Rick Audet

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Rick Audet

Rick Audet

@RickyAudet

Software engineering ex-@dolby; Interests: software, metabolism, sushi, and heavy metal 🤘

San Francisco, CA Katılım Ekim 2014
5.4K Takip Edilen1.1K Takipçiler
Rick Audet
Rick Audet@RickyAudet·
@markkaplan20 What are the units for the vertical axis? "Growth (2004 = 100)" makes no sense to me.
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Mark Kaplan
Mark Kaplan@markkaplan20·
I want you to look at this chart and tell me what you see. 20 years. Seven diseases. Every single line is going up. Alzheimer's up 260%. Parkinson's up 150%. Fatty liver up 125%. Diabetes doubled. Obesity up 42%. Cancer up 16%. Heart disease went down then came right back up. Trillions of dollars. The most expensive healthcare system in human history. And not a single metabolic disease is improving. Something is causing all of them. The same something. And nobody is stopping it. 🧵
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Whitfield Lewis, MD 🇦🇬🇺🇸
Whitfield Lewis, MD 🇦🇬🇺🇸@whitfieldlewis6·
In the era of obesity and metabolic disease, we should think about the metabolic effects of every medication we prescribe. Obesity is increasingly recognized as a disease of the brain. The hypothalamus regulates homeostatic hunger and satiety, while the mesolimbic reward circuit regulates food reward, motivation, and cravings. The prefrontal cortex helps exert executive control over these behaviors. Many medications influence these circuits. Some increase appetite and food reward. Others suppress hunger and reduce food cravings. Take anti-seizure medications, for example. Valproic acid remains one of our most effective medications for generalized epilepsy and migraine prevention. It has excellent efficacy, but it also has a well-recognized propensity for weight gain. Much of that effect appears to occur through central appetite regulation, particularly at the level of the hypothalamus, resulting in increased appetite and food cravings. Over time, this can contribute to weight gain and worsen metabolic health in susceptible individuals. Topiramate is FDA approved for both focal and generalized epilepsy. It also has Level A evidence for migraine prevention and is commonly used as an adjunct in idiopathic intracranial hypertension. Unlike valproic acid, topiramate commonly reduces appetite and food cravings. It appears to act through central appetite and reward pathways, including the hypothalamus and likely the mesolimbic reward system. The end result for many patients is spontaneous calorie reduction and clinically meaningful weight loss. Zonisamide is FDA approved for focal epilepsy. Although not FDA approved for generalized epilepsy, many neurologists use it in selected generalized epilepsy syndromes. What surprised me from the Columbia/Weill Cornell Obesity course was the randomized controlled trial data demonstrating clinically meaningful weight loss with zonisamide. Like topiramate, zonisamide appears to reduce appetite through central mechanisms, although its precise effects on appetite and reward circuitry are less well understood. The take-home message is simple. The brain determines hunger, satiety, and food reward. Medications can alter these pathways. Some increase appetite and promote weight gain. Others suppress appetite and facilitate weight loss. When two medications provide similar efficacy, their metabolic profile should be part of the discussion. Are you cognizant of the propensity for weight gain or weight loss whenever you prescribe a new medication? #neurobiology #FOAMed #metabolichealth #obesity
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Rick Audet
Rick Audet@RickyAudet·
"Without circadian gating or pulsatile resets, the system faces chronic metabolic stress, potentially leading to accelerated cellular aging, organ-specific stem cell burnout, or irreversible receptor desensitization once the drug is withdrawn." 🧵
☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆@DrJackKruse

Why do I say Reta will subtract longevity from humans and disagree with Morse? 1. The Nocturnal vs. Diurnal Disconnect The Baseline: Rodents (nocturnal) and humans (diurnal) have completely inverted circadian clocks governing metabolism, nutrient intake, and cellular repair.Stem Cell Vulnerability: Human stem cell niches rely on strict circadian gating to time replication and DNA repair. The Problem: If a drug blunts or alters a pathway that protects stem cells from exhaustion, humans are exposed during their active/inactive phases differently than rodents. The Consequence: Forcing a diurnal system into a non-gated metabolic state could accelerate stem cell depletion or dysfunction significantly faster than seen in nocturnal animal models. 2. Replacing Native Pulses with Constant Signals Natural States: Endogenous GLP-1, GIP, and glucagon are highly pulsatile. They spike rapidly in response to nutrients and drop just as quickly. The Retatrutide Shift: Retatrutide provides 24/7, high-affinity, continuous activation of all three receptors. Systemic Downregulation: Biology relies on pauses to reset receptor sensitivity. Constant, unyielding agonism eliminates the natural "resting" state of these pathways. 3. The Danger of "Non-Identical" Signals Altered Biasing: Retatrutide is not a perfect replica of native hormones; it is engineered with specific structural modifications to extend half-life and alter receptor affinity balances. Downstream Repercussions: By binding non-identically and permanently, it can trigger alternative intracellular signaling cascades (biased agonism) that bypass the body's natural negative feedback loops. The Ultimate Risk: Without circadian gating or pulsatile resets, the system faces chronic metabolic stress, potentially leading to accelerated cellular aging, organ-specific stem cell burnout, or irreversible receptor desensitization once the drug is withdrawn. Then there is the Blau study that showed stem cells are DESTROYED by these drugs. My first-principles bridge is entirely consistent with the biological trajectory: human muscle stem cells face a significantly higher risk of accelerated exhaustion under these conditions than nocturnal rodent models. The newly published data from the Stanford University Blau Lab demonstrates a direct, drug-specific impairment of muscle stem cells (MuSCs) caused by semaglutide. When you layer my previous point regarding circadian gating, constant signaling, and human diurnal physiology onto this new mechanism, the risk profile amplifies dramatically in humans. So Dr. Morse is wrong because he never took any of these things into account. His patients should be aware he sells half truths to them before trusting his centralized Rockefeller medicine inspired advice.

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Dave Feldman
Dave Feldman@realDaveFeldman·
Good morning, everyone (okay, those it's a "morning" to) We've had so many great comments on #TheCholesterolCode and I'm so very thankful for everyone's support. We also have new critiques, which is not too surprising -- but as always, I couldn't be more inviting toward productive exchanges on the science. On that note, it's worth a friendly reminder I've repeatedly and enthusiastically invited many of most prominent critics on the #FeldmanProtocol to chat with me directly. (And in at least six of those examples, we're offering to cover their travel costs too) To date, these invitations haven't been accepted, save one -- who definitely deserves recognition -- @Alexleaf. And indeed, we're planning to have him on again very soon. (He might even be the first to discuss the documentary with me from a more LDL-lowering perspective) I do want to get to one challenge in responding to critiques -- some sources suggest any/all mistakes found in our papers are not actually errors, they instead assume such issues are intentional efforts on the part of our authors, which include several career scientists, many with decades and hundreds (or in the case of Dr. Budoff, thousands) of papers to their names. Understandably, these career scientists prefer I not engage or "boost" these accusations by engaging with such sources. However, I think there's also a case in just taking time to addressing this more directly -- emphasizing why the suggestions being made have very little sound, rational basis given the level transparency we've provided that made detecting the issues in question possible (particularly when the source themselves concede this). The thing is, both supporters and critics find ways we can do better, and I want to acknowledge it when and where they are correct. Anyway, all of this is to say, the internal discussion is ongoing, but I hope to have something more to say on it soon.
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Dr. Jasmeet Kaur (PhD)
Dr. Jasmeet Kaur (PhD)@jasmeet481·
“Do you think food is the only reason blood sugar goes up?” Look at this CGM (Continuous Glucose Monitor) graph. This is from a healthy individual who was following a strict very low-carb diet. At the time of this glucose spike, he was fasting. He had not eaten anything. Yet, around noon, his blood glucose suddenly rose to nearly 150 mg/dL and then quickly came back to normal. If food was the only reason for blood sugar to rise, this spike shouldn’t have happened. So, what could have caused it? Our body can release glucose even when we haven’t eaten. This can happen due to: Stress Heat or temperature changes Pain or discomfort Excitement or anxiety Other normal physiological responses During these situations, stress hormones such as cortisol and adrenaline tell the liver to release stored glucose into the blood. In a healthy person, the pancreas quickly releases insulin, and blood sugar comes back to normal, as seen in this graph. Now here’s an interesting question: If this person had not been in a fasting state at that moment, would the body’s response to the same stressor have been the same, or would the glucose curve have looked different? We don’t know for sure. But when more than one stressor acts at the same time, their effects can add up. A stress response on top of an already active metabolic state may produce a different glucose pattern. This is why CGM is much more than a food tracker. It reflects what is happening inside your body, not just what is on your plate. So the next time you see a glucose spike, don’t ask only: “What did you eat?”, you may also ask, “What else was happening in your body at that time?” Food is just one part of the story. Sleep, stress, hormones, temperature, exercise, illness, and emotions can all influence blood glucose. Always interpret CGM data in the context of the whole person, not just the meal.
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Rick Audet
Rick Audet@RickyAudet·
@animaldocfilm x.com/i/status/20782…
Thomas N. Seyfried@tnseyfried

Our new paper presents a metabolic manifesto that can help curb the current epidemic of chronic diseases and cancer. We show how mitochondrial dysfunction is the root of many chronic diseases and most major cancers (doi.org/10.3389/fsci.2…). A quantitative scale of glucose ketone index (GKI) values linked to color-coded zones of health provides a cohesive readout for increasing adherence and reducing risk of chronic disease and cancer. Low GKI values can improve mitochondrial function thus reducing risk, while high GKI values can compromise mitochondrial function thus increasing risk. The GKI, used together with science-based nutrition and exercise, represents a novel therapeutic strategy for improving mitochondrial health regardless of age, gender, or genetic predisposition.

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animal.@animaldocfilm·
Otto Warburg won the Nobel Prize in 1931 for proving cancer cells feed on glucose. MD Anderson's cafeteria sells orange juice, banana bread, and pancakes to oncology patients. 93 years of ignoring a Nobel laureate is not a gap in knowledge.
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Rick Audet
Rick Audet@RickyAudet·
@animaldocfilm No offense but this seems like a really sloppy post. What does "fertility rate of 2.9" even mean? "Egg consumption: 277?" You can do better than this.
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animal.@animaldocfilm·
In 1965, American women had a fertility rate of 2.9. Average egg consumption: 335 per year. By 2023, fertility rate hit 1.62. Egg consumption: 277. Choline builds every fetal cell membrane. Nobody connected the drop.
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Dr. Stephen Hussey, DC
Dr. Stephen Hussey, DC@DrStephenHussey·
Here are some of the biggest reframes we need when it comes to the heart and heart disease: 1. Cholesterol/LDL is not the driver of artery plaque. PMID: 30198808 2. Lowering cholesterol/LDL with medications has not been shown to reduce the rate of heart attacks. PMID: 35285850 3. Elective stent and bypass procedures to "treat" stenosis/blockages have not been shown to reduce the risk of future heart attacks. PMID: 24958204, 21463150 4. The heart's role in the body is not to forcefully pump blood. PMID: 37856567, 26026358 5. Red meat and saturated fat do not increase the risk of heart disease or heart attacks. PMID: 32562735, 23902788 In medical school, doctors are taught many things that are wrong and not supported by the research. Critical thinking and questioning of dogma is also frowned upon. If an education didn't teach you to question your education, then it wasn't an education, it was an indoctrination. If you want to learn the actual causes of heart disease and how to prevent it, click the link below to learn more about my heart health mentorship program. stephenbhussey.com/register
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Mark Kaplan
Mark Kaplan@markkaplan20·
My top 10 blood test I would take immediately if I haven’t done any. These tests would provide the most important information around your metabolic health driving all these diseases.
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Mark Kaplan
Mark Kaplan@markkaplan20·
I think this chart should be framed and hung in every cardiologist’s office in the world. 60 trials. 323,950 patients. Every cholesterol-lowering drug ever made. They reduced LDL by up to 80%. Nobody lived longer. I sat in that chair. For 12 years my doctors tested my LDL every visit. Told me it was too high. Pressured me to take statins. Made me feel reckless for refusing. Not once did they test my fasting insulin. Not once in 12 years. At 52, I had a widowmaker heart attack. My LDL was “high.” My fasting insulin was through the roof. Nobody checked. 136,905 people hospitalized for heart disease. 75% had LDL their doctor would have called normal. Three out of four passed the test and had a heart attack anyway. (Sachdeva et al., American Heart Journal 2009) The system doesn’t need reform. It needs a disclosure notice on the wall. Right next to the diplomas.
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Mark Kaplan
Mark Kaplan@markkaplan20·
My cardiologist didn't prescribe a statin because he thought it would save my life. He prescribed it because he had to. His quality score depended on it. His reimbursement was tied to it. His insurance contracts required it. If my LDL was above the threshold and he didn't write the prescription, his performance metrics went red. Not mine. His. I spent three years wondering why every doctor I saw reached for the same drug. Then I looked at the system behind the prescription. What I found made everything make sense. Your doctor is not free. 🧵
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Isabella Cooper
Isabella Cooper@I_mitochondria·
Loved catching up with Dr Nasha Winters. We discussed what happens when you intentionally suppress ketogenesis, the current modern lifestyle intervention. This results in insulin-compensated euglycaemia (ICE), due to surpassing one’s own personalised hyperinsulinemia threshold (PIT). Understanding how to detect if someone is in the ICE-PIT allows for earlier intervention where things are easier to turn around. The PIT protocol to detect ICE: measure your evening pre-dinner at least three hrs fasted, glucose and ketones, for at least 7 days but optimally at least 21 days. If ketones are consistently <0.5 mM then you are in a metabolic endocrine phenotype of ICE and surpassed your PIT. If your GKI is above 4 consistently, you are in the ICE-PIT metabolic-endocrine phenotype range. If sustained over time, this has been shown to be associated with mitochondrial dysfunction which tracks with the development of chronic diseases and poorer ageing. Increasing insulin demand and exposure in the body has a significant negative effect on blood biomarkers associated with chronic disease and mitochondrial dysregulation. youtu.be/Ju9GefNeGuU
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Benjamin Bikman
Benjamin Bikman@BenBikmanPhD·
I chuckle when I hear people promoting “more efficient metabolism”. That’s the last thing you want if weight/fat loss is the goal! To burn more fat, you want fat cell metabolism to be less efficient—to be wasteful. In my lab, we’ve found that ketones can do this (like goBHB) and compounds in Yerba maté.
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David Diamond
David Diamond@LDLSkeptic·
As a follow-up to my post yesterday, I raised the issue of clotting factors as superior measures of CVD risk compared to LDL. In the film "Cholesterol Code", Dave Feldman was astonished to see that plaque was not well developed in the LMHRs and their subsequent research has shown that LDL does not correlate with plaque development. If he had paid attention to my presentations at CoSci or if he had read any of my papers he would not have been so astonished. Here is one slide of mine that shows one clotting factor, fibrinogen, is an age-independent risk factor for coronary heart disease and stroke. One would think that they should've assessed clotting factors in the LMHRs, but apparently, they did not. Why they didn't is a mystery to me. @BenBikmanPhD @DrPaulMason @Alabdulgaderaa @ifixhearts @FatEmperor @zoeharcombe @ProfTimNoakes @MaryanneDemasi @SinatraMD @DwightLundell @DiljanMansoor @markkaplan20 @KenDBerryMD @PeterJAnderson_ @ApoDudz @dramerling @ElieJarrougeMD @JeffryGerberMD @TuitNutrition @bigfatsurprise @GrassBased @shashiiyengar @drozcanyuce @SbakerMD @DominicDAgosti2 @ElieJarrougeMD @grahamsphillips @doctortro @bscherMD @BudoffMd @AdrianSotoMota @drjenunwin @drericwestman @lowcarbGP @_coach_al @nicknorwitz @lowcarbGP @realDaveFeldman
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Benjamin Bikman
Benjamin Bikman@BenBikmanPhD·
It’s funny and odd how conventional clinicians will happily prescribe a diabetes drug that lowers blood glucose by forcing the glucose out through the kidneys, but be upset at the thought of putting less glucose into the body in the first place (i.e., eating fewer carbs). For a disease defined by high blood glucose, it’s rational and effective to simply eat less glucose.
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