems on a scale they had previously been too undernourished to attempt. In 1351 Parliament passed the Statute of Labourers, attempting to cap wages back at pre-plague levels. The peasants noticed. In 1381, well-fed, the same peasants marched on London in the largest popular uprising in medieval English history. The nobility, in the centuries that followed, expanded the Forest Laws. Killing a deer in a royal forest was a capital offence. The Game Laws of the 1600s and 1700s extended the principle. Meat available to the peasant shrank back toward what it had been before the plague. By 1850, the average British army recruit from the industrial slums was so short and so undernourished that the height minimum for enlistment had to be lowered repeatedly to keep the regiments staffed. The single greatest improvement in working-class height and health in English history was caused by a plague that made meat affordable for two generations. The single greatest decline was caused, in significant part, by a political decision to make it expensive again. You can see the whole sequence in the skeletons. The skeletons are in the museums. Go and look.

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Neil Johnson@NeilXJohnson·1d

@chefsevenn Hydrogenated chemically interesterified synthetic fat. Cancer, heart disease, cirrhosis, diabetes and Alzheimer's.

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Chef 👩🏻‍🍳@chefsevenn·1d

What’s your first thought when you see this meal?

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Neil Johnson@NeilXJohnson·1d

@trikomes If genetic, then why isn't diabetes less than 1% like it was in the 1960s? Note the hockey stick inflection in the mid 90s. This lines up with the introduction of MAP packaging. MAP enabled the switch from PHO to high linoleic oils. @ApoDudz @TuckerGoodrich @exfatloss

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Nick Jikomes@trikomes·1d

Likely relocating to St. Petersburg, FL area in the fall.

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Neil Johnson@NeilXJohnson·1d

@Will_of_Europa @PGC1a_RB @exfatloss I'm craving green tea. I'm going to hit up the local tea shop that I've been meaning to visit.

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Will of Europa 🪐@Will_of_Europa·2d

Well well well, how the turntables... @PGC1a_RB @exfatloss What do you know, all the supps the bodybuilder gymbros like also block the polyol pathway

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Mark Kaplan@markkaplan20·4d

@NeilXJohnson Your cardiologist gave up on you. Full of morphine in the ER. No medical intervention remaining. And you healed yourself by addressing insulin resistance. TG 51 and A1C 5.3 are proof that it worked. Your story is not an anecdote. It is evidence. Thank you for sharing it.

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Neil Johnson@NeilXJohnson·2d

@CaryKelly11 Acid reflux fully resolved when I eliminated all refined oils and industrial processed grains from the diet. I still consume grains, I start with live viable grain berries. The grains first tempered (germinated) then milled to flour or flakes.

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Cary Kelly@CaryKelly11·2d

A cousin who had been a nurse for almost 40 years assured me that my acid reflux was because I had a weakened esophageal sphincter and that fatty and spicy foods were triggering my episodes. I believed her. One of my favorite dishes was a spicy shrimp diavolo and I was almost guaranteed to get reflux in the middle of the night after eating it. Little did I know that it wasn't the spice and the fat in the dish. It was the pasta fermenting in my gut. It's well documented. It's called SIBO (Small Intestinal Bacterial Overgrowth). It's when excessive bacteria in the small intestine ferment undigested carbohydrates. This produces gases such as: Hydrogen Methane Hydrogen sulfide That leads to bloating, heartburn and reflux. I was fortunate to accidentally "cure" my acid reflux by going low carb but I never understood the mechanisms until many years later. I just knew that after I quit eating pasta and pancakes, no more reflux. Anyway, I found a science backed article that validates everything I believed and experienced and I'm waiting for the right time to share it with my nurse cousin. Or should I not bother?

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Neil Johnson@NeilXJohnson·3d

@iluminatibot @SamaHoole

QAM

illuminatibot@iluminatibot·4d

Bill Gates' lab-made butter is expected to reach supermarket shelves by 2027. "It looks, smells, and tastes like the butter we're all familiar with, but without the farmland, fertilisers, or emissions." Bill Gates: "The idea of switching to lab-made fats and oils may seem strange at first, but their potential to significantly reduce our carbon footprint is immense." "This is really about how we feed our species and heal our planet at the same time." No Bill, this is really about phasing out agriculture and seizing control of the global food supply, as a way of controlling the global population.

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Nick Norwitz MD PhD@nicknorwitz·4d

Is living with high ApoB is like Smoking? 🚭 I constantly hear the analogy that living with untreated high ApoB is like smoking. The logic goes something like this: “ApoB is causal for cardiovascular disease. Smoking is causal for lung cancer. Not all smokers get lung cancer, but it’s still obviously dumb to smoke because we know smoking causes lung cancer.” And if you force the analogy hard enough, I suppose it sounds superficially reasonable. But in reality, it’s deeply flawed for at least two major reasons. First: risk-benefit. The biological risks of not smoking are essentially nonexistent. The biological risks of taking a pharmaceutical, particularly a statin, to lower ApoB are not nonexistent. Beyond muscle symptoms, there are concerns around insulin resistance, increased diabetes risk, GLP-1 suppression, mitochondrial damage, and broader long-term tradeoffs that are still incompletely understood. So the comparison immediately breaks down because the interventions themselves are not biologically equivalent. Second cancer is a binary event. You either have cancer or you don’t. Atherosclerosis is not binary. It exists on a continuum. So in my case, for example, it’s not merely that I haven’t had a heart attack. I have 0 mm3 of plaque despite exposure to an LDL 500-600 for the better part of a decade. Not calcified plaque. Not soft plaque. Nothing measurable. If the disease process exists on a measurable biological continuum, and you have no measurable evidence of disease whatsoever, that is not analogous to “a smoker who simply hasn’t gotten cancer yet.” It is direct biological evidence that whatever risk variable you are focusing on, whether causal or not. is not manifesting as disease in that organism at that point in time. So please, for the love of nuanced thinking, stop pretending that living with elevated LDL or ApoB is straightforwardly equivalent to smoking cigarettes.

Nick Norwitz MD PhD@nicknorwitz

🚨New Paper: "Seven Years of 700 Cholesterol Without Coronary Atherosclerosis: A Lean Mass Hyper-Responder Case Report" Link: doi.org/10.3390/diseas… For the past 7 years, I’ve been running what is essentially a natural experiment in cholesterol and heart health. During that time, I’ve largely lived with: 👉Total cholesterol around 700 mg/dl 👉LDL cholesterol between 500–600 mg/dL I recently underwent advanced coronary CT angiography imaging with AI-guided analysis. This is not a CAC. It measures all plaque (soft + calcified), with expert interpretation and AI-guided analysis capable of quantifying plaque down to the cubic millimeter (mm3). Now, to address the obvious question: Am I too young for plaque? In brief: No. The clearest comparison is individuals with homozygous familial hypercholesterolemia, who often have similarly extreme LDL/ApoB levels and can develop advanced plaque as toddlers, and even heart attacks as early as age 8. Also, nutrition influencers in their 30s have publicly shared quantified plaque scores from these same imaging technologies. In one recent case, a plant-based influencer in his thirties was found to have 61.3 mm³ of plaque despite having far lower lifetime LDL exposure. (He can identify himself if he so chooses.) My case also isn’t a one-off. There are many individuals like me, including older individuals with similar LDL-C and ApoB without any plaque. The difference is that I’m an unusually well-characterized subject, with extensive metabolic data and health markers tracked over time. You can learn more at the newsletter or open-access paper, linked above. The science of heart health is not settled. And cholesterol is not a simple story. 🚨 If you want to help spread the word... Quote Tweet this post (or create an original post) including the article link with a thought. Academic papers are increasingly evaluated using attention metrics. Original posts from unique users are one way to increase these metrics and help ultimately increase its reach. 🚨 If you want to learn more, I'll include more learning resources below 👇

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exfatloss🥛@exfatloss·3d

Seed oils did 'ronavirus, news at 11. Wild actually: my own EPA:AA ratio fluctuates but averages 0.049, which would (almost?) put me in the BEST group? Known long-term PUFA avoiders average 0.13, or more than 2x off the charts in this study.

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Mark Kaplan@markkaplan20·4d

My statin thread hit over 400k + views yesterday. Thousands of you asked the same question. “What about Repatha?” Here is the answer. It is a bomb shell. You better sit down. I remember sitting on my bathroom floor with a needle in my hand. My cardiologist told me Lipitor was the answer. 80mg. Within months I started losing my memory. Words disappeared mid-sentence. I could not remember my daughter's phone number. He switched me to Crestor. Same thing. Then he told me the future had arrived. A new drug called Repatha. A PCSK9 inhibitor. $14,000 a year. An injection I had to give myself every two weeks. I sat on the cold tile of my bathroom floor, pushed a needle into my own stomach, and injected a foreign substance into my body because a doctor told me a number on a lab report was going to kill me. That was the lowest point of my life. What I did not know yet is what the data actually said about the drug I was injecting. 🧵

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Neil Johnson@NeilXJohnson·4d

@markkaplan20 My story is pretty much exactly the same as yours. I'm now fully healed having tackled, insulin resistance. TRIG=51 A1C=5.3. Four years ago my cardiologist gave up on me while I was pumped full of morphine in the ER. No medical intervention remaining. Heart was dying.

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Mark Kaplan@markkaplan20·4d

I am not telling anyone to stop their medication. I am telling you to ask your doctor one question. "What is my fasting insulin?" If they do not know, or will not test it, you have your answer about whether they are looking for the root cause or just managing a number on a lab report. The truth heals Co-founders of HealthTruth: Dr. Philip Ovadia, Cardiac Surgeon @ifixhearts Dr. Aseem Malhotra, Cardiologist @DrAseemMalhotra Dr. Robert Cywes, Metabolic Surgeon @carbaddictiondr Prof. Tim Noakes @ProfTimNoakes With thanks to @bigfatsurprise @BillAckman @drjasonfung @LDLSkeptic Mark Kaplan Founder, HealthTruth

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Neil Johnson@NeilXJohnson·4d

@ApoDudz Thank you so much. Using Grok with the context of this post I uploaded my CBC W/AUTOMATED DIFF PERFORMABLE lab results. Grok calculated the NLR=1.51. "Excellent".

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Austin Dudzinski, PharmD, BCACP@ApoDudz·4d

“…the objective of this study was to examine the association between NLR and cardiovascular and all-cause mortality among CAD patients with LDL-C less than 1.4 mmol/L in a real-world clinical cohort.” 1.4mmol/l = 55mg/dl

Austin Dudzinski, PharmD, BCACP tweet media

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Sama Hoole@SamaHoole·6d

A small ethical disclosure on the production of this physique. - No field mice sliced in half by combine harvesters. - No skylark nests flushed out and minced by threshers. - No rabbits poisoned by pesticide drift. - No hedgehogs displaced from ripped-out hedgerows. - No bees sterilised by neonicotinoids. - No earthworms churned into paste by deep tillage. - No bats killed by the wind turbines powering the indoor farm. - No deer shot by the gamekeeper protecting the arable field. Two cows a year. Lived outside. Ate the grass that was already growing, under the rain that was already falling. The fact that I'm more vegan than vegans has made a lot of people very angry.

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Neil Johnson@NeilXJohnson·4d

@TuckerGoodrich I've seen it. You check the reference and it says the exact opposite of the claim in the paper.

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Tucker Goodrich@TuckerGoodrich·5d

This is why science has a credibility problem. And no, laziness and sloppiness is not “how science works”.

Lenka Zdeborova@zdeborova

@jimduey @eiszett You absolutely should not trust anyone’s work … that is how science works! You always doubt and look for inconsistencies. Only when many people independently reproduce and extend a concept then it can become accepted.

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Bret Scher, MD@bschermd·5d

A major new trial just showed that dramatically lowering triglycerides didn't reduce heart artery plaque compared to placebo. Does that mean triglycerides (TGs) don't matter for heart disease? Absolutely not, but it does reveal a flaw in how we're thinking about treatment. Here's why. 👇

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Neil Johnson@NeilXJohnson·5d

@TuckerGoodrich @nullbotto @Outdoctrination @mkendrick @malcolmken Would an occasional low dose of mixed tocopherols (100IU) make sense in combination with daily high dose vitamin C?

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Tucker Goodrich@TuckerGoodrich·6d

Yeah, it's interesting, but wrong. He entirely misses the key ingredient. Vitamin E prevents lipid peroxidation, which is a key player in all three conditions he mentions. But E blocks lipid peroxidation by sacrificing itself. When it does so, it becomes a prooxidant itself. Vitamin C resets E so it can continue to protect fats. Lipid peroxidation causes the endothelial damage he talks about.

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Dalton (Analyze & Optimize)@Outdoctrination·6d

Vitamin C shrinks arterial plaques in clinical trial. The picture below shows improvements in under 4 months. 500 mg 3 times daily in people with heart disease - 6/10 people had reduced plaques, while none in control did. Vitamin C has several cardioprotective effects: ➞ Antioxidant ➞ Anti-inflammatory ➞ Collagen supporting ➞ Cholesterol lowering 1954. The old forgotten studies often have the best gems.

Dalton (Analyze & Optimize)@Outdoctrination

An incredible study showed major reductions in arterial plaques simply by shining a form of red light onto the body, more so than even statins. (🧵1/7)

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Neil Johnson@NeilXJohnson·5d

@FoodPleaser I wouldn't eat calamari coated with oxidized hydrogenated chemically inter-esterified seed oils. Otherwise, sure I would eat calamari.