Mehmet E Korkmaz (@MehmetE_Krkmz) profile picture

Prof. Dr. Mehmet Emin Korkmaz Tıp, İç hastalıkları, Kardiyoloji

Joined November 2013
Photo by Mehmet E Korkmaz (@MehmetE_Krkmz)Photo by Mehmet E Korkmaz (@MehmetE_Krkmz)Photo by Mehmet E Korkmaz (@MehmetE_Krkmz)Photo by Mehmet E Korkmaz (@MehmetE_Krkmz)Photo by Mehmet E Korkmaz (@MehmetE_Krkmz)Photo by Mehmet E Korkmaz (@MehmetE_Krkmz)Photo by Mehmet E Korkmaz (@MehmetE_Krkmz)Photo by Mehmet E Korkmaz (@MehmetE_Krkmz)Photo by Mehmet E Korkmaz (@MehmetE_Krkmz)Photo by Mehmet E Korkmaz (@MehmetE_Krkmz)
Çok doğru.
A rant about LDL, HDL & cholesterol... LDL stands for low density lipoprotein. HDL stands for high density lipoprotein. Think of these as taxis that transport lipids around the blood. (There are other taxis). LDL-C is the cholesterol in a LDL. HDL-C is the cholesterol in a HDL. Both LDL & HDL (taxis) also carry protein, phospholipids and triglycerides. People use LDL/LDL-C and HDL/HDL-C interchangeably, which is wrong and misleading. LDL is called bad cholesterol. It's not even cholesterol; it's a carrier of cholesterol (and other lipids). HDL is called good cholesterol. It's not even cholesterol; it's a carrier of cholesterol (and other lipids). The cholesterol in a LDL is the same as the cholesterol in a HDL (C27H46O). There is no good or bad cholesterol - except in the heads of people who should know better (academics, doctors etc). One thing we can all agree on is that lowering cholesterol is eye-wateringly lucrative.
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ACSM Kılavuzu - Daha ağır yükler (1 tekrar maksimumun [1RM] ≥%80'i): kuvvet - Daha yüksek hacim (kas grubu başına haftada ≥10 set) : kas gelişimi - Hızlı bir konsantrik faz ile kaldırılan orta düzey yükler (1RM'nin %30–70'i): patlayıcı güç Basit ve etkili öneriler👇
The American College of Sports Medicine updated its resistance training guidelines after 17 years, based on 137 systematic reviews: - Heavier weights (≥80% of 1RM) favored strength gains - Higher volume (≥10 sets per muscle group per week) favored muscle growth - Moderate loads (30–70% of 1RM), lifted with a fast concentric phase, favored power - Training to failure wasn’t consistently better - Machines and free weights both worked - Complex periodization and advanced set techniques didn’t consistently improve results Full video breakdown: youtu.be/Tu8AyNNlhCQ PMID: 41843416
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"İsveç, 2027/2028 sezonundan itibaren ulusal aşılama kampanyasında yalnızca protein bazlı koronavirüs aşısı kullanacak. Bu, mRNA aşılarını terk eden dünyadaki ilk ülke olacak."
Sweden opts for coronavirus protein vaccine instead of mRNA From the 2027/2028 season onwards, Sweden will use only a protein-based coronavirus vaccine for its national vaccination campaign. It is the first country in the world to say goodbye to the mRNA vaccines. Difference in technology Nuvaxovid is a classic protein vaccine. It contains a ready-made piece of the virus (the spike protein), produced using recombinant technology (a molecular method in which DNA from different organisms is combined in the laboratory and placed into a host cell (such as a bacterium or yeast) to allow it to multiply or produce proteins) and provided with an adjuvant (an excipient that stimulates and strengthens the body's immune response to the antigen, so that the vaccine works better). The body is presented with this protein directly to build an immune response. This differs from mRNA vaccines (such as Comirnaty from Pfizer/BioNTech), where the body's cells must produce the spike protein themselves after receiving the mRNA instruction. This process carries the risk of autoimmune reactions, especially because these products do not remain at the injection site but can spread throughout the body. Furthermore, the quantity and duration of spike protein production are not defined in the mRNA technique. In addition, the lipid coating of the mRNA vaccines is very reactive. All in all, this leads to a disproportionate number of side effects, some very serious and resulting in death (1-3). Sweden chose its own path during the coronavirus years by not enforcing lockdowns or school closures. Although there was much criticism of this at the time, the Swedish approach was later appreciated ( De Morgen, 25 December 2023 ). With the decision to phase out coronavirus mRNA vaccines, Sweden appears set to play a pioneering role once again. The Doctors' Collective, together with European partners, has been advocating for the cessation of mRNA vaccinations for quite some time. Sources: Sanofi press release (April 21, 2026), LäkemedelsVärlden report and Läkemedelsmarknaden report regarding the tender. References Cappelletti-Montano B, Demuru G, Laconi E and Musio M (2023) A comparative analysis on serious adverse events reported for COVID-19 vaccines in adolescents and young adults. Front. Public Health 11:1145645. doi: 10.3389/fpubh.2023.1145645 Szebeni, J. Expanded Spectrum and Increased Incidence of Adverse Events Linked to COVID-19 Genetic Vaccines: New Concepts on Prophylactic Immuno-Gene Therapy, Iatrogenic Orphan Disease, and Platform-Inherent Challenges. Pharmaceutics 2025, 17, 450. Fraiman J, Erviti J, Jones M, Greenland S, Whelan P, Kaplan RM, Doshi P. Serious adverse events of special interest following mRNA COVID-19 vaccination in randomized trials in adults. Vaccine. 2022 Sep 22;40(40):5798-5805. doi: 10.1016/j.vaccine.2022.08.036. Epub 2022 Aug 31. PMID: 36055877; PMCID: PMC9428332. artsencollectief.nl/zweden-k…
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Is high LDL cholesterol (or apoB) harmful ONLY with poor metabolic health, characterized by low HDLc? New study from preeminent lipidologist Sniderman: "when HDL-C is high ... effect of changing apoB vanishes" PS: A low-carb diet potently increases HDLc academic.oup.com/eurjpc/adva…
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Professor Richard Wolff, a highly prominent American Marxian economist, author, and professor emeritus.
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WebMD says too much cholesterol causes heart disease. Then explain this... 136,905 hospital admissions for coronary artery disease. Lipids checked within 24 hours. Almost half had LDL under 100. 17.6% had LDL under 70. Only 21.1% were on a cholesterol drug before they came in. Now the numbers WebMD skipped. More than half had HDL under 40. Fewer than 10% had HDL of 60 or higher. Average triglycerides: 161. Low HDL with high triglycerides is the fingerprint of hyperinsulinemia. Sugar and high carbs cause it. The authors' answer? Push LDL even lower. I'd fix the insulin first... Read the actual study. Link below... – at Tennessee, USA
Too much cholesterol increases your risk of cardiovascular diseases like heart disease and stroke by causing plaque buildup in your arteries, which can restrict blood flow. We answer common questions about cholesterol, including the differences between “good” (HDL) and “bad” (LDL) cholesterol, and more: wb.md/4yAjApG
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Doğru !
Your fat used to be mostly animal. Now it’s mostly soybean. In 1960, about 13% of American adults were obese. Today it’s ~40%. Severe obesity went from under 1% to nearly 10%. That’s the quantity. The composition changed even more quietly. A 2015 review of U.S. adipose tissue samples found linoleic acid (the main fat in seed oils) rose from ~9% of stored fat in 1959 to ~21.5% by 2008 — a 136% increase. It tracked dietary linoleic acid intake almost perfectly as soybean oil flooded the food supply. Your grandparents’ fat cells were built from butter, lard, and tallow. Yours are built from the industrial oils that replaced them. Those oils are more prone to oxidation, more integrated into cell membranes, and part of the same dietary environment that also delivered the refined carbs and ultra-processed calories that expanded the total fat mass. More fat. Different fat. Same timeframe as the obesity epidemic.
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Mehmet E Korkmaz retweeted
“5-21 yaş arası erkeklerde ani kardiyak ölüm için CDC verileri; COVID aşılarının devreye girmesinden bu yana değer, temel oranın 7 standart sapma üzerinde ve hala artmaya devam ediyor.”
I asked @EthicalSkeptic to find CDC data for sudden cardiac death in males ages 5 - 21. The rate since the rollout of the COVID shots is 7 standard deviations above the baseline rate and is still rising. @NIHDirector_Jay @SecKennedy
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CDC ifşacısının gizli kaydı: "MMR aşısı otizm ilişkisini gösteren verilerini gömdük. Utanıyorum."
CDC Whistleblower's Secret Recording: "We Buried the Data on MMR & Autism, I'm Completely Ashamed." Dr. Brian Hooker secretly recorded a senior CDC scientist, Dr. William Thompson, who made a shocking admission. On those recordings, Dr. Thompson freely confessed to a massive cover-up. He admitted that he and his senior associates at the CDC had buried the damning data showing a statistical link between the MMR vaccine and autism. Thompson stated, "Thimerosal causes autism-like features." He expressed profound shame, saying, "I'm completely ashamed of what I did. The higher-ups wanted to do certain things and I went along with it." He named senior officials—Colleen Boyle, Frank DeStefano, Marceline Moulton—as participants. At the helm was Dr. Julie Gerberding, who later became president of Merck Vaccine. This is not a theory. It is a confession from a lead CDC co-author on the pivotal studies used to deny any link. The man inside the machine admitted the fraud. The public deserves the truth. The victims deserve justice.
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Şeker ve meyve suyu tüketimini azaltmak, çocuklarda yağlı karaciğer hastalığını 8 haftada düzeltmekte. Karaciğer yağ oranı şekeri alımını azaltanlarda %25'ten %17'ye indi, kontrollerde değişmedi. Meyve suyu çocuklar için sağlıklı bir besin değildir. pubmed.ncbi.nlm.nih.gov/3066…
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Diğer önemli toksin Omega 6 yağ asitlerdir; yani nebati yağlar. Omega-6/Omega-3 oranı 4:1 olacak şekilde modifiye edilmiş bir diyet, 12 hafta sonunda, çocuklarda kilo kaybı yaşanmasa dahi karaciğer yağ oranında %25,8 azalmaya neden olur. doi.org/10.1093/jn/nxaa183
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Mehmet E Korkmaz retweeted
This was a seemingly problematic post, but Shawn observing that rabbits were a model for cardiovascular research is a fair point, and prompted me to reconsider the suitability for bears. Herbivores get atherosclerosis from cholesterol, carnivores do not. Bears are thus a fair model to examine, at least they are if rabbits were. Humans are somewhere in the middle, we are omnivores who eat a lot of meat, but we evolved from animals that ate mostly vegetables and fruit. Bears are omnivores that eat a lot of meat, but are descended from meat eaters. Linoleic acid in the large amounts found in the modern diet is a novelty in human evolution, and has a clear and well-established role in initiating heart disease in humans. Bears hibernating are still eating their ancestral diet. If we gave bears lots of seed oils, could we induce heart disease? “The fatty acid composition of the triacylglycerols differed substantially from that of the wild [polar] bears, reflecting their diet of fish, domesticated herbivores, bread, and fruit...” onlinelibrary.wiley.com/doi/… Polar bears bears are the most carnivorous of bears, but when fed food closer to a human diet in captivity ("domesticated herbivores”), they start getting human-like illnesses, including visceral fat, a major risk factor for human heart disease. Dogs, another non-human carnivore, are fed a diet that is very close to human diets. There is even a ‘Dietary Guidelines’ for dog food, which closely resembles the human recommendations, including to consume seed oils. Dogs get atherosclerosis that looks very similar to human atherosclerosis. “These histopathological and immunohistochemical features were similar to those of human atherosclerotic lesions.” doi.org/10.1016/S0021-9975(0… We know that wild humans, like wild bears, both eating their natural diet, do not get atherosclerotic heart disease. So. maybe comparing humans to carnivores like bears and dogs is useful, probably more so than rabbits. Oh, by the way, the rabbits who got atherosclerosis from cholesterol were fed cholesterol dissolved in seed oils. Feeding rabbits less seed oils results in less atherosclerosis. “However, sunflower oil provokes a significant progression in lesion development, whereas diet enrichment with extra virgin olive oil and, to a lesser extent, fish oil, stops this progression.” “Sunflower, virgin-olive and fish oils differentially affect the progression of aortic lesions in rabbits with experimental atherosclerosis” sci-hub.ru/storage/2024/2007…
So this post has generated a lot of negative remarks my way. The premise is that I conflated bear physiology with human physiology and “that’s just stooopid” Now of course nowhere in the post do I state this is directly applicable to humans but it is really just an interesting observation As some of you might remember, the earliest work on cholesterol was done on rabbits well over 100 years ago and then that data was later explored in humans. Now most of us are not hibernating bears, even if one of my critics, Jack Kruse somewhat resembles one, and we should not think that the complete lack of cardiovascular disease in bears despite massively elevated cholesterol is an excuse for humans to ignore high cholesterol What is somewhat interesting is the reason why bears have massively elevated cholesterol in the first place- Most likely it is because after they burn through the initial liver glycogen early in hibernation they are then forced to live on their fat stores-now this is arguably exactly what we see on humans that adopt low carb diets and get relatively lean (don’t worry Jack, you don’t have to worry about this)-This phenomenon has been well describe in the scientific literature by the so called “lipid energy model” -which is different from the reason most people see elevations in cholesterol, namely they just get fat and their cells can’t absorb any more circulating fats (maybe Jack needs to worry here) -these are two very different scenarios. Why are the bears protected? Well the authors and some others speculate that the endothelial proteoglycans are somehow different and because they are not as “sticky” the lipoprotein particles are less likely to be trapped in the endothelium. Do we see anything that alters lipoprotein “stickiness” in humans? Actually yes, for instance we know that high blood pressure and hyperglycemia can alter proteoglycans “stickiness” in humans. Does this mean if we improve glycemic control and hypertension with say a low carb diet, we may see an alteration in our endothelial proteoglycans-most likely yes Is it enough to decrease the likelihood of lipoproteins getting trapped in the endothelium? Unknown as far as I’m aware, but perhaps- this is why further study on humans, not bears, on this stuff should be explored. Of course since you can’t make money on a drug for this, I won’t hold my breath!
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Çok doğru!
Why do South Asians get type 2 diabetes at much lower body weights? The answer is in their fat cells. These are fat cells from two young men with the same BMI. The South Asian man's are on the left. The white man's are on the right. At the same BMI as white Europeans, South Asians carry more body fat, bigger fat cells, more liver fat, and higher insulin. Here is what the studies show. 1. Same BMI, much bigger fat cells. In 29 South Asian and 18 white men, average age 27, BMI was 24 vs 23. Body fat was 22% vs 15%. The average belly fat cell was 3,491 vs 1,648 µm² in cross section. Treating the cells as spheres, that is about 3 times the volume of fat per cell on average. The samples in the image show an even larger difference. The larger the fat cells, the worse the insulin resistance. Visceral fat was the same in both groups. 2. Matched for age and BMI, still more insulin. Asian Indians matched to white adults had similar fasting glucose but higher fasting insulin, and they cleared glucose about 40% less well on a clamp test (4.7 vs 7.5 mg/kg/min). 3. Fat cell size explains much of the insulin gap. After adjusting for age, sex and BMI, South Asians had larger fat cells, liver fat of 9.9% vs 2.5%, and higher fasting insulin. Adjusting for fat cell size cut the insulin difference in half. 4. Lean and young. Among 482 lean young adults, insulin resistance was 2 to 3 times more common in Asian Indians than in any other group. The men had about twice the liver fat of white men. 5. It starts in childhood. South Asian children aged 8 to 11 in Britain were not heavier than white children, but their fasting insulin was 53% higher, with similar blood glucose. My view: fat cells can only store so much. When they are full, they become insulin resistant and release more fat into the blood, and that fat ends up in the liver and muscle. Insulin rises to compensate. South Asians appear to reach that limit at a lower body weight. For a South Asian person, a normal BMI does not mean normal metabolism. Fasting insulin, waist size and liver fat say more than weight.
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“5-21 yaş arası erkeklerde ani kardiyak ölüm için CDC verileri; COVID aşılarının devreye girmesinden bu yana değer, temel oranın 7 standart sapma üzerinde ve hala artmaya devam ediyor.”
I asked @EthicalSkeptic to find CDC data for sudden cardiac death in males ages 5 - 21. The rate since the rollout of the COVID shots is 7 standard deviations above the baseline rate and is still rising. @NIHDirector_Jay @SecKennedy
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👍🏻
This time next year, Zelensky will be safely ensconced at a country mansion somewhere in Sussex. There he will be feted and visited by the likes of Boris Johnson, Keir Starmer, Sunak, Obama, Hillary Clinton, von der Leyen, Sean Penn, William and Kate, and Tony Blair et al. His memoir, ghost written, will see him embark on a promotional tour of the chat show and podcast circuit, during which he will be curated as the man who stood up to Putin and was betrayed by Trump. Lucrative Hollywood offers for the rights will follow. As part of this hagiographic carnival, Zelensky will be given an honorary knighthood by King Charles, accompanied by the usual trumpets and banquet. Meanwhile, back in Ukraine, investigators will uncover corruption under his premiership on an industrial scale. These findings will be summarily dismissed as a in the West as a fabrication, cooked up in the Kremlin. For the ordinary Ukrainian, left to pick up the pieces, heartrending stories of men being kidnapped from their families by Zelensky's conscription press gangs --- never to be seen again -- will be commonplace. These stories will be joined by accounts of war pensions denied, compensation payments for the loved ones of fallen soldiers declined, and as will details of widespread torture and abuse within the ranks. No lessons will be learned -- just as none were learned from previous failed military adventures in Afganisation, Iraq, Libya, Syria, etc. The circus will move on to the next, confirming that though the faces change, the game remains the same.
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Harika tespit.
“We ate that ask kids and we turned out fine” NO, NO you didn’t…
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Harika paylaşım... Doymuş yağlara karşı verilen “büyük savaş”, bu kadar saçma.
Doctor: "I'd cut back on the butter. Saturated fat is solid at room temperature, and that's what it does in your arteries." Patient: "What temperature are my arteries?" Doctor: "37." Patient: "What's butter at 37?" Doctor: "...Melted." Patient: "And beef dripping? Lard?" Doctor: "Soft. On their way." Patient: "So what's actually solid in an artery?" Doctor: "Plaque. Cholesterol, calcium, dead white cells." Patient: "Why are the white cells dead?" Doctor: "They go in to mop up damaged cholesterol particles, get overloaded, and die there." Patient: "Damaged how?" Doctor: "Oxidised. Gone rancid, if you like." Patient: "Does butter go rancid?" Doctor: "Not easily. It's stable." Patient: "What does?" Doctor: "Polyunsaturated fat. The vegetable oils. They're fragile." Patient: "Sunflower. Rapeseed. The ones on the healthy-eating sheet you gave me." Doctor: "They're liquid at room temperature. That's the point of them." Patient: "So is petrol. The thing you're frightened of melts before it gets in, and the thing you recommend is the one that rots in there." Doctor: "That's a simplification." Patient: "It was your simplification. You started with the room." Doctor: "..." Patient: "What else is solid at room temperature? Bone. Teeth. Do I want to cut down on those?"
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I spent six rounds challenging Grok on statins. It ended up agreeing with me. Started: "NNT ~20" Ended: hard benefit is "modest": 0.8% absolute reduction in death, 1.3% in heart attacks. In primary prevention, ~0.35% fewer deaths (NNT ~286), and cardiovascular deaths didn't fall significantly. Started: "diabetes ~0.2%/yr" Ended: ~1.3 extra cases per 100 people per year at high intensity. Started: "myopathy <0.1%" Ended: 11 extra muscle complaints per 1,000 in year one. Started: "no infection risk" Ended: "observational shingles signal persists." Grok's final words: "Agreed on the need for absolute, risk-stratified numbers upfront—especially since most statin starts are primary prevention." Every opening claim erred in the drug's favor. It took the trialists' own data to correct each one. Before you start a statin, ask your doctor for YOUR absolute numbers, not the relative ones. I see this as glaring evidence that @grok has pro-pharma biases that should be openly discussed, and corrected, as you can't have informed medical choice without accurate information. @elonmusk @Safety
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