xep

joined 3 weeks ago
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[–] xep@discuss.online 2 points 1 day ago

Or does it need periodic fasting?

Based on what I know now, it sounds to me like periodic fasting sufficient to encourage autophagy is a good practice to have in any diet.

[–] xep@discuss.online 1 points 1 day ago* (last edited 1 day ago) (1 children)

If the government owns every company, maybe you have communism, but most likely what you have is autocracy. If the government owns a 10% stake of one company, that's some nationalisation. There are good reasons for it in capitalism, such as for regulating natural monopolies. I'm not sure Intel falls into "good reasons,' since it appears to me to be some kind of corruption.

[–] xep@discuss.online 2 points 2 days ago* (last edited 2 days ago)

If your frying something without sugar, where does the glycation come from?

I'm guessing implicitly he means don't fry foods containing sugars at high heat, not sure how you'd glycate it otherwise.

Saunas are black boxes

Ha, I see what you did there.

[–] xep@discuss.online 2 points 2 days ago (2 children)

but with devices like air fryers, for example, I’m totally against them because they create advanced glycation end products.

I really like my convection oven :(

Triglycerides are a very good clue. If your triglycerides are absolutely normal—and normal is not less than 150—remember, we fudged a lot of the numbers. It's not 150; it's less than 100. That's normal. It's just that the population today has so much triglycerides that they put the level at that—just like your liver enzymes. When I was in training, liver enzymes greater than 25 were abnormal. Now it's 45 because everyone's got a fatty liver, so they just bumped it up. How daft is that?

Also unfortunately indirectly harming people.

For example, I'll tell you about myself: my "LDL" level is about 170-something—large particles, calcium score zero. My triglycerides are 80; "HDL" 75. That's what you want. You want a good, high "HDL" and a nice, low triglyceride. Then the "LDL" is going to take care of itself. You're going to have large, fluffy particles, and you can test for it. Someone like me—I'm going to test coronary calcium. With my coronary calcium score being zero, I know I'm going to be okay.

I should try to get coronary calcium as part of my yearly medical.

Mycotoxins, phthalates, glyphosate, herbicides, pesticides, and heavy metals all cause inflammation and impair mitochondrial function.

My personal opinion is that it's very likely plant toxins do too.

A major study from Finland showed that people with severe coronary disease who used a regular (not infrared) sauna three times a week had a 40%–50% reduction in sudden cardiac death. If I had a drug that did that, it would be a bestseller. Those who used a sauna five days a week had about a 60% reduction. These findings have been published, but they rarely make the news. Still, sauna clearly offers benefits.

Some argue that sauna raises body temperature and increases heart rate by about 30%, making it comparable to low-level exercise. Maybe. Another likely reason is detoxification, as toxins are excreted through sweat.

I really ought to start.

You can address all these different inflammatory pathways: the endocrine system, the liver, leaky gut, toxins, metals, lifestyle. But there's one thing that touches all the mechanisms and improves them all, and that's fasting.

Glad I started.

I teach patients how to breathe—breathing exercises, breathing in—and how to go into silence. I teach them to cultivate mental, internal silence. That is anti-inflammatory because you’re not sending those messages to the platelets; there is no message when you’re in silence.

I had no idea meditation was anti-inflammatory!

[–] xep@discuss.online 2 points 2 days ago

Our thesis is that when it comes to plaque or blood clots, inflammation is at the root, and this is a systemic process.

I found that 70% of the patients with what they call prediabetes had extremely high insulin levels. So, in spite of decent sugars, they had so much insulin. That identified a whole group of patients at extremely high risk of having a new event—another stent, progressive disease, increasing coronary calcium, heart attacks. So your metabolic condition matters. The biggest metabolic condition I found was prediabetes.

I can walk into the room and tell which patient has fatty liver and visceral fat—and therefore is metabolically abnormal and likely has high insulin levels.

What I often call “leaky gut”—more precisely, intestinal permeability—also plays a role, because inflammation from the gut is first processed in the liver.

You can be inflamed because of your lifestyle. Generally speaking, you’re inflamed because you’re nutritionally insufficient, so you can’t handle even normal stresses, and you develop inflammatory stress responses.

I’ve evolved to include toxicity workups as part of my plans, and I’ve mapped out the biochemical pathways by which toxicity creates atherosclerosis and inflammation in the body. So if you’re heavy-metal toxic, if you have a lot of mycotoxins from mold, if you have a lot of glyphosate, other herbicides and pesticides, plastics, BPA, and phthalates in your body—they don’t belong there. You didn’t evolve with them. Evolution did not include them. Your body’s chemistry—this is common sense, but we don’t want to accept it because we’re so used to this Western lifestyle—was not designed for those chemicals. They’re not supposed to be in your body, and you do not have the mechanisms to cope with them.

The next cause of small, dense LDL is omega-6. If you eat a lot of vegetable oils, it’s almost guaranteed that those oils enter normal LDL, displace cholesterol, and take up space. Now you’ve created small, dense LDL: cholesterol is gone and replaced by omega-6. Omega-6 is pro-inflammatory. That’s why none of my patients eat vegetable oils.

The most compelling case for me for being on a LCHF diet is the fact that multiple independant medical practicioners and researches, in various fields of expertise, have remarkably consistent experiences, theories, and approaches to treating chronic inflammation and improving metabolic health. It makes such a strong case.

[–] xep@discuss.online 2 points 2 days ago* (last edited 2 days ago) (1 children)

Atherosclerosis, or plaque, is not a focal disease. It’s a systemic disease. If you’ve got it in one artery, guess what? You’ve got it in every artery—and you may think you don’t.

A bit terrifying.

Why am I stressing this? Because if you don’t want to develop plaque, don’t want plaque progression, and don’t want the consequences of plaque formation and rupture, you need to know the cause. It’s inflammatory. It’s not linear. It’s not just a scar that keeps growing. It cracks, repairs, cracks, repairs. It’s all related to inflammation. What is your inflammatory status? We are becoming increasingly inflammatory as humans. That’s why this happens. The body reacts, and you get inflammation.

Plaques are both caused by inflammation and inflammatory.

There are two parts to this whole problem. One is plaque formation and plaque rupture—that’s all about the plaque. The next is your blood. If your blood is clotty and your platelets are very jittery, you’re going to get a big blood clot. It’s as much a hematological event as it is an inflammatory process. There are two parts to this equation. That’s why we started paying more attention to the condition of your blood. Do you have clotty blood? Because if you rupture a minor plaque, you can get a big blood clot.

I wonder if grounding, which can decrease the viscosity of blood, can help? Blood donation also helps.

With aggressive lifestyle, dietary, and environmental changes—reducing toxicity, improving your food, and everything else—you can regress it. But the extent—probably the percentage stenosis—is likely very low. That means you can reduce it by maybe 10%.

Unfortunately it seems that lifestyle changes cannot reverse plaque entirely, and it also has to be managed by reducing inflammation as much as possible.

 

Summary


Detailed summary — "The Real Cause of Clogged Arteries and how fasting can help"

  • Core claim: Atherosclerosis (clogged arteries) is primarily driven by chronic inflammation, not merely passive cholesterol deposition, and plaque is a metabolically active, inflammatory process that can rupture and cause heart attacks.

  • Primary triggers that cause vascular inflammation:

    • Metabolic dysfunction (insulin resistance, prediabetes) which promotes harmful lipid profiles including small, dense LDL.
    • Dietary factors (processed foods, high omega‑6 intake, advanced glycation end products) that drive inflammation and oxidative stress.
    • Toxins and impaired detoxification, which increase systemic inflammatory burden.
    • Gut problems (e.g., leaky gut / dysbiosis) that seed inflammation systemically.
    • Lifestyle stressors (poor sleep, chronic stress) that amplify inflammatory cascades.
  • Nature and consequence of plaque: Plaque is described as an inflammatory, metabolically active lesion; when plaque becomes unstable and ruptures the ensuing clot formation leads to heart attacks — so reducing inflammation and stabilizing plaque is central to preventing acute events.

  • How fasting counteracts the causes (mechanisms):

    • Lowers insulin levels, improving insulin sensitivity and reducing production of small, dense LDL, thereby decreasing a major driver of inflammation and atherogenesis.
    • Stimulates autophagy and mitophagy, promoting cellular and mitochondrial cleanup which reduces oxidative stress and inflammatory signaling.
    • Supports detoxification by enhancing liver processing and elimination of toxins that contribute to vascular inflammation.
    • Resets gut health, helping reduce inflammation originating from a leaky or dysbiotic gut.
    • Promotes ketogenesis and fat mobilization during extended fasting, which is framed as anti‑inflammatory and metabolically beneficial.
    • Overall effect: fasting lowers measurable inflammatory markers, improves metabolic health, and creates conditions that can halt or reverse drivers of plaque progression.
  • Practical fasting approaches recommended:

    • Time‑restricted feeding as a daily lifestyle (example: 18:6, eat within 6 hours, fast 18 hours).
    • Periodic prolonged fasts (example: a 3‑day water fast done periodically — cited as helpful for metabolic reset, stem cell mobilization and deeper detoxification; suggested timing varies by individual needs).
    • Use of fasting to achieve ketosis for added anti‑inflammatory and fat‑mobilizing effects.
  • Overall strategy and expectations: Adopt an anti‑inflammatory lifestyle (fasting, improved diet, sleep, stress management, and addressing toxins/gut health) to manage plaque — the goal is usually to prevent progression and rupture rather than promise complete elimination of existing plaque; with these measures individuals can often live with plaque without experiencing fatal events.

  • Takeaway (concise): Targeting systemic inflammation and metabolic dysfunction — with fasting as a central tool among dietary and lifestyle interventions — is presented as the most effective approach to preventing plaque progression and reducing risk of heart attacks.

Dr Jamnadas shares his experience holistically treating patients with heart disease. There is a lot of content, and it's hard to do a write-up when all of it is interesting, so I'd recommend watching the video to anyone who's even at all interested in managing heart disease and staying healthy, since there is a lot of actionable advice.

[–] xep@discuss.online 2 points 2 days ago

but with devices like air fryers, for example, I’m totally against them because they create advanced glycation end products.

I really like my convection oven :(

Triglycerides are a very good clue. If your triglycerides are absolutely normal—and normal is not less than 150—remember, we fudged a lot of the numbers. It's not 150; it's less than 100. That's normal. It's just that the population today has so much triglycerides that they put the level at that—just like your liver enzymes. When I was in training, liver enzymes greater than 25 were abnormal. Now it's 45 because everyone's got a fatty liver, so they just bumped it up. How daft is that?

Pretty damn daft, unfortunately, and indirectly harming far too many people.

For example, I'll tell you about myself: my "LDL" level is about 170-something—large particles, calcium score zero. My triglycerides are 80; "HDL" 75. That's what you want. You want a good, high "HDL" and a nice, low triglyceride. Then the "LDL" is going to take care of itself. You're going to have large, fluffy particles, and you can test for it. Someone like me—I'm going to test coronary calcium. With my coronary calcium score being zero, I know I'm going to be okay.

Too bad I can't get coronary calcium as part of my yearly medical.

Mycotoxins, phthalates, glyphosate, herbicides, pesticides, and heavy metals all cause inflammation and impair mitochondrial function.

My personal opinion is that it's very likely plant toxins do too.

A major study from Finland showed that people with severe coronary disease who used a regular (not infrared) sauna three times a week had a 40%–50% reduction in sudden cardiac death. If I had a drug that did that, it would be a bestseller. Those who used a sauna five days a week had about a 60% reduction. These findings have been published, but they rarely make the news. Still, sauna clearly offers benefits.

Some argue that sauna raises body temperature and increases heart rate by about 30%, making it comparable to low-level exercise. Maybe. Another likely reason is detoxification, as toxins are excreted through sweat.

I really ought to start.

You can address all these different inflammatory pathways: the endocrine system, the liver, leaky gut, toxins, metals, lifestyle. But there's one thing that touches all the mechanisms and improves them all, and that's fasting.

Glad I started.

I teach patients how to breathe—breathing exercises, breathing in—and how to go into silence. I teach them to cultivate mental, internal silence. That is anti-inflammatory because you’re not sending those messages to the platelets; there is no message when you’re in silence.

I had no idea meditation was anti-inflammatory!

[–] xep@discuss.online 1 points 2 days ago (1 children)

Our thesis is that when it comes to plaque or blood clots, inflammation is at the root, and this is a systemic process.

I found that 70% of the patients with what they call prediabetes had extremely high insulin levels. So, in spite of decent sugars, they had so much insulin. That identified a whole group of patients at extremely high risk of having a new event—another stent, progressive disease, increasing coronary calcium, heart attacks. So your metabolic condition matters. The biggest metabolic condition I found was prediabetes.

I can walk into the room and tell which patient has fatty liver and visceral fat—and therefore is metabolically abnormal and likely has high insulin levels.

What I often call “leaky gut”—more precisely, intestinal permeability—also plays a role, because inflammation from the gut is first processed in the liver.

You can be inflamed because of your lifestyle. Generally speaking, you’re inflamed because you’re nutritionally insufficient, so you can’t handle even normal stresses, and you develop inflammatory stress responses.

I’ve evolved to include toxicity workups as part of my plans, and I’ve mapped out the biochemical pathways by which toxicity creates atherosclerosis and inflammation in the body. So if you’re heavy-metal toxic, if you have a lot of mycotoxins from mold, if you have a lot of glyphosate, other herbicides and pesticides, plastics, BPA, and phthalates in your body—they don’t belong there. You didn’t evolve with them. Evolution did not include them. Your body’s chemistry—this is common sense, but we don’t want to accept it because we’re so used to this Western lifestyle—was not designed for those chemicals. They’re not supposed to be in your body, and you do not have the mechanisms to cope with them.

The next cause of small, dense LDL is omega-6. If you eat a lot of vegetable oils, it’s almost guaranteed that those oils enter normal LDL, displace cholesterol, and take up space. Now you’ve created small, dense LDL: cholesterol is gone and replaced by omega-6. Omega-6 is pro-inflammatory. That’s why none of my patients eat vegetable oils.

The most compelling case for me for being on a LCHF diet is the fact that multiple independant medical practicioners and researches, in various fields of expertise, have remarkably consistent experiences, theories, and approaches to treating chronic inflammation and improving metabolic health. It makes such a strong case.

[–] xep@discuss.online 1 points 2 days ago (2 children)

Things I found particularly interesting:

Atherosclerosis, or plaque, is not a focal disease. It’s a systemic disease. If you’ve got it in one artery, guess what? You’ve got it in every artery—and you may think you don’t.

A bit terrifying.

Why am I stressing this? Because if you don’t want to develop plaque, don’t want plaque progression, and don’t want the consequences of plaque formation and rupture, you need to know the cause. It’s inflammatory. It’s not linear. It’s not just a scar that keeps growing. It cracks, repairs, cracks, repairs. It’s all related to inflammation. What is your inflammatory status? We are becoming increasingly inflammatory as humans. That’s why this happens. The body reacts, and you get inflammation.

Plaques are both caused by inflammation and inflammatory.

There are two parts to this whole problem. One is plaque formation and plaque rupture—that’s all about the plaque. The next is your blood. If your blood is clotty and your platelets are very jittery, you’re going to get a big blood clot. It’s as much a hematological event as it is an inflammatory process. There are two parts to this equation. That’s why we started paying more attention to the condition of your blood. Do you have clotty blood? Because if you rupture a minor plaque, you can get a big blood clot.

I wonder if grounding, which can decrease the viscosity of blood, can help? Blood donation also helps.

With aggressive lifestyle, dietary, and environmental changes—reducing toxicity, improving your food, and everything else—you can regress it. But the extent—probably the percentage stenosis—is likely very low. That means you can reduce it by maybe 10%.

Unfortunately it seems that lifestyle changes cannot reverse plaque entirely, and it also has to be managed by reducing inflammation as much as possible.

[–] xep@discuss.online 2 points 3 days ago* (last edited 3 days ago) (1 children)

The vast majority of the content on there is a conservative echo chamber.

TIL. It's always rather amusing as someone outside of America that posts containing factual information get downvotes purely based on the perceived alignment of the subject on the zero-nuance American Political Spectrum. I block ads, so I wouldn't know.

[–] xep@discuss.online 3 points 3 days ago

Really curious about what this leads to. We also know that plants can signal each other via the mycelium, they have awareness of their surroundings and events, just not in the same way we do.

[–] xep@discuss.online 1 points 3 days ago (3 children)

What about Rumble? GN is on there and directly supportable.

 

Summary

  • Brain aging follows a nonlinear trajectory with distinct phases, including a critical window in midlife (ages 40-60) where metabolic interventions may be most effective.
  • The onset of brain aging is marked by increased insulin resistance, which disrupts neuronal glucose metabolism and contributes to cognitive decline.
  • Ketones, which bypass insulin resistance, can stabilize brain networks and potentially reverse early aging effects, particularly in the midlife critical window.
  • The study identifies specific genes (GLUT4, MCT2, APOE) associated with brain aging patterns, highlighting the role of neuronal insulin resistance and ketone transport.
  • Brain network destabilization accelerates after age 40, with the most rapid changes occurring between ages 60-70, indicating a critical period for intervention.
  • The effects of ketones on brain network stability are most pronounced in individuals aged 40-59, suggesting a limited window for effective metabolic intervention.
  • The study suggests that early metabolic stress in neurons, due to insulin resistance, can lead to irreversible damage if not addressed promptly.
  • Gene expression analysis supports the role of insulin resistance in brain aging, with GLUT4 and MCT2 emerging as key factors.
  • The study's findings align with broader aging biomarkers, linking molecular mechanisms to neurobiological outcomes.
  • The research emphasizes the importance of early intervention in brain aging to prevent or delay cognitive decline and neurodegenerative diseases.

Remarks in no particular order:

While suggestive, one obvious caveat of this approach is that the minimally invasive and clinically ubiquitous physiological biomarkers most likely to be available in lifespan studies (e.g., HbA1c, BP, CRP) are not the most sensitive mechanistically.

BP can fluctuate easily and Hba1c is a weighted average of glycation, using an estimated 117 days for men and 106 days in women. Glucose levels on days nearer to the test contribute substantially more to the level of A1c than the levels in days further from the test. If the lifespan of the RBC are not near the average, then the reading will be skewed.

In contrast, blood CRP, indicative of inflammation, showed no significant changes around either landmark. n.s., not statistically significant

Curious that this marker inflammation would be have no statistical significance for brain network instability.

Further supporting the physiological biomarker and gene expression results, we demonstrated that an acute intervention that bypasses neuronal insulin resistance was able to reverse the aging effects. In this case, the fact that ketosis was induced within minutes was key in isolating mechanisms.

It is not clear if they also studied people who eat a diet that would result in more ketosis, or if they only induced ketosis in the participants of the study using exogenous ketones.

While our results implicate metabolic changes as occurring prior to vascular and immune changes, it is also important to consider that neuronal insulin resistance may itself be caused by even earlier age-related changes in neuronal mitochondrial functioning (74, 75)—an important topic for future research.

To be safe, probably best to start being metabolically healthy earlier rather than later.

Meanwhile, in agreement with our previous results in young adults, the glucose bolus calorically matched to each participant’s D-βHB dose did not show stabilizing effects in any of the age groups (Fig. 3C), indicating that the results were specific to non-GLUT4 (and thus noninsulin) mediated pathways.

Our body does not appear to need external sources of glucose to stabilize the networks in our brain.

One key conceptual challenge with devising a strategy for early intervention in brain aging is that the process involves many mutually interacting and reinforcing mechanisms.

Nice that they recognize that reductivism leads to poor conclusions.

For example, mitochondrial dysfunction can generate excessive reactive oxygen species that damage vascular endothelium and activate inflammatory pathways (61). This vascular damage is exacerbated by age-related reductions in cerebral blood flow, which compromise the delivery of nutrients and removal of metabolic waste products (62). The resulting tissue stress triggers microglial activation and promotes chronic low-grade inflammation or “inflammaging,” characterized by elevated proinflammatory cytokines that further impair metabolic and vascular function.

Very succinct summary of metabolic syndrome.

Blood–brain barrier dysfunction emerges as a critical nexus in this interaction, as it affects immune cell trafficking, metabolic substrate availability, and overall brain homeostasis (64). These changes are further complicated by cellular senescence, which affects all three systems through the senescence-associated secretory phenotype (SASP), promoting sustained inflammation and tissue dysfunction (65). This intricate interplay creates self-reinforcing cycles where dysfunction in one system can propagate through the others, potentially accelerating cognitive decline and increasing susceptibility to age-related neurological diseases.

Postulated mechanism for brain network instability as a result of MetS.

Dense paper that took me a while to get through, but worth the read.

 

Personal anecdote: I'm now one month into eating an animal-sources only diet. I eat mainly steaks that I sous vide, and about twice a week I'll eat oily fish, chicken, or pork.

I'd say that I'm currently about 95% adherent. I still drink lattes, and when I'm outside drinking with my friends I don't restrict what foods I eat, although I'll try to politely decline carbohydrates, vegetables, and sweet alcoholic drinks or beer. I really enjoy cooking and baking, and I do miss being able to cook most of what I used to, so that's a little bit of a downside. On the upside, my kitchen has been greatly simplified.

Based on a test I've done today, in mg/dl, my LDL is 212, Tg 98, and HDL 66. My doctor expressed concern about LDL but was happy to observe for a few more months, although he did float the idea of statins. I told him that with my 120/70 BP and ideal waist/height ratio that I'd prefer to wait and see, and he agreed. My tg/hdl ratio of 1.48 was not discussed, although it suggests to me that there isn't anything to worry about.

I found this discussion between Prof. Bart Kay and Dr. Sean Patterson about cholesterol levels helpful, so I'm linking it here:

Summary

  • The speaker discusses their high cholesterol levels and the medical community's approach to diagnosing and treating elevated cholesterol.
  • Cholesterol is a crucial molecule for the human body, serving multiple purposes, and its levels are often pathologized by the pharmaceutical industry.
  • HDL and LDL are not different types of cholesterol but rather lipoproteins that transport cholesterol and other lipids in the bloodstream.
  • The body's lipoprotein levels are regulated by genes that have evolved over billions of years to ensure long-term survival.
  • Doctors often pathologize elevated cholesterol levels based on arbitrary thresholds set by the medical and pharmaceutical industries.
  • The speaker questions whether their high cholesterol levels are a cause for concern or if they are simply a marker of underlying health issues.
  • Chronic inflammation, glycation, and oxidation are the root causes of heart disease, not elevated cholesterol levels.
  • Atherosclerosis is an immune dysfunction caused by chronic systemic inflammation and damage to the vascular epithelial cells.
  • Blood pressure and turbulence in the blood flow due to vessel bifurcations contribute to the development of atherosclerotic lesions.
  • The speaker emphasizes the importance of addressing the root causes of heart disease rather than focusing solely on cholesterol levels.

Another video that's been helpful is the one by Dr. Mason, about blood test results on a ketogenic diet. :

Summary

  • Dr. Paul Mason discusses the interpretation of cholesterol blood tests and the significance of different types of lipoproteins.
  • Cholesterol tests measure lipoproteins, which carry fats around the body, and not just cholesterol itself.
  • There are five major classes of lipoproteins, with VLDL, IDL, LDL, and HDL being the most relevant for health.
  • LDL (low-density lipoprotein) can be healthy or damaged; damaged LDL is linked to heart disease.
  • Damaged LDL is caused by exposure to sugar (glucose), leading to glycation and oxidation, making it small and dense.
  • Standard cholesterol tests often estimate LDL levels, which can be inaccurate; more precise methods involve centrifuging blood samples.
  • High LDL particle count is a better predictor of heart disease than total LDL volume.
  • Damaged LDL can accumulate in blood vessels, leading to atherosclerosis and heart disease.
  • Triglyceride and HDL levels can help determine if someone has a healthy (Pattern A) or unhealthy (Pattern B) LDL profile.
  • The triglyceride-to-HDL ratio is a useful metric for assessing cardiovascular risk.
  • The Feldman protocol suggests that a high-fat diet for three days can significantly lower LDL levels by increasing LDL receptor activity.

Edit: apologies for the placeholder URL, I'd originally intended to only post one youtube video but then decided to do a write-up instead and I don't know how to remove it.

 

I tried fermenting Kefir yesterday. Put some store-bought freeze dried Kefir powder and put them in a 1L tetrapak carton of pasteurized milk, and then I left it for ~24h. Ambient temperature is currently around 28-30'c.

When I opened the milk carton today the Kefir was almost entirely solid and I was unable to pour it out of the carton. I managed eventually to move it to the bottle by scraping it out of the carton, where it now rests.

I've put about 200 ml of milk in a small glass jar and because I was unable to find any grains, added 2 tbsp of the kefir to the glass jar. I wonder if this will let me continue fermenting without using another packet of freeze dried Kefir?

If anyone has any advice about how I should go about doing this I'd really appreciate it.

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