jery_coholic

322 posts

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jery_coholic

jery_coholic

@jerycoholic

Katılım Şubat 2017
313 Takip Edilen19 Takipçiler
Sassy
Sassy@SassyXtr·
... Gun to your head name a Portuguese that played for Arsenal. Level: you are dead💀
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Sassy
Sassy@SassyXtr·
... William Saliba and Thierry Henry aside name a French International that played for Arsenal. Level: Impossible
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jery_coholic
jery_coholic@jerycoholic·
@Turbinetraveler What's the logic of a commercial airliner reaching an altitude where the passengers need to be put on masks?
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Turbine Traveller
Turbine Traveller@Turbinetraveler·
The Boeing 747-400 is the only heavy widebody aircraft that can get up to 45,000 feet. No other aircraft can fly that high weighing this much, not even the newer 747-8 version. Airbus A380, Boeing 787 and B777 max out around 43100ft. Video via Captain Leonardo Silver
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Awojinrin
Awojinrin@XAwojinrin·
@anishmoonka You had me enthralled right up till your last two sentences. Now I have to block you😭
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Anish Moonka
Anish Moonka@anishmoonka·
About a quarter of the ocean's surface is a desert. Hundreds of miles of open water with almost no food in it. So when a big ship crosses one of these empty stretches, it becomes the only interesting thing for miles, and fish start trailing along behind it. Biologists have studied this for decades. Any floating object out there, a log, a clump of seaweed, a drifting coconut, a stray piece of trash, a whole ship, ends up working like a magnet for fish. To something living in all that emptiness, anything floating might mean food, or a place to hide. The effect is so dependable that a big share of the world's tuna fishing is built on it. Boats drop rafts in the open sea, sail away, and come back later to find fish gathered underneath. It builds in stages. A few small fish turn up first, sometimes within hours. Those small fish draw in bigger ones, and before long a whole moving crowd is traveling along under the ship. Sailors noticed this ages ago. In the 1840s a young naturalist fresh out of Yale wrote about little fish that lived for days right beneath a slow ship, and Melville put the same scene in Moby-Dick, a school of fish that drops one ship to follow the next one passing by. So by the time someone leans over the railing with a scrap of food, there's already a hungry audience waiting below. It has been tagging along for who knows how long, maybe days. The corn itself barely matters. Out in open water, fish aren't fussy eaters, grabbing whatever they happen to bump into, so the splash just tells them where to aim. A piece of bread or a chunk of corn gets the same result. The ship had already gathered the crowd. The food only told them where to go.
SİYAH SANCAK@siyahsancakx

⚪️ Büyük yük gemisinde çalışan kişi, denizdeki tehlikeyi suya attığı mısır parçasıyla gösterdi;

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Abu Zeenah
Abu Zeenah@AbuZeenah_·
Guess The National Team ? Level ___100% Impossible
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DSZN8𓀀
DSZN8𓀀@Neduszn8·
Guess the national team? LEVEL: VERY DIFFICULT 🤯
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Il talento di mr Stiglitz🎗️🚁🛴🚚🚚🚚
Sulla vicenda #Maldive, consiglio il docufilm Diving into the Unknown (2016). La storia vera di quanto accadde in una grotta norvegese e del team che si immerse per recuperare i corpi dei loro compagni. Fra loro, Sami Paakkarinen, oggi impegnato a Vaavu. Storia pazzesca.
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Deadly Kalesh
Deadly Kalesh@Deadlykalesh·
📍Kollam, Kerala: A major tragedy was reportedly averted near Chittar after a speeding bus travelling from Madathara to Anchal lost control and overturned when its front tyre allegedly detached mid-journey. Several passengers sustained minor injuries, but no fatalities were reported.
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Chauhan
Chauhan@Platypuss_10·
INDIA 1 | K7076 Smooth touchdown at Amsterdam, Netherlands- AMS yesterday PM Modi was Abroad.
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jyahagi
jyahagi@jyahagi140273·
@Platypuss_10 Is Airbus A380 about the same size as air force one?
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Chauhan
Chauhan@Platypuss_10·
Here’s the size difference between the highest-selling commercial aircraft in history, the Boeing 737, and the Airbus A380 “Superjumbo” — the world’s largest passenger airliner.
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Fairy Gothmother, MD
Fairy Gothmother, MD@jenny2x4·
I already thought Elon’s mom constantly defending him on twitter was embarrassing. I didn’t even consider that Elon was the one tweeting as his own mom and defending himself, which is maybe the most embarrassing thing I’ve ever seen
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Gil Carvalho MD PhD🌈🇵🇸
Gil Carvalho MD PhD🌈🇵🇸@NutritionMadeS3·
Reminder that Canola oil and steel cut oats are health-promoting foods with data consistently showing benefit, impossible to find compelling scientific evidence of harm in humans consuming them Receipts below Happy Wednesday!!!
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jery_coholic
jery_coholic@jerycoholic·
@Drlipid also important to ask the question of what component of the Phospholipid in the lipoprotein molecule is more prone to oxidation? The answer obviously is the PUFA's attached to the glycerol backbone of the Phospholipids/Triglycerides
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jery_coholic
jery_coholic@jerycoholic·
@Tellit007 Once apo B lipoproteins cross the endothelium, which component of the lipoprotein particle is more prone to get oxidised? Its the PUFA's contained in their Triglyceride moeities. But of course you have a bunch of RCTs claiming PUFA's are healthy, don't you?
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Tellit Likeitis
Tellit Likeitis@Tellit007·
Insulin resistance and inflammation are downstream of ApoB retention, not upstream of it. ApoB particles cross the endothelium, get retained, oxidize, and trigger the inflammatory cascade. CANTOS tested the inflammation hypothesis directly: 10,061 patients, CRP halved, 15% MACE reduction, no all-cause mortality benefit. Then there is PESA: atherosclerosis develops above approximately 50 mg/dL LDL-C even when insulin resistance, blood pressure, blood sugar, and inflammation are all optimized. Per 10 mg/dL LDL-C increase: 18% higher atherosclerosis probability. PCSK9 loss-of-function carriers have lifelong low ApoB and 88% fewer coronary events regardless of metabolic state. The lifestyle variable is ApoB. Not the metabolic markers surrounding it. Insulin resistance is a genuine metabolic driver. Lifestyle can reduce it. Chronic inflammation is associated with cardiovascular outcomes. A NYT bestselling author who unlearned everything should ask why the intervention that targets the upstream variable outperforms the one that targets the downstream signal. @DrMarthaGulati has spent her career on exactly this question: which variable to treat first when they diverge. Isn't it ironic.
Robert Lufkin MD@robertlufkinmd

Insulin resistance/inflammation are the great challenges to our health in the 21st century. They are the main drivers for nearly all chronic diseases and determine longevity itself. Fortunately lifestyle choices can dramatically reduce both of them.

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Tellit Likeitis
Tellit Likeitis@Tellit007·
And the Grifter of the Year Award goes to.... @ifixhearts!!! @DoctorTro Close second, better luck next year! What got @ifixhearts over the finish line? Promote the diet. Sell the meat. Skip the outcomes trial. Let the operating room catch what the panel missed. He gets paid either way. @ifixhearts is a cardiac surgeon who wrote a book called Stay Off My Operating Table. His telemedicine practice and his meat brand both depend on high saturated fat diets looking metabolically clean. TG:HDL does that. ApoB often does not. So TG:HDL is in this post. ApoB is not. That brand requires a world where the right markers are TG:HDL, insulin, and fasting glucose. Where ApoB is not the conversation. Because ApoB is where the diet's cost shows up. A patient with a perfect TG:HDL ratio and elevated ApoB is accumulating soft plaque on a protocol that is improving every surrogate his practice tracks. If that patient ends up on his operating table, he collects the surgery fee too. Winning! @drpablocorral on what Stay Off My Operating Table does not mention: TG:HDL estimates the shadow. ApoB measures the object. The replies here are patients sharing their ratios and asking if they are safe. One mentions being in a battle with their doctor over LDL-C. A cardiac surgeon just handed them a surrogate to "win" that argument while the causal particle stays off the panel. Precious.
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Tellit Likeitis
Tellit Likeitis@Tellit007·
You listed six "controversies" in metabolic health. The PCSK9 loss-of-function natural experiment was not one of them. Carriers have lower ApoB from birth, the metabolic markers you cite as protective, and 88% fewer coronary events. That answers Controversy #1 without an additional trial. What answer were you looking for?
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Bret Scher, MD
Bret Scher, MD@bschermd·
In metabolic health, the most dangerous words a clinician can say are 'the science is settled.' Here are six debates that are very much not settled, and that affect every patient I see. 🧵
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jery_coholic
jery_coholic@jerycoholic·
@drterrysimpson You were caught using AI when you literally posted some Arabic words that your AI vomited
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Dr Terry Simpson
Dr Terry Simpson@drterrysimpson·
This is what happens when you let Sama go on and on and ask if he actually read the studies - he didn't. So - lets go through - again, point by point This is the oldest zombie in nutrition discourse. The 1953 graph by Ancel Keys was not a final analysis—it was an early, exploratory presentation. It was preliminary data. More importantly: the full dataset wasn’t even complete or comparable across countries at that time. Mortality data quality varied wildly. When better data became available, Keys didn’t hide—he expanded. And country data is not what you look at - you look at cohorts which brings us to: 2) The Seven Countries Study This wasn’t “cherry-picking.” It was one of the first large, prospective cohort studies in cardiovascular epidemiology. Standardized data collection across countries Measured diet, serum cholesterol, and outcomes longitudinally Showed a graded relationship between saturated fat → LDL → heart disease That relationship has since been reproduced in: Metabolic ward studies Randomized dietary trials Genetic studies (Mendelian randomization) Drug trials lowering LDL This is convergence—not conspiracy. These were not "selected" everyone was invited but seven countries supplied funding for their studies. 3) The “France eats butter and doesn’t die” trope This is the so-called “French paradox.” Reality: Lower smoking-adjusted comparisons change the picture Different portion sizes, meal patterns, and overall diet quality Higher intake of vegetables, legumes, and less ultra-processed food Cherry-picking populations to disprove cherry-picking is… a choice. Finally, this happened 30 years after Keys - not with Keys. And there are seven gastronoical regions of France, including a Med diet region. 4) John Yudkin and sugar Yudkin wasn’t “silenced truth”—he was partly right, partly wrong, like most scientists. Yes, excess sugar is harmful No, that doesn’t invalidate the role of saturated fat and LDL in atherosclerosis Modern consensus: Both refined carbs and atherogenic lipoproteins matter. Science moved forward. It didn’t pick a team. 5) The Procter & Gamble conspiracy Yes, Procter & Gamble donated to the AHA. No, that doesn’t explain: Independent replication across countries Clinical trials lowering LDL and reducing events Genetic disorders like familial hypercholesterolemia causing early heart disease If Crisco caused the entire field of cardiology, that would be impressive branding. 6) “Guidelines caused obesity” This is where the argument collapses. Obesity didn’t rise because: People swapped butter for margarine It rose because: Total calories increased Ultra-processed foods exploded Physical activity declined Food environment changed dramatically The timeline argument is correlation cosplay. 7) The biology they ignore Atherosclerosis isn’t a food fight—it’s a particle problem: ApoB-containing lipoproteins enter the arterial wall They get retained, oxidized, trigger inflammation Plaque develops over decades You can argue diet all day—but LDL/ApoB is necessary for that process. That’s why: Statins work PCSK9 inhibitors work Lower LDL → fewer events (consistently) 8) The “Keys was a villain” narrative Keys was aggressive, opinionated, and very public. So were most mid-century scientists. But turning him into a Bond villain: Ignores decades of confirming evidence Sama just wants you to buy his coaching - and ignore science.
Sama Hoole@SamaHoole

In 1953 an American physiologist called Ancel Keys stood up at a World Health Organization conference in Geneva and presented a graph. The graph plotted fat consumption against heart disease mortality in six countries. The United States at the top. Japan at the bottom. A smooth upward curve in between. The room was convinced. The graph would go on to define global nutrition policy for the next seventy years. There was one small problem with the graph. Keys had data from twenty-two countries. He chose six. The other sixteen, which included France and Switzerland eating vast quantities of butter and cheese with low heart disease, and countries like Chile eating almost no animal fat and having high heart disease, did not produce the line he wanted. So they were not on the graph. When this was pointed out, in print, at the time, Keys did not engage with the science. He launched a career. He became chair of the American Heart Association's nutrition committee. He got himself on the cover of Time magazine. He organised the Seven Countries Study, a sequel to the cherry-picked six, which selected populations and time points that would confirm his hypothesis and excluded those that would not. Crete was measured during Lent. The comparisons were, by design, not fair. Then he did the thing that turned him from a scientist into a politician. He went after the opposition. Dr John Yudkin, a British physiologist, published a book in 1972 called Pure, White and Deadly, arguing that sugar was a better fit for the heart disease data than fat. His data covered more populations, more years, and more accurately matched the rise in cardiovascular mortality across the twentieth century. Keys called him, in print, a charlatan. He used his position at the AHA to block Yudkin's research from conferences. He pressured editors. He lobbied funders. Yudkin's grants dried up. His reputation was systematically dismantled by a man who was, at this point, not doing science but running a protection racket for a hypothesis. Yudkin died in 1995 in obscurity. His work has since been quietly vindicated. Nobody has apologised. Meanwhile the American Heart Association, funded since 1948 by a $1.7 million donation from Procter and Gamble (makers of Crisco, a product that urgently needed a reason for Americans to stop cooking with lard), adopted Keys's recommendations and issued them as medical advice. The American public complied. Butter consumption collapsed. Margarine tripled. Seed oils, negligible in 1950, became the dominant cooking fat. The food industry reformulated thousands of products to remove fat and replace it with sugar, because the fat was the enemy and the sugar was not. American obesity rates, stable for fifty years, began to climb in 1977, the year the McGovern committee translated Keys's hypothesis into federal guidelines. They have not stopped climbing since. Type 2 diabetes followed. Metabolic syndrome followed. Fatty liver disease, which barely existed in 1950, became endemic. The entire constellation of chronic metabolic disease now occupying every doctor surgery in the developed world tracks, almost perfectly, onto the adoption curve of the guidance Keys spent his career promoting. He retired to Italy, drank olive oil, ate cheese, lived to 100, and described himself in interviews as a pioneer. He was a pioneer. He pioneered the practice of producing a predetermined conclusion from selective data, destroying the reputations of anyone who noticed, and using institutional capture to convert the conclusion into policy. Ancel Keys was not wrong the way scientists are sometimes wrong. Ancel Keys was wrong the way politicians are wrong. Deliberately. Profitably. Without consequence. You are still eating the consequences now.

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