@BioLayne @bulletproofexec @thegarybrecka Red light has been shown to have very positive effects on health, hell you champion Huberman who thinks red light is beneficial. You provide no evidence for these techniques being non effective.
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TheElephantExplorer🐘🌴
2K posts
TheElephantExplorer🐘🌴
@ElephantLearner
I am a biophile who loves dissecting and exploring science. I also like exploring spirituality. From time to time I do CS related work. 🖥🌴🧪🌞
Katılım Ocak 2025
31 Takip Edilen49 Takipçiler
People like @bulletproofexec & @thegarybrecka want you to believe that biohacking must be complicated & expensive
This is the biggest scam in wellness
Biohacking is NOT:
hydrogen water
grounding mats
red light therapy
exotic supplements
analemmas (water wands)
overpriced tests
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@schaal2023 @DrJackKruse Are you sure it isn't me.
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@DrJackKruse The elephants in the room are mRNA vaccines, blue light dominance and massive nnEMF saturation.
It’s in most of their homes, offices, schools and autos 24/7. This didn’t exist just 20 years ago.
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Or maybe, something else is going on?
Kids with "genetic diseases" have centralized MDs with no clue what to do.
Healthy teens with minor issues have immune systems so fragile they die from splinters.
Another "healthy teen" dead. But no one asks the real questions, why. They accept the answers. Lattice lock in the immune system doesn't have to be a rare disease any longer to kill you. Few. nypost.com/2026/05/13/us-…
IYKYK
Robbie Mouton@mcgmouton57
It's getting to where you can't trust doctor's anymore. They must be rushing them through medical school. Ethan Cantrell, 18, a fifth generation logger and powerlifter, died from sepsis just 2 months after graduating high school, and one month after getting engaged. Cantrell was stabbed in the right arm while cutting wood. He went to the medical center for treatment where doctors "attempted to irritate" the wound with saline and then sutured it up "tightly." He was quickly discharged and given a week of antibiotics. Later that afternoon, his arm began to swell and he started running fever, then started having trouble breathing. He was brought back to the emergency room and seen by the same doctor who resisted removing the sutures until his arm swelled to 3 times normal. When they removed the sutures, finally, they found dirt, twigs, pine needles and moss that was sown up into his arm. They amputated his arm at the shoulder in an attempt to save his life, but he succumbed to the infection. A $100M lawsuit has been filed. I encourage a prayer for him and his family. Much too young to go. nypost.com/2026/05/13/us-…
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@YounisJoseph He has measured his LDL many times throughout the years showing around the numbers he said.
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The high cholesterol = heart disease theory needs to die
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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@ElephantLearner @MikhailaFuller Yes, and I wasn't suggesting he was outside of a few experiments. I just think it's important for folks to know he has ultimately decided to take not one but two drugs that lower his LDL-C significantly
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@theproof @MikhailaFuller Plus even suppose he was taking statins at the time, statins don't magically reverse extensive plaque, especially the plaque expected the appear at this high of an LDL.
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@theproof @MikhailaFuller Not when he was doing the study though
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QAM
🚨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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High LDL does not automatically equal atherosclerosis.
Great exception to the rule shown here !
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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@ChrisMasterjohn That is really interesting, I would love to hear your thoughts on the Keto-CTA trial!
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Nick is not too young to show soft plaque after seven years of having a cholesterol of 700 mg/dL.
His n=1 case report DOES tell us something incredibly important.
In 1953, it was shown in 300 autopsies of American soldiers who died in the Korean war with a mean age of 22 that 77% had plaque and 15% had luminal narrowing.
Nick is in his 30s so it is expected for him to have some soft plaque even without extremely elevated cholesterol.
Causation can either be necessary, sufficient, or necessary and sufficient.
Nick’s n=1 case shows all on its own that 700 mg/dL cholesterol and its associated high LDL-C and ApoB is not sufficient to cause atherosclerosis.
It may still be necessary to have high LDL-C or ApoB.
In fact, Nick could be the only person on the entire planet who is missing one other factor that, once combined with high LDL-C or high ApoB, is sufficient to cause plaque.
As such it is possible that Nick’s results do not apply to any other person on the planet, when looking at his case report alone.
But that’s totally different from saying we can’t learn a principle from his case report that we know does translate to everyone else.
The principle is that high cholesterol is not sufficient to cause heart disease.
The reason we don’t know if his report generalizes to other people is not because we don’t know if we can generalize that one principle. It’s because we don’t know how Nick is different from other people and we therefore don’t know if anyone else has the same mix of relevant factors.
In other words, it does matter that his n is 1 because for this reason we can’t make a probability statement about the likelihood that someone else can maintain this high cholesterol for the same period of time without showing plaque.
But that’s separate from the point that it only takes a single cause of A coexisting with lack of B to show that A is not sufficient to cause B.
That’s assuming you measured A and B correctly.
Now if we move beyond his case report we can go back to the research showing LDL requires damage to be taken up into plaque and facilitate disease progression.
Maybe Nick is lacking that damage.
Also, the characterization of the LMHR phenotype is suggestive of a generalizable principle connecting Nick with these other folks. It needs a lot more research.
But the point that 700 mg/dL cholesterol for seven years coexists with no plaque is a major demonstration of the insufficiency of high cholesterol or ApoB to cause plaque.
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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@nicknorwitz I feel like the main reason for the dismissal of the keto cta was the fact that they didn't register a primary outcome, and changed it. Then went from cleerly to other types of analyses.
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Response to Rebuttals on: "Seven Years of 700 Cholesterol Without Coronary Atherosclerosis".
It’s been really interesting to watch the first 24-hour response to this new paper. The overwhelming majority has been, if not fully enthusiastic, at least curious. And I sincerely appreciate that.
That said, some of the pushback has also been revealing… even comical. So let me address the most common retorts.
⏳1. “He’s too young.”
Asked and answered. HoFH Children with similar LDL and ApoB levels can develop measurable plaque within the first few years of life and even heart attacks by age 8 or 10. Other people around my age, using similar imaging technology, also show measurable plaque. “He’s young” is not a good explanation.
🙄2. “You have a conflict of interest because you’re the patient.”
LMAO! This one might be my favorite. What exactly did I do? Go into the CT scanner and suck in my plaque like I was sucking in my gut? Ask the AI algorithm, “Hey, I’m the patient — do me a solid?” If you think this is a rebuttal, I suggest you don’t join any debate teams.
🦓3. “He’s an outlier.”
Yes. At a population level, I am an outlier. I don’t have obesity, prediabetes, or metabolic syndrome. But that’s one of the broader points: We have a paucity of data on the risks of elevated LDL in metabolically healthy people without underlying genetic lipid disorders.
Outliers are not reasons to stop thinking. They’re opportunities to learn.
🤷♂️4. “It’s a fluke. He’s a one-off.”
What a remarkably uncurious response. Imagine an oncologist had a patient with stage IV pancreatic cancer (~3% five-year survival rate). And that patient somehow cured himself, then went on to win the 100 meters at the Olympics 12 years later.
Would the oncologist say: “Meh… What’s for lunch?”
Of course not. A good scientist or doctor (or curious human) would ask: what happened here?
🧬5. “Oh, you probably just have protective genetics.”
Oh, really? My father had a 99% occlusion of his left anterior descending artery at age 44. My Lp(a) runs between 100 and 194. And on top of that, I have a history of inflammatory bowel disease, a condition associated with chronic systemic inflammation.
🫀6. “But what about the Keto-CTA paper?”
If you’re trying to beat this drum like it’s a trump card, I’d guarantee you’re stuck in an echo chamber and have incomplete information. It has now been clarified repeatedly that the original CLEERLY dataset published on April 7th was not reliable.
CLEERLY had unblinded scans, anomalously results, and refused to perform a quality-control check. And multiple independent analyses have since shown that the KETO-CTA group do not appear to be a high-progression group. This is why we, the authors, took the initiative to retract the paper (NOT the study). The KETO-CTA Heartflow and QAngio data are available as a pre-print. And I’ve seen nobody legitimately try to defend the CLEERLY dataset.
Also, the data show that LDL and ApoB did not predict plaque progression, and even at high LDL and ApoB levels, confirmed regression was observed.
👇
For supporters, feel free to link this the next time you see someone try to deploy these arguments.
For critics, I suggest taking a read and thinking carefully… either to avoid falling onto the pyramid… or to avoid giving me reason to expand it.
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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@nicknorwitz Never heard this cleerly scan explanation before.
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@LateoRT @Haoshoku @MasalaFry69 The studies I have seen are either super small or not very well controlled from what I understand
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@ElephantLearner @Haoshoku @MasalaFry69 Why would you care minimality vs quality of said studies that you have? Do you have a problem with their quality?
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@Haoshoku @MasalaFry69 The amount of dog food research rcts are minimal, what makes you think we should be concluding off these studies.
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@MasalaFry69 Dogs on a plant-based diet are healthier. Cope and seethe. You're the animal abuser.
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@ChristianJsays Long time no see, Christian James🌿💪
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My Simple Stack that has me Outperforming 99.9% of Men > Age 30:
Daily/EOD:
Algae Oil Omega 3s
Vitamin D3
Zinc+Copper
Vitamin K2 - mk4/7
Beetroot powder
Turmeric + Ginger
Creatine
6mg Boron - on 2 wks/off 1
1-2x Week:
1000mcg methyl b12
12-1500mg NAC
WFPB diet. Exercise.
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@jerry05259307 @YannickBuccella 🤣 I hold my breath at all costs when I come into contact with them.
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High concentrated kerosene kills them all within 30 minutes.
It’s a nice headline, but also in over 90% of cases: what happens in the lab stays in the lab.
It’s just not transferable to humans in a safe and still effective dose.
All day Astronomy@forallcurious
🚨: Dandelion root kills over 90% of colon cancer cells in less than 48 hours, lab experiments reveal
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