xep

joined 2 months ago
MODERATOR OF
[–] xep@discuss.online 1 points 1 day ago (1 children)

For someone called freedom advocate you sure don't sound like one.

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

It's oddly uncommon in my supermarket and twice the price of Aussie beef.

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

I'm primarily also eating Aussie beef and mix epsom salt for magnesium with mountain salt. What minerals do you supplement?

[–] xep@discuss.online 2 points 2 days ago* (last edited 2 days ago) (5 children)

I actually died of scurvy 3 weeks ago, since I stopped eating plants when I started carnivore 11 weeks ago. But then I got better!

 

Dr. Georgia Ede and Dr. Bret Scher discuss the recently released EAT-Lancet diet report.

I found it particularly interesting that they responded to the criticism of the first report by re-releasing it and removing the parts of the report that were criticised, without directly addressing the criticism.

Dr. Sher:

In advance of the release of the 2.0 [diet report], there was actually a release of the "mis-influencers" who have done an organized approach to discredit and attack EAT-Lancet. Their words, not mine. And you were listed as a very high-ranking member of this. So first, how does it feel to be labeled as a "misinfluencer"?

Dr. Ede:

It's interesting. I actually think it's a very good thing. And the reason why is clearly [that] the content that I produced that criticized the EAT-Lancet report came to their attention. I think that that's no small thing, and I would like to believe that the content that I and others produced had a lot to do with the fact that they felt the need to produce this report to try to discredit all of us. I think it may also have had something to do with the way the report was re-released. I noticed that certain things that I criticized about the report are no longer there, and I'm not the only one who produced content critiquing the report.

Also, there are certain concerns that I and others voiced about the content of the report, and it appears as though the authors have gone to great lengths to try to acknowledge and address [these concerns] without actually addressing them. But they're trying to make it look as though they're addressing these shortcomings.

SummaryTitle: Exposing the Truth Behind EAT-Lancet’s Diet Report & MisInfluencer Campaign

  • The EAT-Lancet report aims to control global dietary habits by promoting a plant-based diet for planetary health, but its scientific foundation is questioned.
  • The report's dietary recommendations are criticized for being nutritionally inadequate, particularly for vulnerable groups like pregnant women, children, and the elderly.
  • The EAT-Lancet diet is accused of disregarding the nutritional benefits of animal-based foods, which are essential for optimal human health, including brain development and mental health.
  • The report heavily relies on nutrition epidemiology, which is considered unreliable for making global dietary recommendations.
  • The EAT-Lancet diet is criticized for being overly restrictive and not accounting for individual differences in metabolism, genetics, and cultural food preferences.
  • The report's authors are accused of having conflicts of interest, as they are connected to major food corporations that produce ultra-processed foods and chemical fertilizers.
  • The EAT-Lancet diet is seen as an attempt to control people's eating habits, rather than promoting a flexible and inclusive approach to nutrition.
  • The report's dietary recommendations are criticized for being based on untested theories and guesswork, rather than solid scientific evidence.
  • The EAT-Lancet diet is accused of being environmentally unfriendly, as it does not adequately address the environmental impact of industrial plant food production.
  • The report's authors are criticized for labeling critics as 'mis-influencers' without providing substantial evidence to support their claims.
 

Loved the pictures of all the breeds of cow and also the description of how they've come about and what they taste like. I personally don't actually like A5 Wagyu that much, but plain old Japanese beef and not Wagyu I like a lot.

The colour of the fat showing how nutritious it is (yellow = grass fed) is a nice bit of knowledge to have! I'd also love to be able to dry age my own beef, but I think that's quite an endeavour. Would make a nice project to do on the side, maybe.

::: spoiler Results

[–] xep@discuss.online 2 points 4 days ago* (last edited 4 days ago) (1 children)

This is one of the things I was watching for myself, with the CGM. Turns out, if I eat to satiety (at 60 kg body weight without measuring lean mass, this takes about 650g of moderately fatty ground beef to do) I do get an increase in my blood glucose, at most up to about 110 mg/dL, and I can help it along with a cup of kefir.

In my case, if I drink even a single cup of cafe latte of some sort, that's 100 mg/dL guaranteed, right there. So if this spike is what I'm after, then I'd drink a glass of milk with my one meal of the day. It's dairy, though, so while I don't seem to have trouble tolerating it this may not be for everyone.

[–] xep@discuss.online 1 points 4 days ago* (last edited 4 days ago)

I propose we call a spade a spade:

"Deep fried potatoes, extruded, thin"

"Deep fried potatoes, chopped, thick"

"Deep fried potatoes, thinly sliced"

[–] xep@discuss.online 1 points 5 days ago* (last edited 5 days ago) (1 children)

Ten more days and I'll be three months in. I feel fantastic. My body weight has stabilized around 60 kg, give or take, but I can visibly see that I'm gaining muscle mass and therefore must be still losing fat somewhere. Which is unbelievable for me because I look very lean now, far beyond what I thought was possible for myself. Sometimes I wonder if it's not something temporary and have to check to make sure I'm still lean, like I'm in some kind of dream. I don't want to boast but I can see my abs.

The unusual dry-eye is very very sporadic now. I've noticed two major new improvements. One is that my tinnitus, which I've had since I was a child, is now so quiet that I don't notice it any more. The other improvement is I've always had cold hands and feet below 24'c. Since it was summer when I started carnivore I did not notice this, but it's finally autumn here and 22'c today. Not only are my extremities warm, I tried to put on some warmer clothes out of habit (it's called koromogae here) and had to take them off again because I felt too warm. I've never felt too warm in my entire life, only cold, so it feels unreal. I wouldn't even drink cold drinks in summer before; that's how averse I was to the cold.

Also, I cheated again a week ago and felt the consequences the next day; the joint pain in my the fingers of my right hand came back and stayed for three days. It's better now but it's unreasonable how incommensurate the effect of eating plants and refined sugars is. I didn't eat all that much!

 

I found this really pleasant to listen to so I thought I'd share. It's nice to hear someone talk about the fat loss, satiety, and all the other things that I also experienced when I went carnivore. Murray switched cold turkey and seems to have experienced some unpleasant effects like keto flu, but they resolved after a time.

Summary

  • The speaker discovered the carnivore diet through their son, who had successfully lost weight with it.
  • The speaker had a history of gout and other health issues, which were not effectively treated by conventional medicine.
  • A doctor suggested that diet was the root cause of many diseases, which led the speaker to try the Pritikin diet, resulting in weight loss but not complete gout relief.
  • The speaker initially doubted the carnivore diet but was convinced after seeing the positive results on their son and daughter-in-law.
  • Adopting the carnivore diet led to significant health improvements, including better mobility, reduced inflammation, and better sleep.
  • The speaker experienced a dramatic weight loss, going from 83 kg to 63.7 kg and maintaining a healthy weight around 64-66 kg.
  • The diet has resolved various health issues, including irritable bowel syndrome and bleeding bowels.
  • The speaker and their wife now follow a lifestyle change, including cooking outdoors and walking more, which has improved their overall well-being.
  • The speaker expresses skepticism towards the medical and food industries, believing they contribute to health problems.
  • The speaker views the carnivore diet as a miraculous and life-changing switch that has opened up new possibilities for their future health.

[–] xep@discuss.online 6 points 5 days ago

You can if you're a spider

[–] xep@discuss.online 9 points 6 days ago* (last edited 6 days ago)

Khalifa,

I don't know who you are. I don't know why you are asking. If you are looking for closure, I can tell you that I won't give you any. But what I do have are a very particular set of skills, skills I have acquired over a very long career. Skills that make me a nightmare for people like you. If you let this go now, that'll be the end of it. I will not look for you, I will not pursue you. But if you don't, I will look for you, I will find you, and you will know what a Marine Biologist does.

Regards

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

Apple’s never been on the bleeding edge of phone tech past 2010

Here's the M4 against the Snapdragon X Elite and an Intel processor for good measure: https://www.xda-developers.com/tested-apple-m4-vs-intel-lunar-lake-snapdragon-x-elite/

Edit: I was under the impression the M4 was in phones, it's not.

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

The Chinese government has thrown its weight behind Huawei's HarmonyOS. I wonder what the EU will do?

[–] xep@discuss.online 5 points 1 week ago (1 children)

I'm glad you have all this figured out!

 

Sony's AOSP on Xperia Open Devices page: https://developer.sony.com/open-source/aosp-on-xperia-open-devices

With the recent activity around Google restricting sideloading and not releasing device trees for Pixel, this is a possible alternative. I haven't tried it, but intend to switch to a Sony device for my next phone.

2
submitted 3 weeks ago* (last edited 3 weeks ago) by xep@discuss.online to c/ketogenic@discuss.online
 

There are only three available where I live, so I thought I'd start with my thoughts after having worn all three of them.

Let me start by stating that I wore the sensors as-is, without calibrating with finger-prick readings if calibration is available. I am not diabetic and do not rely on the sensors for accurate readings, so my opinions on these sensors should not inform your decision on which sensor to wear if you do.

Freestyle Libre 1, Abbott Laboratories

The first CGM I tried. Only supports NFC scanning, 6 hour history retention on-sensor. The sensor itself is pretty large and I experienced some aches wearing it. It may be because I didn't apply it properly since I wasn't expecting the loud sound the applicator made. The sensor lasts for 14 days and cost me 8000 yen, in a batch order of 2.

No real-time data and the 6 hour-only history meant gaps in my readings overnight, but I still think that it is alright. Still better than no CGM at all if this is the only sensor available.

Freestyle Libre 2, Abbott Laboratories

I'm wearing this one right now. The sensor is smaller than the Libre 1 and it now supports per-minute live readings via BT. The history retention is longer and I no longer see gaps in overnight readings, but since it updates live that's also less of a concern. The sensor's readings also aren't very noisy compared to the G7. The sensor lasts for 14 days and cost me 7500 yen, in a batch order of 4.

I like this one the best so far, and I haven't noticed any discomfort wearing it yet.

G7, Dexcom

The sensor is an oblong shape and is smaller than the Libre 1 and about the same size as the Libre 2, but longer. The adhesive is much wider and so it feels larger when worn. This was the most uncomfortable one of the three for me. I experienced a lot of aching while wearing this sensor.

The G7 supports live readings every 5 minutes over BT, with a (I think?) 24 hour history on the sensor itself. The readings are quite noisy, and fluctuate up and down a lot. Also, they appear to read generally higher than the Libre1/2, such that my baseline is about ~10% (90) more than on the Libre.

I like the G7 better than the Libre 1, but less than the Libre 2. It is the cheapest of the three, at 6500 yen in a batch of three, but it also only lasts for 10 days.

Phone Apps

LibreLink

The official LibreLink app for the Libre sensors is usable. There is no dark mode, and the amount of detail on the charts aren't user definable. This is probably fine if only used to check immediate readings, but as someone interested in statistics and historical readings I'd use an open source alternative if possible.

Dexcom G7 App

This thing doesn't run on my phone, so I can't review it. I had to use XDrip+ with my G7 sensor.

XDrip+

Open-source app that worked seamlessly with the Dexcom sensor. It's got highly customisable display and alert settings, plus all history data and settings can be exported so it can easily be backed up. It also has a nice widget and a detailed high priority notification display on Android.

It only works on my Libre 2 with Juggluco as a Eversense source. My guess is the OOP2 companion app required does not work with the Japanese Libre 2, since it displays NFC Invalid Data errors. Thankfully, Juggluco can take its place.

This is my preferred app for CGM readings.

Juggluco

By itself I've found this app clunky and hard to use, but it is able to set-up and pair with the Libre 2 sensor easily. In the settings, there is an option to enable Eversense broadcasting so it can send data to XDrip+, turning it into a replacement for OOP2.

 

Maybe a continuous insulin monitor isn't far off the horizon. Unfortunately paywalled.

 

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.

 

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.

view more: next ›