Steven Quartz PhD

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Steven Quartz PhD

Steven Quartz PhD

@StevenQuartz

Professor @Caltech. Computational Neuroscience, fMRI, learning theory. Forthcoming "Dopamine Rules." 2026 return to full-time bike racing & hour record attempt.

Katılım Eylül 2011
646 Takip Edilen3.6K Takipçiler
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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
Dopamine isn't just about individual reward learning. In 2005, my colleagues and I found that a dopaminergic reward prediction error signal extends to social exchange. People use this signal to build a model of others as they develop trust and cooperation. Once formed, this becomes a predictive, anticipatory 'trust signal'. PMID: 15802598 (illustration: cover of science issue featuring the study, which required developing an fMRI 'hyperscanning' platform to probe multiple brains interacting in real-time).
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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
That's not the logic of the analogy at all. I used the analogy to show why the claim that your case study 'reveals that high cholesterol doesn't cause heart disease' - a claim you had the chance to correct but didn't - is wrong. It should be obvious to you why that claim is wrong and what the analogy was intended to show - and reconstructing the logic in such a garbled way suggests that it is obvious to you.
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Nick Norwitz MD PhD
Nick Norwitz MD PhD@nicknorwitz·
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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Alex Leaf
Alex Leaf@Alexleaf·
@StevenQuartz @nicknorwitz A little common sense is all it takes to realize that relying on this monocausal deterministic framework would, quite literally, lead to the conclusion that **nothing** causes heart disease.
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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
Does @nicknorwitz's case study really challenge the entire conventional model of heart disease? That sounds revolutionary - until you realize it relies on a simplistic, outdated understanding of causation that creates a strawman version of the consensus view. This matters because his claim leads to misleading messages like the headline "Why High Cholesterol Doesn't Cause Heart Disease." But it relies on a deterministic, monocausal framework that contemporary causal models have moved far beyond. Using these new models to frame the consensus view requires using numerous causal variables (LDL, blood pressure, smoking, diabetes, genetics, inflammation, etc) in a causal network where the relations among those variables are characterized probabilistically rather than deterministically (by a probability distribution over variables). This fundamentally changes what "X causes Y" means and shows why cases like Norwitz's are exactly the kind of variation such models allow: which variables dominate, offset, delay, or mask effects vary at the individual level. Most importantly, deterministic and monocausal assumptions severely distorts causation when we're dealing with complex, probabilistic, and multifactorial causation in complex systems. Thinking about risk both at the individual and population level requires moving beyond them (this is a follow-up to my sarcastic post yesterday to provide some of its underlying motivation).
Heart Surgeon Dr. Philip Ovadia@ifixhearts

Nick Norwitz Reveals Why High Cholesterol Doesn't Cause Heart Disease In this episode of Stay Off My Operating Table, @nicknorwitz breaks down why the medical world has been treating cholesterol as the disease itself and why that's dead wrong. One extraordinary case of a patient with sky-high LDL and zero arterial plaque is challenging the entire conventional model of heart disease. If you think managing your cholesterol numbers means you're managing your heart health, this conversation will change the way you think.  Watch the full episode here 👉 youtu.be/c2WOEkFpP3M?si…  #CholesterolMyths #HeartHealth #LDLCholesterol #CardiovascularHealth #FunctionalMedicine

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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
@Neuroscope_mp @drmarkhyman There is 0 evidence for this claim. The paper it's based on measured dopamine in the peripheral nervous system, which does not enter the brain. It's a myth used to sell cold plunge pools. The rise in dopamine is related to shivering and peeing...
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Harshi Peiris, Ph.D.
Harshi Peiris, Ph.D.@Neuroscope_mp·
Cold plunges are no joke for dopamine. That 250% increase and the fact it lasts for hours without the crash is pretty powerful compared to coffee. One of my old Post doc advisors did a jump into San Fran Bay every week day for 30 minutes to an hour and he studies aging and neurodegeneration. What interests me even more is how this ties into brain health overall. For conditions like Parkinson’s where dopamine-producing neurons are vulnerable, anything that supports natural dopamine pathways, reduces inflammation, and builds resilience is worth paying attention to. Cold exposure also boosts norepinephrine and BDNF, which help with focus, mood, and neuroprotection. I recommend this because the body adapts if you overdo it. Short and intense seems to work best. Definitely one of the highest return practices once you get past the initial shock.
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Mark Hyman, M.D.
Mark Hyman, M.D.@drmarkhyman·
Your morning coffee gives you a 30% dopamine boost. You know what else does? A cold plunge. Studies show that cold water immersion increases dopamine levels by 250% — and unlike caffeine, the effect lasts up to two hours and doesn't crash. The most alert, focused, unstoppable version of you is a few uncomfortable minutes away. Nobody said it would be warm.
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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
@reallyoptimized @walsh_coman A probabilistic and multifactorial model is the core framework of every major consensus guideline and is built into their risk prediction models, which combine multiple risk factors to output a quantitative probability.
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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
In today's episode, Ovadia will interview a lifelong smoker who doesn't have lung cancer, revealing that smoking doesn't cause lung cancer.
Heart Surgeon Dr. Philip Ovadia@ifixhearts

Nick Norwitz Reveals Why High Cholesterol Doesn't Cause Heart Disease In this episode of Stay Off My Operating Table, @nicknorwitz breaks down why the medical world has been treating cholesterol as the disease itself and why that's dead wrong. One extraordinary case of a patient with sky-high LDL and zero arterial plaque is challenging the entire conventional model of heart disease. If you think managing your cholesterol numbers means you're managing your heart health, this conversation will change the way you think.  Watch the full episode here 👉 youtu.be/c2WOEkFpP3M?si…  #CholesterolMyths #HeartHealth #LDLCholesterol #CardiovascularHealth #FunctionalMedicine

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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
@walsh_coman the post was a sarcastic response to the headline about cholesteroal. It was making the point you also made - causation is probabilistic and multifactorial.
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An Observer
An Observer@walsh_coman·
@StevenQuartz Doesn’t always cause lung cancer. Lry’s try to be more precise with our logic.
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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
@TDoige if that were the case, you wouldn't make a blanket, definitive population-level claim.
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Todd
Todd@TDoige·
@StevenQuartz Maybe, just maybe, Dr. Norwitz is shining a light that our current understanding of heart disease is incomplete.
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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
@AmmousMD Good luck with your $800 video consults to change people’s ’light environment.’ That sounds evidence-based.
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Dr. Ammous
Dr. Ammous@AmmousMD·
@StevenQuartz You're not selling something, you genuinely believe the propaganda. Which is even sadder.
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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
@BradChilmeran no it doesn't. That's the point of the analogy: causation is probabilistic and multifactorial. More broadly, the point is to show why the headline takes a rare exception (a case study with no generalizability) and attempts to make a blanket, population-level claim.
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Bradley Chilmeran, PhD
Bradley Chilmeran, PhD@BradChilmeran·
@StevenQuartz Your analogy assumes that elevated LDLc in all forms and contexts are equally harmful. Is that true? Also, the lifelong smoker would certainly have other health issues attributable to smoking even if free of cancer
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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
@AndrewZywiecMD my post is sarcastic - it shows via analogy why the headline in the post I'm responding to "Nick Norwitz Reveals Why High Cholesterol Doesn't Cause Heart Disease" is the dishonest position.
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Andrew Zywiec, M.D.
Andrew Zywiec, M.D.@AndrewZywiecMD·
@StevenQuartz You're quite aware that this is an exceptionally dishonest position to take, correct? Just making sure we are both on the same page.
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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
@mackinprof @Brady_H I grew up in Canda (of course played hockey & went to the Bobby Orr shool of hockey) - I remember Cherry saying this and something like 'why don't they just put out cheese and crackers for them too.' No commentator better embodied their sport than him!
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Stuart Phillips (he/him)
Stuart Phillips (he/him)@mackinprof·
⚠️Humour Alert (🍁)⚠️ @StevenQuartz & @Brady_H you're both wrong... try playing game 28 in the playoffs after playing 82 games in a regular season. Blocked 33 shots, taken 22 stitches, scored 8 goals, and had 12 assists... to win the Stanley Cup That my boys is tough!😂
Steven Quartz PhD@StevenQuartz

A few hours of jogging sounds tough - until you compare it to a 215 km cycling stage over 3 massive passes in the alps with 14,000 feet of climbing - and then you realize it's only day 2 of a stage race...

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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
@mixedstein My post was half-joking - Bradys post has been generating lots of similar responses
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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
A few hours of jogging sounds tough - until you compare it to a 215 km cycling stage over 3 massive passes in the alps with 14,000 feet of climbing - and then you realize it's only day 2 of a stage race...
Brady Holmer@Brady_H

Comparing 4–5 sets of squats to failure to mile 18 of a marathon is hilarious. By mile 18 you’ve been running for 2+ hours at 85% max heart rate. You get 3–4’ of rest before each set of squats while you scroll Instagram.

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Steven Quartz PhD
Steven Quartz PhD@StevenQuartz·
@nicknorwitz @ifixhearts Does Nick Norwitz really 'Reveal Why High Cholesterol Doesn't Cause Heart Disease.' Is that what his case study really shows? Is the headline framing this responsible science communication?
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Nick Norwitz MD PhD
Nick Norwitz MD PhD@nicknorwitz·
Thanks for a great conversation. I think people will get a lot from it if they take the time. I can't help but add, there is an unbelievable double standard when it comes to assessing clinical cases around cholesterol. Usually, if someone "breaks the rule" is ignored or dismissed. However, if someone falls in line with expectation - it's paraded around... even (or especially) when the reality doesn't match the story people want to tell themselves. Here's an example: x.com/nicknorwitz/st…
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Heart Surgeon Dr. Philip Ovadia
Heart Surgeon Dr. Philip Ovadia@ifixhearts·
Nick Norwitz Reveals Why High Cholesterol Doesn't Cause Heart Disease In this episode of Stay Off My Operating Table, @nicknorwitz breaks down why the medical world has been treating cholesterol as the disease itself and why that's dead wrong. One extraordinary case of a patient with sky-high LDL and zero arterial plaque is challenging the entire conventional model of heart disease. If you think managing your cholesterol numbers means you're managing your heart health, this conversation will change the way you think.  Watch the full episode here 👉 youtu.be/c2WOEkFpP3M?si…  #CholesterolMyths #HeartHealth #LDLCholesterol #CardiovascularHealth #FunctionalMedicine
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Mark Bski🇺🇸Ruggedly Individualistic 🐶 olllllllo
Mark Bski🇺🇸Ruggedly Individualistic 🐶 olllllllo@MarkBski·
The vast throngs of scientists who believe "large-scale, long-term observational studies across diverse global populations, Mendelian randomization studies, clinical interventions, pathophysiological evidence, etc" are at an absolute loss to explain our current pandemics of obesity and diabetes. I blame Groupthink. The smartest and best educated still bleat in unison less they be cast from the group fpr heresy.
Steven Quartz PhD@StevenQuartz

Science is a process of data accumulation and systematic verification, not a spectator sport. And we've known since Plato that debates just award sophistry. Don't be distracted by the fact that the LMHR theory rests on a poorly-designed study (a preprint) and currently a low-quality case study in a low-quality journal. On the other side are large-scale, long-term observational studies across diverse global populations, Mendelian randomization studies, clinical interventions, pathophysiological evidence, etc.

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Keşfet

@KayBwt @Alexleaf @nicknorwitz @Neuroscope_mp @drmarkhyman @reallyoptimized @walsh_coman @TDoige