jet

joined 2 years ago
MODERATOR OF
[–] jet@hackertalks.com 3 points 2 weeks ago (4 children)

https://rentry.co/NSFW-Checkpoint

Not deleted, just they put up a speed bump

[–] jet@hackertalks.com 2 points 2 weeks ago (1 children)

I can't speak to soap, but rendering tallow for food purposes, the impurities can smell a bit wiffy. If I'm trying to render all the cow smell away I have to do the render and filter cycle 3ish times

[–] jet@hackertalks.com 3 points 2 weeks ago (2 children)

I always thought it was a choice for tdw and heat concerns. Intel tends to run a bit cooler (used to)

[–] jet@hackertalks.com 5 points 2 weeks ago (2 children)

Is this about memes?

[–] jet@hackertalks.com 2 points 2 weeks ago (1 children)

How the hell did the medical community go so sideways since then?

From what i've read the doctors who were uncovering the hormonal model of health in the 1930s were German and publishing in German based literature. After the world unpaused in the 1940s there wasn't much enthusiasm in the west for German publications.

Dr. Barry Sears (Biochem PhD, not MD) wrote about all this in the early 90’s in “The Zone” (with references).

Would you recommend reading that book?

[–] jet@hackertalks.com 8 points 2 weeks ago* (last edited 2 weeks ago) (2 children)

Calories are a useful approximation, but not how humans actually operate. A Bomb Calorimeter burns material and the resultant heat generated is what we call a calorie. As a illustrative example of the difference - gasoline is very calorie dense, but not helpful if eaten by a human.

do I gain the calories over the next few hours? Or is it delayed a day or two?

The human body will break down all food and drink into its base components then decide what it will keep, what it will excrete (more or less). So when you consume something you "gain" it immediately (its in your system), the time until its used in the body could be minutes (like carbohydrates), hours (fibre), etc. Often the body will decide to store any excess (carbs again) for later use (weight gain).

Because there will be days when I eat almost NOTHING, and then my scale says I gained 3 lbs. But then there’s other days where I feel I ate like a slob, and somehow lost 2 lbs.

The human body is an amazing homeostatic machine, it's trying to self regulate to optimal body composition. The trouble is lots of modern western food messes with the bodies ability to self regulate..... which brings us to the real topic

Losing weight is hard, but it might be easier if I understood the rules of how this all works.

The big secret is hormones, don't interfere with your hormones and the body will self regulate body composition to optimal (lose weight if your obese).

[Paper] The Carbohydrate-Insulin Model of Obesity - Beyond “Calories In, Calories Out” - 2018

TLDR - Eating sugar and carbohydrates forces blood glucose levels to rise (within minutes), elevated blood glucose forces insulin to rise (to reduce blood glucose), elevated insulin forces the body to go into anabolic (gain weight) state. Basically you can't lose any fat while your insulin is high, so every time someone eats a bunch of sugar or carbohydrates with a meal/snack they are putting a 2-4 hour pause on any fat loss.

[–] jet@hackertalks.com 5 points 2 weeks ago* (last edited 2 weeks ago) (7 children)

The importance of this cannot be understated, humans are amazing hormonal machines. Hormones control every aspect of our biology. The hormonal insulin model has dramatic application to human health and specifically obesity / insulin resistance / metabolic health.

TLDR: Insulin is the cause of almost all obesity you see. Carbohydrates drive blood sugar, blood sugar drives insulin, insulin drives weight gain. As a good example - T1Ds who don’t take their insulin wont gain weight, no matter how much they eat..

Notes:

rates of obesity remain intractably high despite intensive focus on reducing calorie intake (eat less) and increasing calorie expenditure (move more), with major implications to well-being, life-expectancy, and health care costs.

this model considers fat cells as central to the etiology of obesity, not passive storage sites of calorie excess.

Insulin decreases the circulating concentration of all major metabolic fuels by stimulating glucose uptake into tissues, suppressing release of fatty acids from adipose tissue, inhibiting production of ketones in the liver, and promoting fat and glycogen deposition.

Insulin is a super hormone, when its elevated the body stops feeding itself and stores everything.

inadequate insulin treatment of type 1 diabetes and drugs that inhibit insulin secretion cause weight loss.

Dietary fat has little direct effect on insulin, providing a theoretical basis for the efficacy of high-fat diets.

the carbohydrate-insulin model of obesity (CIM) proposes that a high-carbohydrate diet—including large amounts of refined starchy foods and sugar, as commonly consumed in the lowfat diet era—produces postprandial hyperinsulinemia, promotes deposition of calories in fat cells instead of oxidation in lean tissues, and thereby predisposes to weight gain through increased hunger, slowing metabolic rate, or both

Carbs/Sugars drive weight gain and hunger, its a vicious cycle.

calorie restriction can be viewed as symptomatic treatment, destined to fail for most people in the modern food environment. Low-calorie, low-fat diets may actually exacerbate the underlying metabolic problem by further restricting energy available in the blood—triggering the starvation response comprised of rising hunger, falling metabolic rate, and elevated stress hormone levels

People eating a high carb diet are always hungry because all of their internal stored energy (fat) is unavailable to them. They are always starving even though they have plenty of fat.

Even when calorie-restricted to prevent excessive weight gain, insulin-treated animals still developed excessive body fat consistent with a prediction of the CIM regarding fuel partitioning

CICO / Eat Less Move More - Would say that the food doesnt matter, but in animals adding insulin without changing the diet causes weight gain! This disproves the simplistic CICO advice of weight loss.

calorie restriction to prevent excessive weight gain in animals on a high-GI diet did not prevent excessive adiposity or the associated cardiometabolic risk factors

If the insulin is elevated (carbs/sugar in the diet) even calorie restriction does not prevent obesity in animals.

[–] jet@hackertalks.com 2 points 2 weeks ago (1 children)

The only thing unhealthy in your neighbors diet is the sugar substitute in the coke zero. If he reduced his obesity down to a normal weight, his life has massively improved.

should eat their veggies

This is the party line, but its actually up for debate because the actual scientific literature doesn't have evidence that this is necessary.

I’m still thinking that can’t be healthy, but he does look healthier in comparison to morbidly obese.

Carnivores (which it sounds like your neighbor is) tend to be very data focused, ask if he would share his health metrics with you (lipid panel, hba1c, etc)... When you look at those metrics you will have to decide what "healthy" means (what outcomes you care about)

[–] jet@hackertalks.com 2 points 2 weeks ago (2 children)

If you know of a link to the full paper, I'd love to read it

[–] jet@hackertalks.com 1 points 2 weeks ago

Blue prince is a wonder experience! I'm glad your enjoying it.

[–] jet@hackertalks.com 4 points 2 weeks ago* (last edited 2 weeks ago)

This was one of the papers referenced in @xep@fedia.io 's cholesterol paper from a few days ago. Thought it was interesting for its own post.

Notes:

evidence from the Kuopio Ischemic Heart Disease Risk-Factor Study suggested that egg protein intake was associated with significantly reduced risk for T2D in Finnish men [6].

Subjects who were pregnant, planning to be pregnant during the study period, lactating, or of child-bearing potential and unwilling to commit to the use of a medically approved form of contraception throughout the study period were also excluded.

That really complicates analysis, if someone is using hormonal birth control that will change the hormones, but also if they start it for the study then it's skewing the results.

However, HOMA-IR was significantly increased following the Non- Egg (24.4%) compared with the Egg condition (1.4%). Although this finding suggests that replacing higher-CHO (primarily sugar) foods with egg-based foods at breakfast may have a favorable effect on whole-body insulin sen-sitivity, caution is warranted. The HOMA-IR value is calculated using a linear model based on population-derived estimates, whereas HOMA2-%S is calculated using a nonlinear model, which is theoretically more robust [19, 20, 27]. No significant differences were present between the Egg and Non-Egg conditions for HOMA2-% S based on fasting values, or the ISI from the short IVGTT

Short intervention study, where the Egg population was still consuming carbohydrates saw a very modest improvement in insulin sensitivity. I speculate this is because of the reduction of carbohydrates for a single meal.

Another potentially relevant factor regarding effects of different meals on CHO metabolism is time of day. Dif-ferences in sympathetic nervous system activity and/or diurnal patterns related to the release of incretin hormones (e.g., glucagon-like peptide-1 and gastric inhibitory poly-peptide in response to a meal) may affect insulin sensitivity [31], and markedly higher (~40%) insulin sensitivity has been observed in the morning compared with mid-afternoon or evening [32]. Jakubowicz et al. conducted a randomized crossover trial where subjects with T2D were fed either a meal pattern that included a high-energy breakfast plus a low-energy dinner (breakfast: 2946 kJ, lunch: 2523 kJ, and dinner: 858 kJ) or a meal pattern with a low-energy break-fast plus a high-energy dinner (breakfast: 858 kJ, lunch: 2523 kJ, and dinner: 2946 kJ) [32]. Despite isoenergetic intakes, those consuming the higher energy breakfast meal pattern had reduced postprandial hyperglycemia and higher levels of intact and total glucagon-like peptide-1. In the present trial, study products were consumed at the breakfast meal, when insulin sensitivity would be expected to be at its highest. It is uncertain whether similar results would be obtained with consumption of the study products in the afternoon or evening.

This is a curious result, and speaks to the point Xep made about eating and time of day, I'm still very curious if this holds in a fully ketogenic diet.

I think the variability of thus study compared to other egg studies indicates that the eggs are not the main variable of interest, its the carbohydrates that are accounting for the fluctuating signal across these studies.

 

250th Anniversary of the U.S. Merchant Marine June 12, 2025

In this episode, Sal Mercogliano — a maritime historian at Campbell University (@campbelledu) and former merchant mariner — discusses the Battle of Machias, the first naval battle of the American Revolution and the founding of the U.S. Merchant Marine.

 

A absolutely excellent film, great cinematography, story pacing. It takes itself seriously enough that you can get immersed.

Set in the 1920s south amongst a racially divided farming community, two cousins start a new business.

Snarky Jay Review https://youtu.be/4Fkc_qo4qX0

It's great to watch, worth the time, I do recommend.

2
submitted 1 month ago* (last edited 1 month ago) by jet@hackertalks.com to c/carnivore@dubvee.org
 

I see you're quite passionate about the carnivore diet but I'd suggest some adjustments to the diet guide that address key health concerns:

Could you add a section about kidney stone prevention? The carnivore diet significantly increases kidney stone risk due to high animal protein intake, acidic urine, and zero plant-based alkalizing compounds. Studies show 5.9% incidence rate vs 0.25-0.3% in general population: Incidence and Characteristics of Kidney Stones in Patients on Ketogenic Diet: A Systematic Review and Meta-Analysis

Could you include guidance on fiber supplementation? Since carnivore diets provide zero dietary fiber, users miss the 23% reduction in all-cause mortality and 26% reduction in cardiovascular mortality that fiber provides. Consider discussing supplementation strategies: Dietary fiber intake and all-cause and cause-specific mortality: An updated systematic review and meta-analysis

Could you include guidance on digestive health management? Since fiber feeds beneficial gut bacteria and prevents constipation, carnivore dieters may need specific strategies to maintain gut health without any plant foods: Dietary fiber intake and total mortality: a meta-analysis of prospective cohort studies

Could you add a section on micronutrient monitoring? A nutrient analysrt in multiple essential nutrients including thiamin, magnesium, calcium, vitamin C, folate, and potassium (you can even see it in the nutrient table in the guide). Regular blood work and targeted supplementation may be necessary: Assessing the Nutrient Composition of a Carnivore Diet: A Case Study Model

Could you include cardiovascular monitoring recommendations? Given the significant dietary shift, more frequent lipid panels and blood pressure monitoring could help track how individuals respond to higher saturated fat intake, since responses vary considerably between people. Meta-analyses show both processed and unprocessed red meat consumption are associated with increased CVD, stroke, and heart failure risk: Red meat consumption, cardiovascular diseases, and diabetes: a systematic review and meta-analysis and Health effects associated with consumption of unprocessed red meat: a Burden of Proof study

Could you add a section on cancer risk awareness? A comprehensive analysis of 148 studies found red meat increases breast cancer risk by 9%, endometrial cancer by 25%, and colorectal cancer by 10%. Users should be aware of these risks for informed decision-making: Consumption of red meat and processed meat and cancer incidence: a systematic review and meta-analysis

As with most highly restrictive diets there's lots of bloodwork and supplementation required to make sure you don't damage your body long term and while it may be much harder than having a more varied diet it may be useful if you don't have any other choice.


@zeezee@slrpnk.net Originally expressed these concerns in a comment but due to some federation issues outside of our control it didn't federate properly, so I'm reposting it here so it can be seen by everyone.

12
submitted 1 month ago* (last edited 1 month ago) by jet@hackertalks.com to c/fedigrow@lemmy.zip
 

So we have A (aussie.zone) H (hackertalks.com) S (slrpnk.net) and D (dubvee.org)

  • UserS is banned from dubvee.org but not the community
  • UserS respond to a post from H, and H and A see this comment
  • D does not see UserS's comment (makes sense, since they were banned).
  • S has no community subscribers
  • S does not see H, or A's response to UserS's comment

  • 2 - Why does A see UserS's comment at all?
  • 3 - Why doesn't S see A's response, or H's response to the comment? No local subscribers?

exact post details

https://aussie.zone/post/21517299

vs

https://hackertalks.com/post/11881040

however on dubvee...

https://lemmy.dubvee.org/post/3575707

neither of our posts made it back to S.

And on slrpnk.net neither of our comments made it.... https://slrpnk.net/post/23201137

I think because UserS was banned from dubvee.org https://lemmy.dubvee.org/modlog?page=1&actionType=All&userId=6263415

 

Grant Genereux is a chemical engineer turned health researcher and advocate, known for his work exploring the role of vitamin A toxicity in chronic disease. After resolving his own health issues by eliminating vitamin A from his diet, Grant began sharing his findings through self-published books and public interviews. His research challenges conventional nutritional wisdom, offering a provocative perspective on the potential dangers of vitamin A consumption.

Grant and I explore the controversial topic of vitamin A toxicity and its overlooked role in modern chronic illnesses. We also discuss the science behind his elimination diet and the radical improvements in health that many have experienced after cutting out vitamin A. Be sure to watch the full interview to learn more.

0:00 Intro
2:38 Who is Grant Genereux?
6:53 Signs of vitamin A toxicity
9:10 How much vitamin A is safe?
18:45 Synthetic vs natural vitamin A
23:04 Thoughts on too many organ supplements
29:05 Is vitamin A really essential?
32:15 Foods high in hidden vitamin A
36:07 Chronic illness link to vitamin A
42:56 Should you stop milk and eggs?
48:49 Why cod liver helps 
56:51 Vitamin A’s link to cancer
1:05:21 Should you test vitamin A levels?
1:14:54 Where can people find Grant Genereux?

summerizerSummary

In this in-depth discussion, Judy Cho, a board-certified holistic nutritionist, revisits the controversial topic of vitamin A toxicity, especially as it relates to the consumption of liver products such as beef liver, cod liver, and cod liver oil. Alongside Grant Genu, a former engineer turned health advocate who has adhered to a low vitamin A diet for nearly a decade, Cho challenges the conventional wisdom that vitamin A is universally beneficial and highlights the risks tied to its excessive intake. The dialogue addresses the concept of hypervitaminosis A—a condition caused by vitamin A accumulation in the body—and explores how it may contribute to various health issues, including insulin resistance, skin problems, hair loss, bone pain, and potentially even chronic liver damage.

Despite vitamin A’s recognized role in essential physiological functions such as protein synthesis and cellular growth, their conversation reveals how overconsumption can disrupt these processes. The speakers explain how excess vitamin A can interfere with the DNA-to-protein synthesis pathway, leading to defective protein production, which may exacerbate insulin resistance and other metabolic disorders. They point out that many people, including those following carnivore diets, may unknowingly suffer from vitamin A toxicity even without obvious symptoms.

The discussion critiques the health industry’s heavy promotion of liver and organ supplements, cautioning about imbalances in nutrients like copper and zinc when consuming high amounts of liver. Cho and Grant encourage a more individualized approach to diet and vitamin A intake, suggesting that factors such as liver function and overall health status significantly influence vitamin A tolerance. They also note a growing but still cautious community advocating for awareness about vitamin A toxicity, with many experiencing notable health improvements on a low vitamin A regimen, albeit sometimes facing detox-related setbacks.

Furthermore, they warn against the long-term use of retinoids and vitamin A supplements, which can cause severe complications due to cumulative toxicity. The conversation emphasizes the importance of education, research, and personalized dietary strategies to prevent vitamin A overload and optimize health outcomes. Ultimately, the interview calls for a nuanced, balanced understanding of vitamin A’s role in nutrition, advocating for more widespread discourse regarding its potential dangers.

Highlights

  • 🥩 Vitamin A toxicity is a growing concern, especially from liver and organ meat consumption.
  • ⚠️ Excess vitamin A can cause symptoms like dry skin, hair loss, bone pain, and liver damage.
  • 🔬 Vitamin A’s interference with protein synthesis may contribute to insulin resistance and metabolic issues.
  • 🌿 Some individuals benefit from a low vitamin A diet, experiencing improved health after detoxification.
  • 💊 Long-term use of vitamin A supplements and retinoids may lead to serious health risks.
  • 🔄 Personalized vitamin A intake recommendations are essential, considering liver function and individual health.
  • 📈 Awareness about vitamin A toxicity is increasing, though skepticism and diet dropout remain challenges. Key Insights

⚖️ Vitamin A’s Dual Nature: Essential Yet Potentially Toxic Though vitamin A is vital for vision, immune function, and cellular growth, its narrow therapeutic window means excessive intake can lead to hypervitaminosis A, disrupting key biological processes and causing cumulative tissue damage over time.

🔄 Mechanism of Toxicity: Impact on Protein Synthesis and Insulin Resistance Vitamin A can bind to DNA blueprints responsible for protein assembly, causing the production of defective proteins. This malfunction potentially drives insulin resistance even in low-sugar diets, highlighting vitamin A toxicity’s metabolic implications often overlooked in nutritional science.

🌱 Individual Variation in Vitamin A Tolerance Liver health and detoxification capacity vary widely; thus, while some may thrive on liver-heavy diets, others—particularly with compromised liver function or chronic illnesses—may experience negative effects, underscoring the need for personalized dietary advice rather than blanket recommendations.

❗ Underrecognized Public Health Issue Despite decades of research on hypervitaminosis A, discussion on this condition within mainstream nutrition is limited, leading to a misconception that high vitamin A intake from “nutrient-dense” foods is universally safe. This gap contributes to the rise of undiagnosed vitamin A toxicity cases.

🔄 Detox and Adaptation Periods Are Critical Adopting a low vitamin A diet can cause temporary detoxification symptoms; patience and support during this phase are crucial for success. These setbacks are often mistaken for failure, contributing to a high dropout rate among adherents to low vitamin A regimens.

🚫 Risks Associated with Synthetic Retinoids and Supplements Beyond dietary sources, synthetic retinoids and vitamin A supplements pose significant risks for toxicity, especially with prolonged use, demanding greater caution and transparency regarding their effects and monitoring in clinical practice.

📢 Need for Balanced Nutritional Messaging and Research The health community and consumers must engage in more nuanced discussions about vitamin A, balancing its benefits against risks, tailoring intake to individual health profiles, and fostering further research into chronic low-level vitamin A toxicity and its long-term consequences.

This comprehensive overview underscores the vital importance of reexamining vitamin A’s role in nutrition and encourages informed, personalized approaches to avoid the potential harms of overconsumption.

 

We have had a few YPTB posts since this community was started

One was yesterday. We just moved to a new instance, so our ban lists and people's block lists got reset - Only natural that we would have more attention

I have completed the migration of the archival posts from the old instance to this instance, apologies for the flood of posts today - it is complete now.

Our subscriber count went from 140 to 50 - I'll post the we have moved message to the old lemm.ee community every few days until it goes offline.

The pinned posts should only link to posts within the new community, let me know if I missed anything.

Nutrition brings out the passion in people!

 

Buckle up! This is a 400 page book published in 1888 discussing the benefits of a ASF diet

It's sad how much we "knew", but didn't use in the last 150 years, how many lives could have been improved?

In this book Salisbury putting people on Red Meat and water (indian diet), he found he could reverse rheumatoid arthritis, Ulcerative colitis, gout. He specifically was interested in how the Red Meat diet improved Tuberculosis, and how those already on a red meat diet were far less susceptible to Tuberculosis

The fact this book is old does NOT INVALIDATE IT. This doctor was able to visit and live amongst people who ate "carnivore" diets, and compare their health vs people eating lots of PBF. That is a unique perspective we don't have access to anymore. This is a time capsule that should be the basis of more modern research.

https://collections.nlm.nih.gov/catalog/nlm:nlmuid-62210780R-bk

https://archive.org/details/b2150796x/page/n7/mode/2up

A bit on James Salisbury - https://en.wikipedia.org/wiki/James_H._Salisbury

He did, in fact, invent the Salisbury steak.

his advocacy of a meat-centered diet to promote health, and the term Salisbury steak for a ground beef patty served as the main course has been used in the United States since 1897.

Salisbury recommended this recipe (somewhat different from modern Salisbury steak recipes) for the treatment of alimentation (digestive disorders):

Heat the muscle pulp of lean beef made into cakes and broiled. This pulp should be as free as possible from connective or glue tissue, fat and cartilage. [...]

Previous to chopping, the fat, bones, tendons and fasciae should all be cut away, and the lean muscle cut up in pieces an inch or two square. Steaks cut through the centre of the round are the richest and best for this purpose. Beef should be procured from well fatted animals that are from four to six years old.

The pulp should not be pressed too firmly together before broiling, or it will taste livery. Simply press it sufficiently to hold it together. Make the cakes from half an inch to an inch thick. Broil slowly and moderately well over a fire free from blaze and smoke. When cooked, put it on a hot plate and season to taste with butter, pepper, salt; also use either Worcestershire or Halford sauce, mustard, horseradish or lemon juice on the meat if desired. Celery may be moderately used as a relish.[5]

Look at that, no carbs in Salisbury's version of the Salisbury steak.

 

Background/Objectives: The rise in chronic metabolic diseases has led to the exploration of alternative diets. The carnivore diet, consisting exclusively of animal products, has gained attention, anecdotally, for imparting benefit for inflammatory conditions beyond that possible by other restrictive dietary approaches. The aim was to assess the micronutrient adequacy of four versions of the carnivore diet against national nutrient reference values (NRVs). Methods: This study assessed the nutrient adequacy of the carnivore diet against national NRVs from the Australian National Health and Medical Research Council (NHMRC) and New Zealand Ministry of Health. Four meal plans for hypothetical average Australian adults were developed and analysed using Foodworks.online (Version 1, Xyris Pty Ltd., Brisbane, Australia, 2024), dietary software. Two female and two male plans were included; one set including dairy products and the other set including offal. Results: The carnivore diet met several NRV thresholds for nutrients such as riboflavin, niacin, phosphorus, zinc, Vitamin B6, Vitamin B12, selenium, and Vitamin A, and exceeded the sodium threshold. However, it fell short in thiamin, magnesium, calcium, and Vitamin C, and in iron, folate, iodine and potassium in some cases. Fibre intake was significantly below recommended levels. Conclusion: The carnivore diet may offer benefits for managing certain chronic conditions. Whether the metabolic contexts from consuming such a diet facilitates a lower requirement of certain nutrients, or whether it poses risks of micronutrient inadequacies remains to be determined. Tailored nutritional guidance and supplementation strategies are recommended to ensure careful consideration of micronutrient intake to prevent deficiencies.

Full paper at above link https://doi.org/10.3390/nu17010140

 

TLDR - There is far from consensus in the vilification of red meat in dietary guidelines. This article dives into the details of the ongoing schism.

Mainstream dietary recommendations now commonly advise people to minimize the intake of red meat for health and environmental reasons. Most recently, a major report issued by the EAT-Lancet Commission recommended a planetary reference diet mostly based on plants and with no or very low (14 g/d) consumption of red meat. We argue that claims about the health dangers of red meat are not only improbable in the light of our evolutionary history, they are far from being supported by robust scientific evidence.

Full paper at https://pubmed.ncbi.nlm.nih.gov/31486336/

 

https://pubmed.ncbi.nlm.nih.gov/38354868/

TLDR - Meat has been unfairly blamed by bad (possibly biased) statistical analysis.

some investigators may test many alternative analytic specifications and selectively report results for the analysis that yields the most interesting findings.

when investigators analyze data from observational studies, there are often hundreds of equally justifiable ways of analyzing the data, each of which may produce results that vary in direction, magnitude, and statistical significance

Evidence shows that investigators’ prior beliefs and expectations influence their results [5]. In the presence of strong opinions, investigators’ beliefs and expectations may shape the literature to the detriment of empirical evidence

Basically given a all the possible variable permutations they took a very large sampling of inputs to outcomes and looked at the resultant hazard ratio, demonstrating that you can cherry pick to get the results you want (good or bad). This is the core weakness of observational studies.

Curve analysis demonstrates itself as a valuable too in iterating through many of the combinations of observational data to show stronger trends.

The left/blue side of the graph are outcomes that show meat decreased all cause mortality, the right/red side of the graph are outcomes that show meat increases all cause mortality. If you were a hungry researcher, you could publish unending papers indicating either way from this same observational data pool! - Hence the constant news cycle driven by dietary agendas - not based on hard science RCTs.

 

TLDR : Weak Science, Low Relationship, Healthy User Confounders - Nothing burger.

Results: The dementia analysis included 133,771 participants (65.4% female) with a mean baseline age of 48.9 years, the objective cognitive function analysis included 17,458 female participants with a mean baseline age of 74.3 years, and SCD analysis included 43,966 participants (77.1% female) with a mean baseline age of 77.9 years. Participants with processed red meat intake ≥0.25 serving per day, compared with <0.10 serving per day, had a 13% higher risk of dementia (hazard ratio [HR] 1.13; 95% CI 1.08-1.19; plinearity < 0.001) and a 14% higher risk of SCD (relative risk [RR] 1.14; 95% CI 1.04-1.25; plinearity = 0.004). Higher processed red meat intake was associated with accelerated aging in global cognition (1.61 years per 1 serving per day increment [95% CI 0.20-3.03]) and in verbal memory (1.69 years per 1 serving per day increment [95% CI 0.13-3.25], both plinearity = 0.03). Unprocessed red meat intake of ≥1.00 serving per day, compared with <0.50 serving per day, was associated with a 16% higher risk of SCD (RR 1.16; 95% CI 1.03-1.30; plinearity = 0.04). Replacing 1 serving per day of nuts and legumes for processed red meat was associated with a 19% lower risk of dementia (HR 0.81, 95% CI 0.75-0.86), 1.37 fewer years of cognitive aging (95% CI -2.49 to -0.25), and a 21% lower risk of SCD (RR 0.79, 95% CI 0.68-0.92).

Discussion: Higher intake of red meat, particularly processed red meat, was associated with a higher risk of developing dementia and worse cognition. Reducing red meat consumption could be included in dietary guidelines to promote cognitive health. Further research is needed to assess the generalizability of these findings to populations with diverse ethnic backgrounds.

https://pubmed.ncbi.nlm.nih.gov/39813632/ https://doi.org/10.1212/WNL.0000000000210286

Sounds really bad! But, Association is not causation, "could" also means "cloud not"

(I can't find the full paper, if you know a link please share it, I want to read the full paper)

Prospective cohort study, epidemiology, another slice of the Nurses Health Study, and the HPFS. Observational Research, cannot prove causation. The Hazard ratio is 1.13, that's nothing. You have to be at least 2 to even justify further research (unless there is an agenda). As a reference the hazard ratio for smoking was 30!

As always in observational studies, healthy patient confounders need to be considered. The person ignoring current advice eating pizza, fast food, etc is considered a "meat eater", but the person following the guidelines is more or less vegetarian (no processed meat, no red meat at least, not smoking, not drinking) at this point. The big difference between these groups? SUGAR AND CARBS.

Even with this massive confounder the Hazard Ratio was only 1.13 (1.0 means NO Correlation at all)

From this tiny data point, the news is flooded with "Red Meat Causes Dementia"

The research director at Harvard has a well established PBF bias, as well as funding from industry. This paper is just one is a series (there will be another for the next news cycle with the same hazard ratios, saying the same thing). At BEST this type of low probability correlation should be used to setup a real study, a RCT... not to set policy or demonize red meat.

Recall our previous discussion of how you slice the data looking for relationships is just as important as the results with a large body of observational data https://lemmy.dubvee.org/post/2623649

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