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Guide Lord's Nutrition Handbook [MEGA-THREAD] (1 Viewer)

Guide Lord's Nutrition Handbook [MEGA-THREAD]

Lord's Nutrition Handbook
By Lord Lord

I'm providing evidence-based information synthesized from peer-reviewed research. This is not medical advice, and individual nutritional needs vary based on health status, activity level, age, and other factors. If you have specific health conditions, particularly metabolic disorders, kidney disease, or cardiovascular conditions, consult with a qualified healthcare professional before making significant dietary changes.


1771339951001.png
"To eat is a necessity, but to eat intelligently is an art." - La Rochefoucauld

INTRODUCTION
Nutrition is undoubtedly of the most studied fields in all of science, and simultaneously one of the most confidently misunderstood. I find that genuinely fascinating in a frustrating sort of way, as you've got decades of rigorous, peer-reviewed research sitting in journals that almost nobody reads, and right next to it is some retard on tiktok with 4 million followers telling you that olive oil or seed oil is slowly killing you. And people believe him. A lot of people.

I would consider myself a somewhat understanding individual, so I kind of get it, honestly. Nutrition research is notoriously difficult to communicate. Not only do studies contradict each other, but headlines misrepresent findings, and the actual papers are locked behind scientific jargon dense enough to make anyone's eyes glaze over. So people turn to whoever sounds the most confident and tells the most compelling story. And the most compelling stories in nutrition are almost always the most wrong ones.

There's a shit ton of examples I can provide, but we can always think back to the trajectory of dietary advice over the past 60 years. Fat was the enemy through the 70s and 80s. So food manufacturers replaced fat with sugar, gave everything a "low-fat" label, and obesity rates climbed anyway. Then, of course, followed carbohydrate, gluten, lectins, and seed oils.

When it comes to nutrition, there is always something new to be terrified of, always a new villain, always someone selling the solution. The 'villain' conveniently changes every decade but the structure of the argument stays identical:


1. Mainstream nutrition is always hiding the truth
2. This one food or food group is destroying your health
3. Here's what you should really be eating


What's actually happening is a combination of:

Genuine scientific uncertainty being exploited + Preliminary findings get reported as established fact + Some financial incentives (supplement companies, diet book deals, supplement-shilling influencers) transforms what information reaches people.

I would also include human psychology in the considering we're wired to respond to threat, to novelty, and to simple explanations for complex problems.

From personal experience, I've watched a couple of friends spend years cycling through elimination diets, cutting out entire food groups, spending money on supplements that do essentially nothing, and genuinely believing they were optimizing their health while ignoring the basics. I'm not exempt from this. Early on I went through phases of obsessing over meal timing, tracking every gram, and other nonsensical shit. It's honestly exhausting and unnecessary as fuck.

I then, fortunately, started actually reading the research. And what you find when you do that is so much less dramatic and draining than the content ecosystem wants you to believe. The fundamentals of a healthy diet are not controversial within nutrition science. They are, however, aggressively unprofitable to promote, because they don't require any 'special' products, any elimination protocols, or any influencer to explain them.

That's what this thread is. I hope you see this as an honest attempt to lay out what peer-reviewed evidence actually shows, how to eat in a way that satisfies your nutritional needs, and why a great portion of what's circulating online right now is either overstated, misinterpreted, or outright wrong.
BASELINE AND HOW TO EAT ACCORDINGLY
Your body needs three macronutrients to function:

1. Protein
2. Carbohydrates
3. Fats


The Institute of Medicine has established acceptable macronutrient distribution ranges (AMDRs) based on decades of metabolic research and epidemiological evidence.

According to this research on macronutrient requirements, these ranges are:


1771327082900.png

"carbohydrate (45%-65% of energy), protein (10%-35% of energy), and fat (20%-35% of energy; limit saturated and trans fats)"
These are RANGES, meaning there's flexibility. I promise you, your body doesn't spontaneously combust if you hit 44% carbohydrates one day.

They particularly exist due to different populations and activity levels require different distributions. If you're physically active, you'll trend toward higher carbohydrate intake (5-12 g/kg body weight depending on activity). Protein needs scale similarly, from 1.2-1.8 g/kg body weight for active individuals.

This Korean study on macronutrient distributions and hypertension found that deviating from appropriate macronutrient ranges was associated with increased hypertension risk even after adjusting for other factors.

The study tracked participants who consumed outside the Korean AMDR (carbohydrate 55-70%, fat 15-25%, protein 7-20%) and found:


1771345513842.png

"odds ratio of the non-AMDR group was 1.25 (95% CI, 1.02-1.53) in the hypertensive subjects."

Now, I know this may all seem confusing, but it practically means that balance matters more than anything. You don't have to obsess over macro-nutrients.

- Extremely low-fat diets can reduce testosterone production.
- Extremely low-carb diets can impair high-intensity performance.
- Inadequate protein compromises muscle maintenance and satiety.

You need all three in reasonable amounts.


PROTEIN:

The RDA for protein is 0.8 g/kg body weight. This number has been unchanged for over 70 years because it represents the minimum needed to prevent nitrogen loss.

What's particularly interesting to me about this is that the RDA was never meant to represent optimal intake.

This research examining protein requirements points out that
:

1771348391031.png

"the lowest level of protein intake reflected in the AMDR is higher than that of the RDA."
The AMDR allows up to 35% of calories from protein, which for most people translates to significantly more than 0.8 g/kg.

Recent studies, particularly in older adults, show benefits at intakes exceeding the RDA. For most people, aiming for 1.2-1.6 g/kg body weight makes sense, with higher intakes (1.6-2.2 g/kg) justified for those doing resistance training or in caloric deficits.

It literally:


1. Has the highest thermic effect of all macronutrients (meaning your body burns more calories digesting it)
2. Promotes satiety better than carbs or fats
3. Is essential for maintaining lean mass.


The study below on protein and cognitive function found that:

1771351205602.png



PROTEIN SOURCES
1771349763508.png


Yes, plant proteins count. No, you don't need to eat 200g of chicken breast daily.

CARBOHYDRATES:

There are two types of carbohydrates:

1. Complex carbohydrates
2. Simple carbohydrates


Carbs are not poisonous nor are they universally benign.

The type matters enormously.

We can tell by looking at the same research on macronutrients and cognitive function from earlier that found a clear distinction:

1771351429944.png

"Intake of simple carbohydrates ('sugars') is consistently associated with decreased global cognition whereas consumption of complex carbohydrates correlates with successful brain aging and improved memory both in the short- and long-term."
Complex carbohydrates include:

- Whole grains
- Legumes
- Vegetables
- Fruits


They provide fiber, vitamins, minerals, and sustained energy. Simple carbohydrates (added sugars, refined grains) spike blood glucose rapidly and provide little nutritional value beyond calories.

We can see the difference in mortality data. There are multiple meta-analyses that show that whole grain consumption reduces all-cause mortality.


One comprehensive analysis
examining prospective cohort studies found this about whole grain intake:

1771358922467.png

The dose-response showed benefits up to 210-225 g/day (about 7-7.5 servings)

Another meta-analysis found that comparing highest to lowest whole grain intake categories yielded a pooled relative risk of 0.84 for cardiovascular mortality and 0.91 for total mortality. For every 48g (about 1.5 servings) of whole grains consumed daily, there was a 7% reduction in all-cause mortality and a 9% reduction in CVD mortality.

1771359605002.png

Refined grains show the opposite pattern or no significant association, and in some analyses, higher refined grain intake correlates with increased mortality risk.


CARBOHYDRATE SOURCES
1771359996954.png


FATS:
Dietary fat is essential. You need it for:

- Hormone production
- Vitamin absorption (A, D, E, K are fat-soluble)
- Cell membrane integrity
- Brain function


The question is which fats?

The evidence is clear on trans fats: avoid them. They're associated with increased cardiovascular disease risk and were banned in many countries for good reason. Saturated fat is more nuanced. If your intake is excessive, it does tend to correlate with elevated LDL cholesterol. HOWEVER, moderate consumption within the 20-35% fat range appears fine for most people.

The ACTUAL discussion should focus on unsaturated fats, particularly:


1. Omega-3
2.
Omega-6 fatty acids


Both are essential (your body cannot synthesize them), but their ratio in the diet matters.

Linoleic acid (LA), the primary omega-6 fatty acid, has been highly demonized online. The "seed oil" panic is one of the most persistent nutrition myths of the 2020s. Hence why I want to show you guys what the research actually shows.


A 2024 review of omega-6 fatty acids
examining literature from January 2023 to August 2024 concluded that:
1771360741564.png

"Contrary to previous concerns that high LA intake may increase inflammation, most recent evidence supports the benefits of LA for cardiometabolic health. Several large studies report that higher blood LA levels correlate with reduced risks of coronary heart disease, stroke, and type 2 diabetes."

The mechanisms include activation of peroxisome proliferator-activated receptors (PPARs) + modulation of oxylipins involved in glucose and lipid metabolism. Current intakes around 5-10% of energy appear beneficial.

A systematic review specifically addressing the "LA causes inflammation" hypothesis examined 15 clinical trials, stating:

1771361185851.png

"failed to find any support for the 'diet LA causes inflammation hypothesis.'"

1771406411586.png

"LA appears to reduce inflammation and reduce risk for CMD" (cardiometabolic disease).

Above that, the review also stated that the dogma positioning LA as pro-inflammatory because it's an omega-6 fatty acid is false when examined in human studies.

This study on omega-6 fatty acids and inflammation concluded:

1771407417535.png

"studies in healthy human adults have found that increased intake of ARA or LA does not increase the concentrations of many inflammatory markers. Epidemiological studies have even suggested that ARA and LA may be linked to reduced inflammation."
The confusion basically comes from the mechanistic thinking that omega-6 fatty acids CAN be metabolized into pro-inflammatory eicosanoids. But in practice, humans consuming normal amounts of LA don't show increased inflammatory markers. The theoretical pathway =/= clinical inflammation in well-nourished humans.

Am I saying there is no legitimate discussion about omega-6 to omega-3 ratios? No. Not at all. In fact, research on this topic literally states that Western diets provide omega-6/3 ratios around 20:1, whereas ratios of 4:1 or less may be more optimal.

Now, is the solution to eliminate omega-6 (which would require avoiding nuts, seeds, and many healthy foods)? No. That would be, quite frankly, insanely retarded. All you need to do is increase omega-3 intake from fatty fish, flaxseeds, walnuts, and chia seeds.


One legitimate concern about seed oils came from this research on heating vegetable oils. When oils high in linoleic acid are heated to high temperatures, they can form toxic aldehydes like 4-hydroxynonenal (4-HNE). The study found that oils high in linoleic acid (soybean, sunflower, some canola products) generated significant 4-HNE when heated to 200°C for extended periods, while oils low in polyunsaturated fats (coconut oil) generated negligible amounts.

Now, THIS is a somewhat reasonable concern for deep frying, but it doesn't justify the blanket condemnation of all seed oils. The issue is oxidative stress from prolonged high-heat cooking, which affects any PUFA-rich oil.



METHOD:

Using high-heat stable oils (avocado, refined olive, coconut) for cooking above 180°C and reserving PUFA-rich oils for lower-heat applications or actual use would be a sensible approach.
SOURCES
1771410507541.png




MICRO-NUTRIENTS:
Vitamins and minerals don't get the attention macronutrients do, but deficiencies cause actual, measurable problems. This research on micronutrients basically identifies 13 essential vitamins and 10 essential trace elements that humans require.

Water-soluble vitamins (B-complex, C) need regular replenishment since your body doesn't store them long-term. Fat-soluble vitamins (A, D, E, K) can be stored, which means both deficiency and toxicity are possible.

This study on micronutrient deficiencies globally notes that:

1771412013828.png

"deficiencies of vitamin A and zinc increase the risk of child mortality, and zinc deficiency increases infectious morbidity and reduces linear growth as well. Deficiencies of iodine and iron are significant primarily for their effects on development and cognition and consequent disabilities."
The most commonly deficient micronutrients in developed countries, according to recent research, are:

1. Vitamin D
2. Iron
3. Vitamin A
4. Zinc
5. Folate
6. Iodine


Vitamin D deserves special mention.

Most people in non-equatorial climates are deficient or insufficient. Supplementation of 1000-2000 IU/day is reasonable for most adults, though individual needs vary based on baseline levels, sun exposure, and skin pigmentation.
Iron deficiency is pretty common in menstruating individuals and can cause negative effects on the body like fatigue and cognitive impairment.

This research on iron and cognition showed that significant effects on neurological function happens when deficient.


1771412589624.png
B vitamins, particularly B12, folate, and B6, are also really important for neurological function and energy metabolism. B12 is found almost exclusively in animal products, making supplementation necessary for strict vegans.


MICRO-NUTRIENT SOURCES
You get micronutrients from eating varied, minimally processed foods. A diet with:
1771412845039.png

FIBER
Fiber is technically a carbohydrate, but since humans lack the enzymes to digest it fully, it functions differently. It's classified as:

1. Soluble (dissolves in water, found in oats, beans, apples)
Or
2. Insoluble (doesn't dissolve, found in whole wheat, vegetables, nuts)

This research on fiber and cardiovascular health found that:


1771413227345.png

"regular consumption of dietary fiber, particularly fiber from cereal sources, may improve CVD health through multiple mechanisms including lipid reduction, body weight regulation, improved glucose metabolism, blood pressure control, and reduction of chronic inflammation."

The umbrella review I provided below of fiber meta-analyses found that individuals consuming the highest amounts of dietary fiber showed statistically significant reductions in cardiovascular disease mortality (RR = 0.77-0.83), CVD incidence (RR = 0.72-0.91), coronary heart disease (RR = 0.76-0.93), and stroke (RR = 0.83-0.93) compared to lowest intake groups.

1771423994515.png
And this systematic review on fiber and mortality concluded that:

1771425209296.png

"greater dietary fibre intake is associated with a lower risk of both cardiovascular disease and coronary heart disease." The dose-response analysis found benefits for each 7 g/day increase in total fiber intake.
This updated meta-analysis data from 64 studies with over 3.5 million subjects found that:

1771425891692.png

"higher consumption of total dietary fiber, significantly decreased the risk of all-cause mortality, CVD-related mortality, and cancer-related mortality by 23, 26 and 22%."
The mechanisms involve multiple pathways, like:

Fiber feeds beneficial gut bacteria -> slows glucose absorption -> increases satiety -> binds bile acids (forcing cholesterol use for replacement) -> modulates inflammation through short-chain fatty acid production.

Current recommendations suggest 25-30g daily for most adults. The average American consumes around 15g. The gap isn't small.


FIBER SOURCES
1771426623033.png


You will NOT hit adequate fiber eating primarily meat, dairy, and refined carbohydrates. You just won't.

PLANT-BASED FOODS:

The research on plant-based diets has exploded in the past decade.

A comprehensive review of plant-based diets and cardiovascular health found that:


1771427647153.png

"plant-based diets, especially when rich in high quality plant foods such as whole grains, fruits, vegetables, and nuts" were "associated with lower risk of cardiovascular outcomes and intermediate risk factors."
Does quality matter at all? Yes, it does. Enormously.

In fact, this research distinguishing healthy from unhealthy plant-based diets found that even though overall plant-based diet adherence associated with 8% lower cardiovascular mortality, unhealthy plant-based diets (high in refined grains, potatoes/fries, sugar-sweetened beverages) showed INCREASED cardiovascular mortality risk (HR: 1.05).

Conversely, healthy plant-based diets rich in whole grains, fruits, vegetables, nuts, and legumes showed decreased CVD incidence (HR: 0.87).


1771428269741.png

1771428920987.png

"participants in the highest versus lowest quintile for adherence to overall plant-based diet index or provegetarian diet had a 16%, 31% to 32%, and 18% to 25% lower risk of cardiovascular disease, cardiovascular disease mortality, and all-cause mortality, respectively."

1771429438689.png

Interestingly enough, this research in African American populations found no significant association between plant-based diet adherence and CVD or mortality.
What this basically suggests is that population-specific factors or different baseline dietary patterns may possibly modify effects.

Meta-analysis across multiple ethnicities in the Multiethnic Cohort Study found that:


1771429650531.png

"healthy plant-based dietary pattern emphasizing the quality of plant foods was associated with a lower risk of all-cause and CVD mortality in both men and women," though magnitude is varied by other factors such as race and ethnicity.

Do you see the consistent pattern? Specifically diets rich in minimally processed plant foods correlate with better health outcomes. This doesn't require veganism or vegetarianism.
How do we know they don't? Well, if we look at this research, it explicitly notes that:

1771440032951.png

"plant-based diets do not have to be vegan or vegetarian. For most people, complete elimination of meat or animal products is unrealistic and not necessary for cardiovascular health."
The takeaway to all of this is that what matters is the proportion and quality of plant foods consumed and not the complete exclusion of animal products.

CONCLUSION
Human nutrition is complex enough that rigid rules fail for most people. So, as far as we know, your optimal diet depends on:

1. Activity level (athletes need more carbs and protein than sedentary individuals)
2. Age (protein requirements increase with age, caloric needs typically decrease)
3. Health status (diabetes changes carbohydrate metabolism, kidney disease modifies protein needs)
4. Genetics (some people process saturated fat differently, lactose intolerance varies by ancestry)
5. Food availability and culture
6. Personal preferences and sustainability


Based on the research I've provided so far, the evidence consistently supports:

1. Base your diet on minimally processed foods. This single principle addresses, like, 80% of nutritional concerns. Whole grains instead of refined. Whole fruits instead of juice. Nuts instead of nut-flavored cereal. The closer food is to its original form, the more likely it retains beneficial nutrients and fiber.

2. Eat sufficient protein distributed throughout the day. Aim for 1.2-1.6 g/kg for most people, higher if very active or older. Include it at each meal for optimal muscle protein synthesis.

3. Prioritize complex carbohydrates over simple sugars.
Your carbohydrate intake should come primarily from whole grains, legumes, vegetables, and fruits. You CAN eat refined grains and added sugars, but try to limit them.

4. Include varied sources of fat. Emphasize
unsaturated fats from nuts, seeds, avocados, olive oil, and fatty fish. Don't fear saturated fat in moderate amounts, but don't center your diet around it. Omega-3 intake deserves attention.

5. Eat enough fiber. If you're following points 1-4, this happens automatically. If you're not hitting 25-30g daily, something's wrong with your food choices.

6. Include a wide variety of plant foods. Vegetables and fruits provide micronutrients, phytochemicals, and fiber that are difficult to obtain elsewhere. Different colors typically indicate different nutrient profiles.

7. Don't obsess over minor details.
The difference between 45% and 50% carbohydrate intake is so little compared to whether those carbohydrates come from whole grains or refined flour. Focus on the big patterns before micromanaging macros.

Notice that calorie counting, macronutrient calculation to the gram, food timing rules, supplement stacks, meal frequency dogma is absent in this entire guide. That's simply because those things can matter for specific goals (athletic performance, bodybuilding, metabolic conditions), but for general health, food quality and variety matter far more than being precise.

You don't need to be perfect. In fact, a diet that's 80% whole foods and includes regular vegetables, adequate protein, and sufficient fiber will outperform a "perfect" diet that's abandoned after two weeks because it's unsustainable.

The best diet is one that's:

- Nutritionally adequate

- Practically sustainable
- Culturally appropriate

- Enjoyable enough to be consistent about it

This might look like Mediterranean for some, like traditional Asian diets for others, or like modernized versions of indigenous food patterns. The common thread behind all of this is principles. Minimal processing, plant emphasis, adequate protein, healthy fats.
 

coloringhalo

jbg @sensitive sapphire
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By Lord Lord

I'm providing evidence-based information synthesized from peer-reviewed research. This is not medical advice, and individual nutritional needs vary based on health status, activity level, age, and other factors. If you have specific health conditions, particularly metabolic disorders, kidney disease, or cardiovascular conditions, consult with a qualified healthcare professional before making significant dietary changes.

INTRODUCTION
Nutrition is undoubtedly of the most studied fields in all of science, and simultaneously one of the most confidently misunderstood. I find that genuinely fascinating in a frustrating sort of way, as you've got decades of rigorous, peer-reviewed research sitting in journals that almost nobody reads, and right next to it is some retard on tiktok with 4 million followers telling you that olive oil or seed oil is slowly killing you. And people believe him. A lot of people.

I would consider myself a somewhat understanding individual, so I kind of get it, honestly. Nutrition research is notoriously difficult to communicate. Not only do studies contradict each other, but headlines misrepresent findings, and the actual papers are locked behind scientific jargon dense enough to make anyone's eyes glaze over. So people turn to whoever sounds the most confident and tells the most compelling story. And the most compelling stories in nutrition are almost always the most wrong ones.

There's a shit ton of examples I can provide, but we can always think back to the trajectory of dietary advice over the past 60 years. Fat was the enemy through the 70s and 80s. So food manufacturers replaced fat with sugar, gave everything a "low-fat" label, and obesity rates climbed anyway. Then, of course, followed carbohydrate, gluten, lectins, and seed oils.

When it comes to nutrition, there is always something new to be terrified of, always a new villain, always someone selling the solution. The 'villain' conveniently changes every decade but the structure of the argument stays identical:


1. Mainstream nutrition is always hiding the truth
2. This one food or food group is destroying your health
3. Here's what you should really be eating


What's actually happening is a combination of:

Genuine scientific uncertainty being exploited + Preliminary findings get reported as established fact + Some financial incentives (supplement companies, diet book deals, supplement-shilling influencers) transforms what information reaches people.

I would also include human psychology in the considering we're wired to respond to threat, to novelty, and to simple explanations for complex problems.

From personal experience, I've watched a couple of friends spend years cycling through elimination diets, cutting out entire food groups, spending money on supplements that do essentially nothing, and genuinely believing they were optimizing their health while ignoring the basics. I'm not exempt from this. Early on I went through phases of obsessing over meal timing, tracking every gram, and other nonsensical shit. It's honestly exhausting and unnecessary as fuck.

I then, fortunately, started actually reading the research. And what you find when you do that is so much less dramatic and draining than the content ecosystem wants you to believe. The fundamentals of a healthy diet are not controversial within nutrition science. They are, however, aggressively unprofitable to promote, because they don't require any 'special' products, any elimination protocols, or any influencer to explain them.

That's what this thread is. I hope you see this as an honest attempt to lay out what peer-reviewed evidence actually shows, how to eat in a way that satisfies your nutritional needs, and why a great portion of what's circulating online right now is either overstated, misinterpreted, or outright wrong.
BASELINE AND HOW TO EAT ACCORDINGLY
Your body needs three macronutrients to function:

1. Protein
2. Carbohydrates
3. Fats


The Institute of Medicine has established acceptable macronutrient distribution ranges (AMDRs) based on decades of metabolic research and epidemiological evidence.

According to this research on macronutrient requirements, these ranges are:


View attachment 29166
"carbohydrate (45%-65% of energy), protein (10%-35% of energy), and fat (20%-35% of energy; limit saturated and trans fats)"
These are RANGES, meaning there's flexibility. I promise you, your body doesn't spontaneously combust if you hit 44% carbohydrates one day.

They particularly exist due to different populations and activity levels require different distributions. If you're physically active, you'll trend toward higher carbohydrate intake (5-12 g/kg body weight depending on activity). Protein needs scale similarly, from 1.2-1.8 g/kg body weight for active individuals.

This Korean study on macronutrient distributions and hypertension found that deviating from appropriate macronutrient ranges was associated with increased hypertension risk even after adjusting for other factors.

The study tracked participants who consumed outside the Korean AMDR (carbohydrate 55-70%, fat 15-25%, protein 7-20%) and found:


View attachment 29238
"odds ratio of the non-AMDR group was 1.25 (95% CI, 1.02-1.53) in the hypertensive subjects."
Now, I know this may all seem confusing, but it practically means that balance matters more than anything. You don't have to obsess over macro-nutrients.

- Extremely low-fat diets can reduce testosterone production.
- Extremely low-carb diets can impair high-intensity performance.
- Inadequate protein compromises muscle maintenance and satiety.

You need all three in reasonable amounts.


PROTEIN:

The RDA for protein is 0.8 g/kg body weight. This number has been unchanged for over 70 years because it represents the minimum needed to prevent nitrogen loss.

What's particularly interesting to me about this is that the RDA was never meant to represent optimal intake.

This research examining protein requirements points out that
:

View attachment 29255
"the lowest level of protein intake reflected in the AMDR is higher than that of the RDA."
The AMDR allows up to 35% of calories from protein, which for most people translates to significantly more than 0.8 g/kg.

Recent studies, particularly in older adults, show benefits at intakes exceeding the RDA. For most people, aiming for 1.2-1.6 g/kg body weight makes sense, with higher intakes (1.6-2.2 g/kg) justified for those doing resistance training or in caloric deficits.

It literally:


1. Has the highest thermic effect of all macronutrients (meaning your body burns more calories digesting it)
2. Promotes satiety better than carbs or fats
3. Is essential for maintaining lean mass.


The study below on protein and cognitive function found that:

Yes, plant proteins count. No, you don't need to eat 200g of chicken breast daily.

CARBOHYDRATES:

There are two types of carbohydrates:

1. Complex carbohydrates
2. Simple carbohydrates


Carbs are not poisonous nor are they universally benign.

The type matters enormously.

We can tell by looking at the same research on macronutrients and cognitive function from earlier that found a clear distinction:

View attachment 29283
"Intake of simple carbohydrates ('sugars') is consistently associated with decreased global cognition whereas consumption of complex carbohydrates correlates with successful brain aging and improved memory both in the short- and long-term."
Complex carbohydrates include:

- Whole grains
- Legumes
- Vegetables
- Fruits


They provide fiber, vitamins, minerals, and sustained energy. Simple carbohydrates (added sugars, refined grains) spike blood glucose rapidly and provide little nutritional value beyond calories.

We can see the difference in mortality data. There are multiple meta-analyses that show that whole grain consumption reduces all-cause mortality.


One comprehensive analysis
examining prospective cohort studies found this about whole grain intake:

View attachment 29326
The dose-response showed benefits up to 210-225 g/day (about 7-7.5 servings)

Another meta-analysis found that comparing highest to lowest whole grain intake categories yielded a pooled relative risk of 0.84 for cardiovascular mortality and 0.91 for total mortality. For every 48g (about 1.5 servings) of whole grains consumed daily, there was a 7% reduction in all-cause mortality and a 9% reduction in CVD mortality.
Refined grains show the opposite pattern or no significant association, and in some analyses, higher refined grain intake correlates with increased mortality risk.


CARBOHYDRATE SOURCES
View attachment 29335

FATS:
Dietary fat is essential. You need it for:

- Hormone production
- Vitamin absorption (A, D, E, K are fat-soluble)
- Cell membrane integrity
- Brain function


The question is which fats?

The evidence is clear on trans fats: avoid them. They're associated with increased cardiovascular disease risk and were banned in many countries for good reason. Saturated fat is more nuanced. If your intake is excessive, it does tend to correlate with elevated LDL cholesterol. HOWEVER, moderate consumption within the 20-35% fat range appears fine for most people.

The ACTUAL discussion should focus on unsaturated fats, particularly:


1. Omega-3
2.
Omega-6 fatty acids


Both are essential (your body cannot synthesize them), but their ratio in the diet matters.

Linoleic acid (LA), the primary omega-6 fatty acid, has been highly demonized online. The "seed oil" panic is one of the most persistent nutrition myths of the 2020s. Hence why I want to show you guys what the research actually shows.


A 2024 review of omega-6 fatty acids
examining literature from January 2023 to August 2024 concluded that:
View attachment 29339
"Contrary to previous concerns that high LA intake may increase inflammation, most recent evidence supports the benefits of LA for cardiometabolic health. Several large studies report that higher blood LA levels correlate with reduced risks of coronary heart disease, stroke, and type 2 diabetes."
The mechanisms include activation of peroxisome proliferator-activated receptors (PPARs) + modulation of oxylipins involved in glucose and lipid metabolism. Current intakes around 5-10% of energy appear beneficial.

A systematic review specifically addressing the "LA causes inflammation" hypothesis examined 15 clinical trials, stating:

View attachment 29343
"failed to find any support for the 'diet LA causes inflammation hypothesis.'"

View attachment 29531
"LA appears to reduce inflammation and reduce risk for CMD" (cardiometabolic disease).

Above that, the review also stated that the dogma positioning LA as pro-inflammatory because it's an omega-6 fatty acid is false when examined in human studies.

This study on omega-6 fatty acids and inflammation concluded:

View attachment 29537
"studies in healthy human adults have found that increased intake of ARA or LA does not increase the concentrations of many inflammatory markers. Epidemiological studies have even suggested that ARA and LA may be linked to reduced inflammation."
The confusion basically comes from the mechanistic thinking that omega-6 fatty acids CAN be metabolized into pro-inflammatory eicosanoids. But in practice, humans consuming normal amounts of LA don't show increased inflammatory markers. The theoretical pathway =/= clinical inflammation in well-nourished humans.

Am I saying there is no legitimate discussion about omega-6 to omega-3 ratios? No. Not at all. In fact, research on this topic literally states that Western diets provide omega-6/3 ratios around 20:1, whereas ratios of 4:1 or less may be more optimal.

Now, is the solution to eliminate omega-6 (which would require avoiding nuts, seeds, and many healthy foods)? No. That would be, quite frankly, insanely retarded. All you need to do is increase omega-3 intake from fatty fish, flaxseeds, walnuts, and chia seeds.


One legitimate concern about seed oils came from this research on heating vegetable oils. When oils high in linoleic acid are heated to high temperatures, they can form toxic aldehydes like 4-hydroxynonenal (4-HNE). The study found that oils high in linoleic acid (soybean, sunflower, some canola products) generated significant 4-HNE when heated to 200°C for extended periods, while oils low in polyunsaturated fats (coconut oil) generated negligible amounts.

Now, THIS is a somewhat reasonable concern for deep frying, but it doesn't justify the blanket condemnation of all seed oils. The issue is oxidative stress from prolonged high-heat cooking, which affects any PUFA-rich oil.



METHOD:

Using high-heat stable oils (avocado, refined olive, coconut) for cooking above 180°C and reserving PUFA-rich oils for lower-heat applications or actual use would be a sensible approach.



MICRO-NUTRIENTS:
Vitamins and minerals don't get the attention macronutrients do, but deficiencies cause actual, measurable problems. This research on micronutrients basically identifies 13 essential vitamins and 10 essential trace elements that humans require.

Water-soluble vitamins (B-complex, C) need regular replenishment since your body doesn't store them long-term. Fat-soluble vitamins (A, D, E, K) can be stored, which means both deficiency and toxicity are possible.

This study on micronutrient deficiencies globally notes that:

View attachment 29540
"deficiencies of vitamin A and zinc increase the risk of child mortality, and zinc deficiency increases infectious morbidity and reduces linear growth as well. Deficiencies of iodine and iron are significant primarily for their effects on development and cognition and consequent disabilities."
The most commonly deficient micronutrients in developed countries, according to recent research, are:

1. Vitamin D
2. Iron
3. Vitamin A
4. Zinc
5. Folate
6. Iodine


Vitamin D deserves special mention.

Most people in non-equatorial climates are deficient or insufficient. Supplementation of 1000-2000 IU/day is reasonable for most adults, though individual needs vary based on baseline levels, sun exposure, and skin pigmentation.
Iron deficiency is pretty common in menstruating individuals and can cause negative effects on the body like fatigue and cognitive impairment.

This research on iron and cognition showed that significant effects on neurological function happens when deficient.

B vitamins, particularly B12, folate, and B6, are also really important for neurological function and energy metabolism. B12 is found almost exclusively in animal products, making supplementation necessary for strict vegans.


MICRO-NUTRIENT SOURCES
You get micronutrients from eating varied, minimally processed foods. A diet with:
View attachment 29544
FIBER
Fiber is technically a carbohydrate, but since humans lack the enzymes to digest it fully, it functions differently. It's classified as:

1. Soluble (dissolves in water, found in oats, beans, apples)
Or
2. Insoluble (doesn't dissolve, found in whole wheat, vegetables, nuts)

This research on fiber and cardiovascular health found that:


View attachment 29545
"regular consumption of dietary fiber, particularly fiber from cereal sources, may improve CVD health through multiple mechanisms including lipid reduction, body weight regulation, improved glucose metabolism, blood pressure control, and reduction of chronic inflammation."

The umbrella review I provided below of fiber meta-analyses found that individuals consuming the highest amounts of dietary fiber showed statistically significant reductions in cardiovascular disease mortality (RR = 0.77-0.83), CVD incidence (RR = 0.72-0.91), coronary heart disease (RR = 0.76-0.93), and stroke (RR = 0.83-0.93) compared to lowest intake groups.

View attachment 29555
And this systematic review on fiber and mortality concluded that:

View attachment 29556
"greater dietary fibre intake is associated with a lower risk of both cardiovascular disease and coronary heart disease." The dose-response analysis found benefits for each 7 g/day increase in total fiber intake.
This updated meta-analysis data from 64 studies with over 3.5 million subjects found that:

View attachment 29561
"higher consumption of total dietary fiber, significantly decreased the risk of all-cause mortality, CVD-related mortality, and cancer-related mortality by 23, 26 and 22%."
The mechanisms involve multiple pathways, like:

Fiber feeds beneficial gut bacteria -> slows glucose absorption -> increases satiety -> binds bile acids (forcing cholesterol use for replacement) -> modulates inflammation through short-chain fatty acid production.

Current recommendations suggest 25-30g daily for most adults. The average American consumes around 15g. The gap isn't small.


FIBER SOURCES
View attachment 29562

You will NOT hit adequate fiber eating primarily meat, dairy, and refined carbohydrates. You just won't.

PLANT-BASED FOODS:

The research on plant-based diets has exploded in the past decade.

A comprehensive review of plant-based diets and cardiovascular health found that:


View attachment 29577
"plant-based diets, especially when rich in high quality plant foods such as whole grains, fruits, vegetables, and nuts" were "associated with lower risk of cardiovascular outcomes and intermediate risk factors."
Does quality matter at all? Yes, it does. Enormously.

In fact, this research distinguishing healthy from unhealthy plant-based diets found that even though overall plant-based diet adherence associated with 8% lower cardiovascular mortality, unhealthy plant-based diets (high in refined grains, potatoes/fries, sugar-sweetened beverages) showed INCREASED cardiovascular mortality risk (HR: 1.05).

Conversely, healthy plant-based diets rich in whole grains, fruits, vegetables, nuts, and legumes showed decreased CVD incidence (HR: 0.87).


View attachment 29589
"participants in the highest versus lowest quintile for adherence to overall plant-based diet index or provegetarian diet had a 16%, 31% to 32%, and 18% to 25% lower risk of cardiovascular disease, cardiovascular disease mortality, and all-cause mortality, respectively."

View attachment 29590
Interestingly enough, this research in African American populations found no significant association between plant-based diet adherence and CVD or mortality.
What this basically suggests is that population-specific factors or different baseline dietary patterns may possibly modify effects.

Meta-analysis across multiple ethnicities in the Multiethnic Cohort Study found that:


View attachment 29597
"healthy plant-based dietary pattern emphasizing the quality of plant foods was associated with a lower risk of all-cause and CVD mortality in both men and women," though magnitude is varied by other factors such as race and ethnicity.

Do you see the consistent pattern? Specifically diets rich in minimally processed plant foods correlate with better health outcomes. This doesn't require veganism or vegetarianism.
How do we know they don't? Well, if we look at this research, it explicitly notes that:

View attachment 29643
"plant-based diets do not have to be vegan or vegetarian. For most people, complete elimination of meat or animal products is unrealistic and not necessary for cardiovascular health."
The takeaway to all of this is that what matters is the proportion and quality of plant foods consumed and not the complete exclusion of animal products.

CONCLUSION
Human nutrition is complex enough that rigid rules fail for most people. So, as far as we know, your optimal diet depends on:

1. Activity level (athletes need more carbs and protein than sedentary individuals)
2. Age (protein requirements increase with age, caloric needs typically decrease)
3. Health status (diabetes changes carbohydrate metabolism, kidney disease modifies protein needs)
4. Genetics (some people process saturated fat differently, lactose intolerance varies by ancestry)
5. Food availability and culture
6. Personal preferences and sustainability


Based on the research I've provided so far, the evidence consistently supports:

1. Base your diet on minimally processed foods. This single principle addresses, like, 80% of nutritional concerns. Whole grains instead of refined. Whole fruits instead of juice. Nuts instead of nut-flavored cereal. The closer food is to its original form, the more likely it retains beneficial nutrients and fiber.

2. Eat sufficient protein distributed throughout the day. Aim for 1.2-1.6 g/kg for most people, higher if very active or older. Include it at each meal for optimal muscle protein synthesis.

3. Prioritize complex carbohydrates over simple sugars.
Your carbohydrate intake should come primarily from whole grains, legumes, vegetables, and fruits. You CAN eat refined grains and added sugars, but try to limit them.

4. Include varied sources of fat. Emphasize
unsaturated fats from nuts, seeds, avocados, olive oil, and fatty fish. Don't fear saturated fat in moderate amounts, but don't center your diet around it. Omega-3 intake deserves attention.

5. Eat enough fiber. If you're following points 1-4, this happens automatically. If you're not hitting 25-30g daily, something's wrong with your food choices.

6. Include a wide variety of plant foods. Vegetables and fruits provide micronutrients, phytochemicals, and fiber that are difficult to obtain elsewhere. Different colors typically indicate different nutrient profiles.

7. Don't obsess over minor details.
The difference between 45% and 50% carbohydrate intake is so little compared to whether those carbohydrates come from whole grains or refined flour. Focus on the big patterns before micromanaging macros.

Notice that calorie counting, macronutrient calculation to the gram, food timing rules, supplement stacks, meal frequency dogma is absent in this entire guide. That's simply because those things can matter for specific goals (athletic performance, bodybuilding, metabolic conditions), but for general health, food quality and variety matter far more than being precise.

You don't need to be perfect. In fact, a diet that's 80% whole foods and includes regular vegetables, adequate protein, and sufficient fiber will outperform a "perfect" diet that's abandoned after two weeks because it's unsustainable.

The best diet is one that's:

- Nutritionally adequate

- Practically sustainable
- Culturally appropriate

- Enjoyable enough to be consistent about it

This might look like Mediterranean for some, like traditional Asian diets for others, or like modernized versions of indigenous food patterns. The common thread behind all of this is principles. Minimal processing, plant emphasis, adequate protein, healthy fats.
mirin effort
 

Mandy

No longer the biggest fish in the tank
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No offense, but for someone making this claim:



Yet to be recommending that users avoid foods with consistent epidemiological evidence showing reduced mortality, based ENTIRELY on mechanistic speculation that directly contradicts clinical trial data, I wouldn't want their approval.

Seriously, this advice is absurd:

View attachment 30160

I need you to define what you mean by "inflammation" and "oxidative stress" in this specific context. Are you talking about measured inflammatory biomarkers (CRP, IL-6, TNF-α)? Are you talking about clinically diagnosed inflammatory conditions? I'm genuinely confused on what you're referring to.
Maybe if you read my thread properly,you’ll see that I was talking about the enhanced peripheral serotonin synthesis by the enterochromaffin cell.s
"Oxidative stress and inflammation are both issues many people struggle with today,and you can just see that with how much Omega 6 fatty acids people are consuming."

I've already cited a systematic review of 15 clinical trials that directly tested this hypothesis and found no support for it. That review specifically examined whether increasing linoleic acid intake increases inflammatory markers in humans. It doesn't.
Have you counted in accumulation which is differed from tissue to tissue?
So before I go any further, can you tell me what specific evidence are you relying on that contradicts those FIFTEEN trials? What human data shows that dietary linoleic acid at typical consumption levels increases measured inflammation? I'm curious.
https://pubmed.ncbi.nlm.nih.gov/10102242/
https://bbrfoundation.org/content/f...-serotonin-transport-and-depression-severity?
https://www.nature.com/articles/1600783?
https://www.sciencedirect.com/science/article/pii/S0022227520397728?
https://www.nature.com/articles/1600783?


Some studies, not exactly lenolic acid but what most matters is that they’re PUFA. I have more if you want.

"it's simply the oil itself which is just pure polyunsaturated fats"

As if that's self-evidently problematic. Defend the claim and not the premise.

Just because polyunsaturated fats have multiple double bonds and those bonds are more susceptible to oxidation than single bonds does not automatically mean one of that shows harm in humans consuming them at normal dietary levels through normal cooking methods. The human body has quite literally evolved with extensive antioxidant systems (like glutathione, superoxide dismutase, catalase, vitamins E and C) specifically to manage oxidative processes.
You need other stress factors,PUFA just contributes.
You're making this logic leap of thinking "PUFAs can oxidise, therefore dietary PUFAs cause harmful oxidation in vivo," which is not how this works AT ALL. Water can oxidise iron into rust. Does drinking water cause you to rust from the inside? No, that would be insanely fucking retarded to think. This is all because context and biological systems matter.
I didn’t say thats the only thing that oxides,seems like you understood me wrong based of what you’re describing of my belief on the.
"First thing you can easily do is get rid of any fish oil supplements,if you for example take 1-2g of omega 3 fatty acids everyday via fish oil then you’re causing unecessary inflammation and oxidative stress because guess what DHA and EPA are also polyunsaturated fats. What you should instead do is eat fish at least once a week,I like to eat fish once or twice a week and therefore you get the same dosages of DHA and EPA but the differences is at least you’re not abusing everyday. DHA and EPA have a long brain half life,about 2.5 years,this way it’s not even an issue if you go weeks without consuming it."

What are you talking about, lmfao?

Let me make sure I understand your position correctly. You're claiming that:

1. DHA and EPA in supplement form cause inflammation
2. DHA and EPA in fish form are fine
3. The difference is... frequency of consumption??

That literally doesn't make any sense. If DHA and EPA are inflammatory (your claim), they're inflammatory REGARDLESS of whether they come from a capsule or a salmon fillet. The molecule is the same. Your body doesn't distinguish between "fish oil DHA" and "cooked salmon DHA" once it's absorbed. They're biochemically identical.
Again,I didn’t just say “they’re the only fats that oxidize”. Biochemically they’re ideal,and frequency of consumption makes sense,I literally said that the brain half life is 2.5 years therefore you’re essentially just overloading yourself if you spam omega 3s every day.
If your argument is actually about dose (supplements provide concentrated amounts daily, fish provides it less frequently), that's would be a completely different claim than "fish oil supplements cause inflammation." That's a claim about dose-response, which would require YOU to specify: at what dose does EPA/DHA switch from beneficial to harmful? What's the threshold? Show me the data demonstrating that 1-2g daily causes problems but eating fish twice weekly (which can easily provide similar or higher amounts depending on portion size and fish type) doesn't.
Dosen’t have a specific threshold,other factors play in.
"DHA and EPA have a long brain half life,about 2.5 years"

Lmfao, where did you get 2.5 years? The literature on DHA kinetics shows turnover rates varying by tissue, with brain DHA having relatively slow turnover, but 2.5 years is not a standard figure I've encountered. Cite your source.
https://www.mdpi.com/1422-0067/26/1...ly, however, the theoretical half,mg/day [70].

You know that it’s just a simple google search?
Fuck it. Even if we grant that DHA has slow turnover in neural tissue, that wouldn't even support your argument that you only need 2-3g per week. The half-life tells you how long it takes for concentration to decrease by half, not what your intake frequency should be to maintain optimal levels. Those are quite literally separate questions.
Like I said,your brain would already be saturated unless you’re deficient.
"avoid nuts and seeds in general" because they're "calorically dense due to fat content which mostly consist of polyunsaturated fats."

Many foods are calorically dense. That's would just be an argument for portion awareness. People also overconsume calorically dense ice cream. That would not mean we should conclude ice cream is problematic because of caloric density. It would just mean portion control matters.
I never talked about the caloric density,no idea where you get that. Yeah not only PUFA is the only factor,I’m just saying this because nuts are rich in PUFA,get the example.
AGAIN, what I'm really surprised about the most is that you're telling users to avoid foods (nuts, seeds, fatty fish in supplement form) that have been CONSISTENTLY associated with positive health outcomes in epidemiological research.
What I’m consistently seeing is that you rely a lot on public research,why don’t you explain specific mechanisms for example that would otherwise strengthen your point? Just curious.
I cited data earlier showing that nut consumption is associated with reduced cardiovascular mortality. Higher blood levels of linoleic acid (which comes partly from nuts and seeds) correlated with reduced risk of coronary heart disease, stroke, and diabetes.
Just state a confirmed result,no need for correlations because for example (not saying that you’re saying it) you can just say “Red meat is linked to heart cancer” yet you would need to explain why
It would honestly be REALLYY interesting to see how you reconcile your advice to avoid these foods with the mortality data showing benefits from consuming them. Because you can't both be right. Either:

1. nuts are harmful and we should see worse outcomes in nut consumers (we see better outcomes), or
2. you're spreading misinformation.

If you want to argue that avoiding PUFAs improves health, then the burden is on YOU to show that populations or individuals avoiding PUFAs have measurably better outcomes than those consuming moderate amounts on ACTUAL outcomes in ACTUAL humans. Where's that data?



Okay.



It is, considering you're using a tool that is fundamentally unreliable (documented extensively, by the way) because they're trained on statistical patterns in text (word frequency, sentence structure, predictability) and not whether something was actually written by AI. They literally flag formal writing, non-native English speakers, and anyone who writes clearly and structurally as "AI-generated" at high rates.

OpenAI THEMSELVES stated that their own classifier "correctly identifies 26% of AI-written text as 'likely AI-written,' while incorrectly labeling human-written text as AI-written 9% of the time." They shut the shit down in July 2023 because it was practically useless.

View attachment 30171
View attachment 30172
DNR this part.


I can get where you’re meaning,but I seriously in all respect am telling you’re already getting many things wrong and oversimplifying many things that I said instead of thinking outwards to other points. You’re taking my words from a thread that is especifically simplified for others,so yeah I might say “PUFA is bad” with minimal explanation but at least it’s broad in a sense where people understand what I’m implying directly.

Also,
https://raypeat.com/articles/articles/fats-functions-malfunctions.shtml?utm_source=chatgpt.com

I don’t know if you think Ray Peat is a good source,but genuinely read.
 

Mandy

No longer the biggest fish in the tank
Joined
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Posts
1,060
Reputation
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Maybe if you read my thread properly,you’ll see that I was talking about the enhanced peripheral serotonin synthesis by the enterochromaffin cell.s

Have you counted in accumulation which is differed from tissue to tissue?

https://pubmed.ncbi.nlm.nih.gov/10102242/
https://bbrfoundation.org/content/f...-serotonin-transport-and-depression-severity?
https://www.nature.com/articles/1600783?
https://www.sciencedirect.com/science/article/pii/S0022227520397728?
https://www.nature.com/articles/1600783?


Some studies, not exactly lenolic acid but what most matters is that they’re PUFA. I have more if you want.


You need other stress factors,PUFA just contributes.

I didn’t say thats the only thing that oxides,seems like you understood me wrong based of what you’re describing of my belief on the.

Again,I didn’t just say “they’re the only fats that oxidize”. Biochemically they’re ideal,and frequency of consumption makes sense,I literally said that the brain half life is 2.5 years therefore you’re essentially just overloading yourself if you spam omega 3s every day.

Dosen’t have a specific threshold,other factors play in.

https://www.mdpi.com/1422-0067/26/19/9343#:~:text=Interestingly, however, the theoretical half,mg/day [70].

You know that it’s just a simple google search?

Like I said,your brain would already be saturated unless you’re deficient.

I never talked about the caloric density,no idea where you get that. Yeah not only PUFA is the only factor,I’m just saying this because nuts are rich in PUFA,get the example.

What I’m consistently seeing is that you rely a lot on public research,why don’t you explain specific mechanisms for example that would otherwise strengthen your point? Just curious.

Just state a confirmed result,no need for correlations because for example (not saying that you’re saying it) you can just say “Red meat is linked to heart cancer” yet you would need to explain why

DNR this part.


I can get where you’re meaning,but I seriously in all respect am telling you’re already getting many things wrong and oversimplifying many things that I said instead of thinking outwards to other points. You’re taking my words from a thread that is especifically simplified for others,so yeah I might say “PUFA is bad” with minimal explanation but at least it’s broad in a sense where people understand what I’m implying directly.

Also,
https://raypeat.com/articles/articles/fats-functions-malfunctions.shtml?utm_source=chatgpt.com

I don’t know if you think Ray Peat is a good source,but genuinely read.

But yeah Lord Lord I can see why you’re not exactly understanding what I’m implying,and I take fault on that,that thread should’ve been more detailed. But in general you misunderstood me partially.
 

coloringhalo

jbg @sensitive sapphire
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Maybe if you read my thread properly,you’ll see that I was talking about the enhanced peripheral serotonin synthesis by the enterochromaffin cell.s

Have you counted in accumulation which is differed from tissue to tissue?

https://pubmed.ncbi.nlm.nih.gov/10102242/
https://bbrfoundation.org/content/f...-serotonin-transport-and-depression-severity?
https://www.nature.com/articles/1600783?
https://www.sciencedirect.com/science/article/pii/S0022227520397728?
https://www.nature.com/articles/1600783?


Some studies, not exactly lenolic acid but what most matters is that they’re PUFA. I have more if you want.


You need other stress factors,PUFA just contributes.

I didn’t say thats the only thing that oxides,seems like you understood me wrong based of what you’re describing of my belief on the.

Again,I didn’t just say “they’re the only fats that oxidize”. Biochemically they’re ideal,and frequency of consumption makes sense,I literally said that the brain half life is 2.5 years therefore you’re essentially just overloading yourself if you spam omega 3s every day.

Dosen’t have a specific threshold,other factors play in.

https://www.mdpi.com/1422-0067/26/19/9343#:~:text=Interestingly, however, the theoretical half,mg/day [70].

You know that it’s just a simple google search?

Like I said,your brain would already be saturated unless you’re deficient.

I never talked about the caloric density,no idea where you get that. Yeah not only PUFA is the only factor,I’m just saying this because nuts are rich in PUFA,get the example.

What I’m consistently seeing is that you rely a lot on public research,why don’t you explain specific mechanisms for example that would otherwise strengthen your point? Just curious.

Just state a confirmed result,no need for correlations because for example (not saying that you’re saying it) you can just say “Red meat is linked to heart cancer” yet you would need to explain why

DNR this part.


I can get where you’re meaning,but I seriously in all respect am telling you’re already getting many things wrong and oversimplifying many things that I said instead of thinking outwards to other points. You’re taking my words from a thread that is especifically simplified for others,so yeah I might say “PUFA is bad” with minimal explanation but at least it’s broad in a sense where people understand what I’m implying directly.

Also,
https://raypeat.com/articles/articles/fats-functions-malfunctions.shtml?utm_source=chatgpt.com

I don’t know if you think Ray Peat is a good source,but genuinely read.
wow
 

Lord

Iron
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I was talking about the enhanced peripheral serotonin synthesis by the enterochromaffin cell.s

Right, so I asked you to define what you meant by "inflammation" and "oxidative stress" in your original PUFA claims, and your response is... serotonin synthesis in gut cells?

You're not answering my question. You're quite literally changing the subject entirely.

Your original claim was, quote on quote, that omega-6 consumption causes "oxidative stress and inflammation" and that "many people struggle with today." I asked whether you meant measured inflammatory biomarkers or clinical conditions. You didn't answer. Instead you pivoted to enterochromaffin cell serotonin synthesis, which is a completely different physiological process.

Are you now claiming that your PUFA concerns are primarily about serotonin metabolism rather than inflammation? If so, those are different claims requiring different evidence. Pick one framework and defend it. Why are you sliding between "PUFAs cause inflammation" and "PUFAs affect serotonin" whenever one line of argument gets challenged? Lmfao.

While we're at it:

https://looksmax.gg/threads/simple-changes-that-could-help-your-health-mandys-nutrition.22159/
1771597158357.png


WHAT are you talking about?

Where's the human data showing that "fast-acting tryptophan" from meat causes measurable problems compared to "slow-acting tryptophan" from dairy? You're making physiological assertions without clinical outcomes. This is exactly the problem I identified with Peat's work, which is mechanism without demonstrated harm in humans.

Have you counted in accumulation which is differed from tissue to tissue?

No, I haven't "counted in accumulation," because YOU haven't demonstrated that tissue accumulation of linoleic acid at dietary intake levels causes harm. That's your claim to defend, not mine to disprove.

The 15 clinical trials I cited tested people consuming linoleic acid over weeks to months. If accumulation was causing the inflammatory effects you claim, those trials would have detected it. But, they didn't. Either the accumulation doesn't occur at harmful levels, or it occurs but doesn't produce the inflammatory effects you're asserting, or the trials would have shown something.

You're proposing that there's a harm mechanism operating over longer timescales that short-term studies miss. Cool. Now, with that being said, can you show me the long-term epidemiological data demonstrating worse outcomes in populations with higher tissue LA levels. I've already shown you the opposite, which is higher blood LA correlates with REDUCED cardiovascular disease and diabetes risk.

YOUR burden is to reconcile YOUR accumulation hypothesis with that epidemiological data. How are people with higher LA accumulation showing better outcomes if accumulation is harmful?


Dude...

1. https://pubmed.ncbi.nlm.nih.gov/10102242/

This just discusses how dietary PUFAs affect neuronal membrane composition and function. It's examining mechanisms by which PUFAs might influence brain function through membrane fluidity and receptor activity. It's not a clinical trial showing that dietary PUFA consumption causes harm. It's not showing that people who eat more PUFAs have worse neurological outcomes. It's describing biochemical pathways.

This is exactly the problem I identified. You're just citing mechanism without outcome data.

Even your own sources acknowledges that:
1771602672154.png


In other words, even in 1999, the author was saying we don't fully understand how dietary PUFA changes translate to functional outcomes in the nervous system.

And you're using this as evidence that PUFAs are harmful? Based on what clinical endpoint?

2. https://www.nature.com/articles/1600783

Okay, so you finally found a human study showing increased oxidative markers with PUFA intake.

But... you didn't mention that this was a 4-6 week study with 19 people. The high-PUFA group consumed 15% PUFAs as food energy, which is SUBSTANTIALLY HIGHER than typical dietary intake (most guidelines suggest 5-10%).

Even the conclusion of your own source states this:
1771603174162.png


So the actual finding of your own source is that VERY HIGH PUFA intake may increase oxidative markers, and adequate antioxidant intake may be protective. Now... how in the fuck is that the same as "avoid all PUFAs"? That would just be "don't consume excessive amounts and ensure adequate antioxidants."

Also, oxidative stress markers are surrogate endpoints. They're not clinical outcomes. Showing elevated LDL oxidation markers in a 6-week study doesn't show that this translates to cardiovascular disease, especially when the long-term epidemiological data I provided in my guide showed the opposite association (higher LA intake, lower CVD risk).

3. https://bbrfoundation.org/content/f...e-serotonin-transport-and-depression-severity

Mandy, this is a news article about research and not a primary research paper.

Correlation. In people who already have depression. This tells us NOTHING about whether dietary PUFA CAUSES the altered brain fatty acid levels or whether depression alters fatty acid metabolism or whether both are downstream effects of something else entirely.

The directionality problem is so massive here that it's honestly insane. If depression causes metabolic changes that alter brain fatty acid composition, then the fatty acid levels are a consequence rather than the cause. You can't use this to argue that dietary PUFA causes depression unless you have intervention data showing that PUFA restriction improves depression outcomes. Where is that?

4. https://www.sciencedirect.com/science/article/pii/S0022227520397728

This is cell culture...

Cell. Culture.

Cells in a dish exposed to pro-oxidant conditions show lipid peroxidation when loaded with PUFAs. This tells us that in a completely artificial environment with no antioxidant defenses, PUFAs can be oxidized. We already knew this. PUFAs are susceptible to oxidation. No shit. That's chemistry.

How would this tell us whether dietary PUFA consumption in humans with intact antioxidant systems, normal metabolism, and complex regulatory feedback causes clinically meaningful oxidative damage?

You cannot extrapolate from "endothelial cells in a dish with added iron show PUFA oxidation" to "eating salmon causes vascular damage in humans." The inferential gap is enormous.

So far, the evidence you've provided has been:

1. A review discussing PUFA mechanisms in neuronal membranes (mechanism, no clinical outcomes)
2. A small 6-week study showing increased oxidative markers with very high PUFA intake (15% of energy, not typical dietary amounts, surrogate markers are not clinical outcomes)
3. A correlation between brain fatty acid levels and depression in depressed patients (correlation =/= no causation, this is common sense, directionality unclear)
4. A cell culture study showing PUFA oxidation under artificial pro-oxidant conditions (cell culture, not humans)

What you have NOT provided, though, is:

1. Clinical trials showing that dietary PUFA at typical intake levels causes measurable harm
2. Long-term outcome data showing worse health in PUFA consumers
3. Intervention studies showing that PUFA restriction improves clinical endpoints
4. ANY DATA WHATSOEVER contradicting the 15 clinical trials I cited showing no inflammatory effects from LA consumption

You gave me mechanism, correlation, and cell culture. Not only did I give you clinical trials measuring inflammatory markers in humans but epidemiological data on cardiovascular outcomes and mortality.

No offense, but you have to be out of your mind to think that those are equivalent forms of evidence. When mechanism contradicts outcome data in humans, the outcome data wins. Every single time. Because what matters is what actually happens in living humans eating real food and not what happens to cells in a dish or what theoretical pathways might be activated.

Your evidence is insufficient to support your recommendations. That's it.

You need other stress factors,PUFA just contributes.

You keep contradicting yourself that I honestly can't even keep up anymore.

So now PUFA isn't THE problem but a contributor that requires other stress factors to cause harm? This more weaker than the original claim you made. If PUFA only causes problems in the presence of other stressors, then you would tell users on this forum to focus on identifying and removing those stressors and not the total evisceration of PUFA altogether.

Also, this completely undermines your position on nuts and fish. If someone is managing stress well, sleeping adequately, not obese, exercising regularly... then by your own logic, moderate PUFA intake wouldn't be problematic. So why would you make a blanket recommendation to avoid nuts, seeds, and daily fish oil?

"PUFAs are bad enough to eliminate entirely, but also they're only harmful in combination with other factors."

Bro, pick one.

I didn’t say thats the only thing that oxides,seems like you understood me wrong based of what you’re describing of my belief on the.

I didn't claim you said that. I said your logic of "PUFAs can oxidize → dietary PUFAs cause harmful oxidation in vivo" is flawed because the capacity to oxidize doesn't automatically translate to harmful oxidation in living systems with antioxidant defenses.

You still haven't addressed this. The human body manages oxidative processes constantly. The mere fact that a molecule CAN be oxidized doesn't demonstrate that consuming it CAUSES net oxidative harm. You need to show that dietary PUFA overwhelms antioxidant systems and produces measurable oxidative damage. Where's that data?

Again,I didn’t just say “they’re the only fats that oxidize”. Biochemically they’re ideal,and frequency of consumption makes sense,I literally said that the brain half life is 2.5 years therefore you’re essentially just overloading yourself if you spam omega 3s every day.

You didn't understand what I said. So, I'll restate it again.

The same molecules (DHA and EPA) are inflammatory when taken daily in supplement form but not inflammatory when consumed 1-2x weekly from fish, and the difference is... dose frequency based on neural tissue half-life?

If someone, say, eats 200g of salmon twice weekly, they're getting roughly 3-4g of EPA/DHA per week, which averages to about 0.5-0.6g daily. That's LESS than the 1-2g daily from supplements you claim causes problems. So your fish recommendation actually provides lower weekly intake than the supplement regimen you're condemning.

If dose frequency matters, at what interval does DHA/EPA switch from harmful to beneficial? Daily is bad, twice weekly is good... what about every other day? Every third day? You need to specify the threshold and provide evidence for it.

And you STILL haven't explained why the molecule would be inflammatory from a capsule but not from fish. They're biochemically identical once absorbed. Your body doesn't have different metabolic pathways for "supplement DHA" V.S. "salmon DHA." That's not how it works.

Dosen’t have a specific threshold,other factors play in.

Stop evading.

If you're claiming that 1-2g daily of fish oil causes problems, you're implicitly claiming there's a dose above which harm occurs. You might not know the exact number, but you're asserting that 1-2g exceeds it.

Either there's a threshold or there isn't. If there isn't, then even trace amounts would be harmful and your recommendation to eat fish at all would be wrong. If there is, then you need to have some basis for claiming that supplement doses exceed it but fish consumption doesn't.

"Other factors play in" dude you're just admitting that dose alone doesn't predict harm, which means your advice to avoid fish oil supplements specifically isn't justified by the dose argument, therefore your advice is, quite frankly, bullshit.


I'll accept that brain DHA has a long half-life.

That still wouldn't tell you optimal intake frequency.

Half-life tells you how quickly existing stores deplete. Intake requirements depend on turnover rate across all tissues (not just brain), baseline stores, biosynthesis from ALA, and functional needs.

Your argument is that:

"brain DHA has a 2.5-year half-life, therefore weekly intake is sufficient, therefore daily supplementation is "overloading."

This makes no sense.

Overloading would mean exceeding the body's capacity to metabolize or store DHA, leading to spillover into harmful pathways. Where's the evidence that 1-2g daily exceeds metabolic capacity? Red blood cell and plasma DHA levels respond to dietary intake, which would literally suggest that testing the body is incorporating it, not "overloading."

If you're saturated (your claim), further intake would simply not be absorbed or would be oxidized for energy. It wouldn't cause inflammation unless you can show me a specific mechanism by which excess DHA produces inflammatory metabolites.

Like I said,your brain would already be saturated unless you’re deficient.

BASED ON WHAT??

What defines "saturated" brain DHA levels? Is this measured in humans or are you assuming saturation from the half-life data?

The populations with highest fish consumption (Japan, Mediterranean regions, Nordic countries with high fatty fish intake) consume FAR MORE than 2-3g EPA/DHA weekly. They consume it multiple times weekly, sometimes daily. If your saturation hypothesis was correct, these populations should show no additional benefit from high intake and possibly harm from "overloading."

Instead, they show among the best cardiovascular and cognitive outcomes globally.

How do you explain that?

I never talked about the caloric density,no idea where you get that. Yeah not only PUFA is the only factor,I’m just saying this because nuts are rich in PUFA,get the example.

You literally wrote: "nuts and seeds are known to be calorically dense due to the fat content which mostly consist of polyunsaturated fats."

1771605674199.png


That's you. That's your words. You specifically mentioned caloric density as a property of nuts and seeds in the context of recommending avoidance.

If caloric density wasn't part of your reasoning for avoiding them, why mention it? And if it wasn't relevant, then your only remaining argument is PUFA content, which brings us back to: where's the evidence that nuts cause harm despite epidemiological data showing the opposite?

What I’m consistently seeing is that you rely a lot on public research,why don’t you explain specific mechanisms for example that would otherwise strengthen your point? Just curious.

Because mechanisms don't override outcomes, and I've already provided the outcome data.

I cited 15 clinical trials on LA and inflammation. I cited epidemiological data on nut consumption and mortality. I cited cardiovascular outcome data. I cited whole grain mortality data. These are OUTCOMES in humans. Actual results.

I can also explain mechanisms.

Linoleic acid gets incorporated into cell membranes, modulates eicosanoid production, activates PPAR receptors involved in glucose and lipid metabolism, and serves as a precursor to various oxylipins with diverse functions. The net effect in humans consuming moderate amounts is neutral to beneficial for inflammation and reduced risk for cardiometabolic disease.

But I don't NEED to explain the mechanism for the outcome data to be valid. If clinical trials show no increase in inflammatory markers with LA consumption, that's the answer. The mechanism is interesting for understanding WHY, but the outcome is what matters for dietary recommendations.

You're trying to reverse the burden. You're arguing from mechanism and wanting me to provide counter-mechanisms. That's not how this works. I have outcome data. You have mechanistic speculation. Outcomes trump mechanisms when they conflict.

Just state a confirmed result,no need for correlations

Mandy Mandy, do you understand how epidemiological research works??

We can't randomize people to eat or avoid nuts for 40 years and measure mortality. That's not feasible. So we use prospective cohort studies tracking dietary patterns and outcomes over decades, controlling for confounders.

When I say "higher blood LA levels correlate with reduced cardiovascular disease," I'm describing findings from multiple large prospective studies. Mind you, these are dose-response relationships that persist after multivariate adjustment.

Yes, correlation doesn't prove causation. But when you have:

1. biological plausibility (mechanisms by which LA could be beneficial)
2. dose-response relationships (more LA, better outcomes)
3. consistency across multiple populations and studies
4. temporal relationship (exposure precedes outcome)
5. strength of association (meaningful risk reductions)

...that's strong epidemiological evidence. Am I saying it's proof? No. Is it substantially better evidence than the mechanistic speculation you're providing? Yes, lmfao.

I like the read meat example, though. The association between red meat and colorectal cancer shows similar epidemiological patterns, and we DO have mechanistic explanations (heme iron, heterocyclic amines from cooking, N-nitroso compounds). The combination of epidemiology and mechanism is why dietary guidelines suggest moderating red meat.

The same exact logic would apply to nuts and LA. We have both favorable epidemiology AND mechanistic plausibility. You have unfavorable mechanism claims but contradictory epidemiology. When those conflict, I'm going with the actual human outcomes.

DNR this part.

Surprising, considering the question was straightforward.

I'll repeat so that I know you're not condeding without explicity doing so.

How do you reconcile your advice to avoid nuts with mortality data showing benefits from nut consumption? Simple. This is the central tension in your entire position. You're recommending avoidance of foods that consistently associate with better health outcomes. That would require you to provide an explanation.

but I seriously in all respect am telling you’re already getting many things wrong and oversimplifying many things that I said instead of thinking outwards to other points.

Lmfao.

You don't get to say "avoid nuts and seeds" to a general audience and then claim you meant something more nuanced when challenged.

Either your advice is appropriate for the audience you're giving it to, or it's oversimplified to the point of being wrong. Which is it?

And if you think I'm STILL misunderstanding or oversimplifying your position, clarify it now. State precisely:

1. What you claim PUFAs do in humans at typical dietary intakes
2. What evidence supports this
3. Why epidemiological data showing benefits from PUFA-containing foods doesn't contradict your position
4. What the threshold is for harmful versus benign PUFA intake

Also,
https://raypeat.com/articles/articles/fats-functions-malfunctions.shtml?utm_source=chatgpt.com

I don’t know if you think Ray Peat is a good source,but genuinely read.

I've already gone through Peat's work extensively. Peat's positions are what we're evaluating. I can't use Peat to validate Peat.

No offense,but why the fuck did you take that seriously?

I didn't. I just reappropriated the joke for the purpose of demonstrating how you being in that position couldn't be the case. I obviously knew it was satire, lmao.
 

Nardicus102

1G Test, NW1
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472
Right, so I asked you to define what you meant by "inflammation" and "oxidative stress" in your original PUFA claims, and your response is... serotonin synthesis in gut cells?

You're not answering my question. You're quite literally changing the subject entirely.

Your original claim was, quote on quote, that omega-6 consumption causes "oxidative stress and inflammation" and that "many people struggle with today." I asked whether you meant measured inflammatory biomarkers or clinical conditions. You didn't answer. Instead you pivoted to enterochromaffin cell serotonin synthesis, which is a completely different physiological process.

Are you now claiming that your PUFA concerns are primarily about serotonin metabolism rather than inflammation? If so, those are different claims requiring different evidence. Pick one framework and defend it. Why are you sliding between "PUFAs cause inflammation" and "PUFAs affect serotonin" whenever one line of argument gets challenged? Lmfao.

While we're at it:

https://looksmax.gg/threads/simple-changes-that-could-help-your-health-mandys-nutrition.22159/
View attachment 30284

WHAT are you talking about?

Where's the human data showing that "fast-acting tryptophan" from meat causes measurable problems compared to "slow-acting tryptophan" from dairy? You're making physiological assertions without clinical outcomes. This is exactly the problem I identified with Peat's work, which is mechanism without demonstrated harm in humans.



No, I haven't "counted in accumulation," because YOU haven't demonstrated that tissue accumulation of linoleic acid at dietary intake levels causes harm. That's your claim to defend, not mine to disprove.

The 15 clinical trials I cited tested people consuming linoleic acid over weeks to months. If accumulation was causing the inflammatory effects you claim, those trials would have detected it. But, they didn't. Either the accumulation doesn't occur at harmful levels, or it occurs but doesn't produce the inflammatory effects you're asserting, or the trials would have shown something.

You're proposing that there's a harm mechanism operating over longer timescales that short-term studies miss. Cool. Now, with that being said, can you show me the long-term epidemiological data demonstrating worse outcomes in populations with higher tissue LA levels. I've already shown you the opposite, which is higher blood LA correlates with REDUCED cardiovascular disease and diabetes risk.

YOUR burden is to reconcile YOUR accumulation hypothesis with that epidemiological data. How are people with higher LA accumulation showing better outcomes if accumulation is harmful?



Dude...

1. https://pubmed.ncbi.nlm.nih.gov/10102242/

This just discusses how dietary PUFAs affect neuronal membrane composition and function. It's examining mechanisms by which PUFAs might influence brain function through membrane fluidity and receptor activity. It's not a clinical trial showing that dietary PUFA consumption causes harm. It's not showing that people who eat more PUFAs have worse neurological outcomes. It's describing biochemical pathways.

This is exactly the problem I identified. You're just citing mechanism without outcome data.

Even your own sources acknowledges that:
View attachment 30300

In other words, even in 1999, the author was saying we don't fully understand how dietary PUFA changes translate to functional outcomes in the nervous system.

And you're using this as evidence that PUFAs are harmful? Based on what clinical endpoint?

2. https://www.nature.com/articles/1600783

Okay, so you finally found a human study showing increased oxidative markers with PUFA intake.

But... you didn't mention that this was a 4-6 week study with 19 people. The high-PUFA group consumed 15% PUFAs as food energy, which is SUBSTANTIALLY HIGHER than typical dietary intake (most guidelines suggest 5-10%).

Even the conclusion of your own source states this:
View attachment 30302

So the actual finding of your own source is that VERY HIGH PUFA intake may increase oxidative markers, and adequate antioxidant intake may be protective. Now... how in the fuck is that the same as "avoid all PUFAs"? That would just be "don't consume excessive amounts and ensure adequate antioxidants."

Also, oxidative stress markers are surrogate endpoints. They're not clinical outcomes. Showing elevated LDL oxidation markers in a 6-week study doesn't show that this translates to cardiovascular disease, especially when the long-term epidemiological data I provided in my guide showed the opposite association (higher LA intake, lower CVD risk).

3. https://bbrfoundation.org/content/f...e-serotonin-transport-and-depression-severity

Mandy, this is a news article about research and not a primary research paper.

Correlation. In people who already have depression. This tells us NOTHING about whether dietary PUFA CAUSES the altered brain fatty acid levels or whether depression alters fatty acid metabolism or whether both are downstream effects of something else entirely.

The directionality problem is so massive here that it's honestly insane. If depression causes metabolic changes that alter brain fatty acid composition, then the fatty acid levels are a consequence rather than the cause. You can't use this to argue that dietary PUFA causes depression unless you have intervention data showing that PUFA restriction improves depression outcomes. Where is that?

4. https://www.sciencedirect.com/science/article/pii/S0022227520397728

This is cell culture...

Cell. Culture.

Cells in a dish exposed to pro-oxidant conditions show lipid peroxidation when loaded with PUFAs. This tells us that in a completely artificial environment with no antioxidant defenses, PUFAs can be oxidized. We already knew this. PUFAs are susceptible to oxidation. No shit. That's chemistry.

How would this tell us whether dietary PUFA consumption in humans with intact antioxidant systems, normal metabolism, and complex regulatory feedback causes clinically meaningful oxidative damage?

You cannot extrapolate from "endothelial cells in a dish with added iron show PUFA oxidation" to "eating salmon causes vascular damage in humans." The inferential gap is enormous.

So far, the evidence you've provided has been:

1. A review discussing PUFA mechanisms in neuronal membranes (mechanism, no clinical outcomes)
2. A small 6-week study showing increased oxidative markers with very high PUFA intake (15% of energy, not typical dietary amounts, surrogate markers are not clinical outcomes)
3. A correlation between brain fatty acid levels and depression in depressed patients (correlation =/= no causation, this is common sense, directionality unclear)
4. A cell culture study showing PUFA oxidation under artificial pro-oxidant conditions (cell culture, not humans)

What you have NOT provided, though, is:

1. Clinical trials showing that dietary PUFA at typical intake levels causes measurable harm
2. Long-term outcome data showing worse health in PUFA consumers
3. Intervention studies showing that PUFA restriction improves clinical endpoints
4. ANY DATA WHATSOEVER contradicting the 15 clinical trials I cited showing no inflammatory effects from LA consumption

You gave me mechanism, correlation, and cell culture. Not only did I give you clinical trials measuring inflammatory markers in humans but epidemiological data on cardiovascular outcomes and mortality.

No offense, but you have to be out of your mind to think that those are equivalent forms of evidence. When mechanism contradicts outcome data in humans, the outcome data wins. Every single time. Because what matters is what actually happens in living humans eating real food and not what happens to cells in a dish or what theoretical pathways might be activated.

Your evidence is insufficient to support your recommendations. That's it.



You keep contradicting yourself that I honestly can't even keep up anymore.

So now PUFA isn't THE problem but a contributor that requires other stress factors to cause harm? This more weaker than the original claim you made. If PUFA only causes problems in the presence of other stressors, then you would tell users on this forum to focus on identifying and removing those stressors and not the total evisceration of PUFA altogether.

Also, this completely undermines your position on nuts and fish. If someone is managing stress well, sleeping adequately, not obese, exercising regularly... then by your own logic, moderate PUFA intake wouldn't be problematic. So why would you make a blanket recommendation to avoid nuts, seeds, and daily fish oil?

"PUFAs are bad enough to eliminate entirely, but also they're only harmful in combination with other factors."

Bro, pick one.



I didn't claim you said that. I said your logic of "PUFAs can oxidize → dietary PUFAs cause harmful oxidation in vivo" is flawed because the capacity to oxidize doesn't automatically translate to harmful oxidation in living systems with antioxidant defenses.

You still haven't addressed this. The human body manages oxidative processes constantly. The mere fact that a molecule CAN be oxidized doesn't demonstrate that consuming it CAUSES net oxidative harm. You need to show that dietary PUFA overwhelms antioxidant systems and produces measurable oxidative damage. Where's that data?



You didn't understand what I said. So, I'll restate it again.

The same molecules (DHA and EPA) are inflammatory when taken daily in supplement form but not inflammatory when consumed 1-2x weekly from fish, and the difference is... dose frequency based on neural tissue half-life?

If someone, say, eats 200g of salmon twice weekly, they're getting roughly 3-4g of EPA/DHA per week, which averages to about 0.5-0.6g daily. That's LESS than the 1-2g daily from supplements you claim causes problems. So your fish recommendation actually provides lower weekly intake than the supplement regimen you're condemning.

If dose frequency matters, at what interval does DHA/EPA switch from harmful to beneficial? Daily is bad, twice weekly is good... what about every other day? Every third day? You need to specify the threshold and provide evidence for it.

And you STILL haven't explained why the molecule would be inflammatory from a capsule but not from fish. They're biochemically identical once absorbed. Your body doesn't have different metabolic pathways for "supplement DHA" V.S. "salmon DHA." That's not how it works.



Stop evading.

If you're claiming that 1-2g daily of fish oil causes problems, you're implicitly claiming there's a dose above which harm occurs. You might not know the exact number, but you're asserting that 1-2g exceeds it.

Either there's a threshold or there isn't. If there isn't, then even trace amounts would be harmful and your recommendation to eat fish at all would be wrong. If there is, then you need to have some basis for claiming that supplement doses exceed it but fish consumption doesn't.

"Other factors play in" dude you're just admitting that dose alone doesn't predict harm, which means your advice to avoid fish oil supplements specifically isn't justified by the dose argument, therefore your advice is, quite frankly, bullshit.



I'll accept that brain DHA has a long half-life.

That still wouldn't tell you optimal intake frequency.

Half-life tells you how quickly existing stores deplete. Intake requirements depend on turnover rate across all tissues (not just brain), baseline stores, biosynthesis from ALA, and functional needs.

Your argument is that:

"brain DHA has a 2.5-year half-life, therefore weekly intake is sufficient, therefore daily supplementation is "overloading."

This makes no sense.

Overloading would mean exceeding the body's capacity to metabolize or store DHA, leading to spillover into harmful pathways. Where's the evidence that 1-2g daily exceeds metabolic capacity? Red blood cell and plasma DHA levels respond to dietary intake, which would literally suggest that testing the body is incorporating it, not "overloading."

If you're saturated (your claim), further intake would simply not be absorbed or would be oxidized for energy. It wouldn't cause inflammation unless you can show me a specific mechanism by which excess DHA produces inflammatory metabolites.



BASED ON WHAT??

What defines "saturated" brain DHA levels? Is this measured in humans or are you assuming saturation from the half-life data?

The populations with highest fish consumption (Japan, Mediterranean regions, Nordic countries with high fatty fish intake) consume FAR MORE than 2-3g EPA/DHA weekly. They consume it multiple times weekly, sometimes daily. If your saturation hypothesis was correct, these populations should show no additional benefit from high intake and possibly harm from "overloading."

Instead, they show among the best cardiovascular and cognitive outcomes globally.

How do you explain that?



You literally wrote: "nuts and seeds are known to be calorically dense due to the fat content which mostly consist of polyunsaturated fats."

View attachment 30307

That's you. That's your words. You specifically mentioned caloric density as a property of nuts and seeds in the context of recommending avoidance.

If caloric density wasn't part of your reasoning for avoiding them, why mention it? And if it wasn't relevant, then your only remaining argument is PUFA content, which brings us back to: where's the evidence that nuts cause harm despite epidemiological data showing the opposite?



Because mechanisms don't override outcomes, and I've already provided the outcome data.

I cited 15 clinical trials on LA and inflammation. I cited epidemiological data on nut consumption and mortality. I cited cardiovascular outcome data. I cited whole grain mortality data. These are OUTCOMES in humans. Actual results.

I can also explain mechanisms.

Linoleic acid gets incorporated into cell membranes, modulates eicosanoid production, activates PPAR receptors involved in glucose and lipid metabolism, and serves as a precursor to various oxylipins with diverse functions. The net effect in humans consuming moderate amounts is neutral to beneficial for inflammation and reduced risk for cardiometabolic disease.

But I don't NEED to explain the mechanism for the outcome data to be valid. If clinical trials show no increase in inflammatory markers with LA consumption, that's the answer. The mechanism is interesting for understanding WHY, but the outcome is what matters for dietary recommendations.

You're trying to reverse the burden. You're arguing from mechanism and wanting me to provide counter-mechanisms. That's not how this works. I have outcome data. You have mechanistic speculation. Outcomes trump mechanisms when they conflict.



Mandy Mandy, do you understand how epidemiological research works??

We can't randomize people to eat or avoid nuts for 40 years and measure mortality. That's not feasible. So we use prospective cohort studies tracking dietary patterns and outcomes over decades, controlling for confounders.

When I say "higher blood LA levels correlate with reduced cardiovascular disease," I'm describing findings from multiple large prospective studies. Mind you, these are dose-response relationships that persist after multivariate adjustment.

Yes, correlation doesn't prove causation. But when you have:

1. biological plausibility (mechanisms by which LA could be beneficial)
2. dose-response relationships (more LA, better outcomes)
3. consistency across multiple populations and studies
4. temporal relationship (exposure precedes outcome)
5. strength of association (meaningful risk reductions)

...that's strong epidemiological evidence. Am I saying it's proof? No. Is it substantially better evidence than the mechanistic speculation you're providing? Yes, lmfao.

I like the read meat example, though. The association between red meat and colorectal cancer shows similar epidemiological patterns, and we DO have mechanistic explanations (heme iron, heterocyclic amines from cooking, N-nitroso compounds). The combination of epidemiology and mechanism is why dietary guidelines suggest moderating red meat.

The same exact logic would apply to nuts and LA. We have both favorable epidemiology AND mechanistic plausibility. You have unfavorable mechanism claims but contradictory epidemiology. When those conflict, I'm going with the actual human outcomes.



Surprising, considering the question was straightforward.

I'll repeat so that I know you're not condeding without explicity doing so.

How do you reconcile your advice to avoid nuts with mortality data showing benefits from nut consumption? Simple. This is the central tension in your entire position. You're recommending avoidance of foods that consistently associate with better health outcomes. That would require you to provide an explanation.



Lmfao.

You don't get to say "avoid nuts and seeds" to a general audience and then claim you meant something more nuanced when challenged.

Either your advice is appropriate for the audience you're giving it to, or it's oversimplified to the point of being wrong. Which is it?

And if you think I'm STILL misunderstanding or oversimplifying your position, clarify it now. State precisely:

1. What you claim PUFAs do in humans at typical dietary intakes
2. What evidence supports this
3. Why epidemiological data showing benefits from PUFA-containing foods doesn't contradict your position
4. What the threshold is for harmful versus benign PUFA intake



I've already gone through Peat's work extensively. Peat's positions are what we're evaluating. I can't use Peat to validate Peat.



I didn't. I just reappropriated the joke for the purpose of demonstrating how you being in that position couldn't be the case. I obviously knew it was satire, lmao.
HIGH IQ take

n honestly when it comes to nutrition as a whole there can be more nuance, Human/Population data usually beat theoretical mechanism data
Mandy Mandy take somewhat makes sense from mechanistic POV n you could also make the argument due to genetic polymorphism everyone in population could respond somewhat differently to said thing, thus making mechanistic theory more passable from a metabolic contex.

But once Human data enter's the room, theory has to take a seat most of the time Lord Lord
I mean if we really think about it logically, before anything gets published, it goes Theory -> Mechanism -> Rat -> Human studies
With population data being the number 1 in terms of reliability of information we can go off of.

This is quite litteraly how HairCafe cooked FaceIQ in a nutrition debate
 

Lord

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HIGH IQ take

n honestly when it comes to nutrition as a whole there can be more nuance, Human/Population data usually beat theoretical mechanism data
Mandy Mandy take somewhat makes sense from mechanistic POV n you could also make the argument due to genetic polymorphism everyone in population could respond somewhat differently to said thing, thus making mechanistic theory more passable from a metabolic contex.

But once Human data enter's the room, theory has to take a seat most of the time Lord Lord
I mean if we really think about it logically, before anything gets published, it goes Theory -> Mechanism -> Rat -> Human studies
With population data being the number 1 in terms of reliability of information we can go off of.

This is quite litteraly how HairCafe cooked FaceIQ in a nutrition debate

Mechanistic plausibility is fine as a starting point. It generates hypotheses worth testing. The problem that I personally have with these takes is that it just stops at mechanism and is basically treated as conclusive when the human data doesn't support it.
 

Mandy

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Right, so I asked you to define what you meant by "inflammation" and "oxidative stress" in your original PUFA claims, and your response is... serotonin synthesis in gut cells?

You're not answering my question. You're quite literally changing the subject entirely.

Your original claim was, quote on quote, that omega-6 consumption causes "oxidative stress and inflammation" and that "many people struggle with today." I asked whether you meant measured inflammatory biomarkers or clinical conditions. You didn't answer. Instead you pivoted to enterochromaffin cell serotonin synthesis, which is a completely different physiological process.
It’s part of the process because that is the main driver in my opinion. Excess peripheral serotonin->CRH->ACTH->Cortisol. I talked about this in another thread,yet you only seem to have read one.
And generally if stress responses are further induced from example a modern diet+PUFA then of course what would excessive ATDH stimulation do? Not an anti inflammatory result as obvious .
Are you now claiming that your PUFA concerns are primarily about serotonin metabolism rather than inflammation? If so, those are different claims requiring different evidence. Pick one framework and defend it. Why are you sliding between "PUFAs cause inflammation" and "PUFAs affect serotonin" whenever one line of argument gets challenged? Lmfao.
as stated before,lots of the inflammatory response is downstream from excess endochromaffin stimulation.
While we're at it:

https://looksmax.gg/threads/simple-changes-that-could-help-your-health-mandys-nutrition.22159/
View attachment 30284

WHAT are you talking about?

Where's the human data showing that "fast-acting tryptophan" from meat causes measurable problems compared to "slow-acting tryptophan" from dairy? You're making physiological assertions without clinical outcomes. This is exactly the problem I identified with Peat's work, which is mechanism without demonstrated harm in humans.
there’s no chemical “slow acting” or “fast acting” and I know that and isn’t it obvious? It’s digestion speed and endrochromaffin sensory rate.
No, I haven't "counted in accumulation," because YOU haven't demonstrated that tissue accumulation of linoleic acid at dietary intake levels causes harm. That's your claim to defend, not mine to disprove.

The 15 clinical trials I cited tested people consuming linoleic acid over weeks to months. If accumulation was causing the inflammatory effects you claim, those trials would have detected it. But, they didn't. Either the accumulation doesn't occur at harmful levels, or it occurs but doesn't produce the inflammatory effects you're asserting, or the trials would have shown something.

You're proposing that there's a harm mechanism operating over longer timescales that short-term studies miss. Cool. Now, with that being said, can you show me the long-term epidemiological data demonstrating worse outcomes in populations with higher tissue LA levels. I've already shown you the opposite, which is higher blood LA correlates with REDUCED cardiovascular disease and diabetes risk.

YOUR burden is to reconcile YOUR accumulation hypothesis with that epidemiological data. How are people with higher LA accumulation showing better outcomes if accumulation is harmful?

I’ll look into the trial studies properly soon,I have to admit I don’t understand what you exactly want me to counter here not.

Dude...

1. https://pubmed.ncbi.nlm.nih.gov/10102242/

This just discusses how dietary PUFAs affect neuronal membrane composition and function. It's examining mechanisms by which PUFAs might influence brain function through membrane fluidity and receptor activity. It's not a clinical trial showing that dietary PUFA consumption causes harm. It's not showing that people who eat more PUFAs have worse neurological outcomes. It's describing biochemical pathways.

This is exactly the problem I identified. You're just citing mechanism without outcome data.

Even your own sources acknowledges that:
View attachment 30300

In other words, even in 1999, the author was saying we don't fully understand how dietary PUFA changes translate to functional outcomes in the nervous system.

And you're using this as evidence that PUFAs are harmful? Based on what clinical endpoint?

2. https://www.nature.com/articles/1600783

Okay, so you finally found a human study showing increased oxidative markers with PUFA intake.

But... you didn't mention that this was a 4-6 week study with 19 people. The high-PUFA group consumed 15% PUFAs as food energy, which is SUBSTANTIALLY HIGHER than typical dietary intake (most guidelines suggest 5-10%).

Even the conclusion of your own source states this:
View attachment 30302

So the actual finding of your own source is that VERY HIGH PUFA intake may increase oxidative markers, and adequate antioxidant intake may be protective. Now... how in the fuck is that the same as "avoid all PUFAs"? That would just be "don't consume excessive amounts and ensure adequate antioxidants."
You can’t avoid PUFA completely. And thats my point that just proved,but for you the “excessive” amount is higher than what I state is “excessive”. It’s like, if I’d tell to do the most lowest fat diet possible,you would still end up with a few grams of dietary fat. And didn’t I state that I recommend fish consumption?
IMG_2782.jpeg

Like I said,your “excessive limit” in your belief is just higher than mine.

Also, oxidative stress markers are surrogate endpoints. They're not clinical outcomes. Showing elevated LDL oxidation markers in a 6-week study doesn't show that this translates to cardiovascular disease, especially when the long-term epidemiological data I provided in my guide showed the opposite association (higher LA intake, lower CVD risk).

3. https://bbrfoundation.org/content/f...e-serotonin-transport-and-depression-severity

Mandy, this is a news article about research and not a primary research paper.

Correlation. In people who already have depression. This tells us NOTHING about whether dietary PUFA CAUSES the altered brain fatty acid levels or whether depression alters fatty acid metabolism or whether both are downstream effects of something else entirely.

The directionality problem is so massive here that it's honestly insane. If depression causes metabolic changes that alter brain fatty acid composition, then the fatty acid levels are a consequence rather than the cause. You can't use this to argue that dietary PUFA causes depression unless you have intervention data showing that PUFA restriction improves depression outcomes. Where is that?
Well generally being in a state of neurotransmitter signal irregulation would just show louder results than a person that isn’t in such a state. But yeah tbh these aint the best studies.
4. https://www.sciencedirect.com/science/article/pii/S0022227520397728

This is cell culture...

Cell. Culture.

Cells in a dish exposed to pro-oxidant conditions show lipid peroxidation when loaded with PUFAs. This tells us that in a completely artificial environment with no antioxidant defenses, PUFAs can be oxidized. We already knew this. PUFAs are susceptible to oxidation. No shit. That's chemistry.
Then does saturated fat still show more stability in a Petri dish according to another one,I’ll try finding it later.
How would this tell us whether dietary PUFA consumption in humans with intact antioxidant systems, normal metabolism, and complex regulatory feedback causes clinically meaningful oxidative damage?
It’s infront of you,no?
You cannot extrapolate from "endothelial cells in a dish with added iron show PUFA oxidation" to "eating salmon causes vascular damage in humans." The inferential gap is enormous.
I consume Salmon and other fish, huh? That would go against my stand itself.
So far, the evidence you've provided has been:

1. A review discussing PUFA mechanisms in neuronal membranes (mechanism, no clinical outcomes)
2. A small 6-week study showing increased oxidative markers with very high PUFA intake (15% of energy, not typical dietary amounts, surrogate markers are not clinical outcomes)
3. A correlation between brain fatty acid levels and depression in depressed patients (correlation =/= no causation, this is common sense, directionality unclear)
4. A cell culture study showing PUFA oxidation under artificial pro-oxidant conditions (cell culture, not humans)

What you have NOT provided, though, is:

1. Clinical trials showing that dietary PUFA at typical intake levels causes measurable harm
2. Long-term outcome data showing worse health in PUFA consumers
3. Intervention studies showing that PUFA restriction improves clinical endpoints
4. ANY DATA WHATSOEVER contradicting the 15 clinical trials I cited showing no inflammatory effects from LA consumption
does it have to be lenolic acid? Just asking so I can pick specific studies to send later.
You gave me mechanism, correlation, and cell culture. Not only did I give you clinical trials measuring inflammatory markers in humans but epidemiological data on cardiovascular outcomes and mortality.

No offense, but you have to be out of your mind to think that those are equivalent forms of evidence. When mechanism contradicts outcome data in humans, the outcome data wins. Every single time. Because what matters is what actually happens in living humans eating real food and not what happens to cells in a dish or what theoretical pathways might be activated.
I’m not claiming what I think is purely superior,I’m still open minded in this conversation yet there’s a lot of confusion here which throws me and probably you out of different shuttles.
Your evidence is insufficient to support your recommendations. That's it.
Just If you wish,I can send some more that would be more specific.
You keep contradicting yourself that I honestly can't even keep up anymore.
Like I said,confusion in this discussion.
So now PUFA isn't THE problem but a contributor that requires other stress factors to cause harm? This more weaker than the original claim you made. If PUFA only causes problems in the presence of other stressors, then you would tell users on this forum to focus on identifying and removing those stressors and not the total evisceration of PUFA altogether.
Other recommendations clearly indicated to remove other stressors,I never necessarily said PUFA intake while having everything else om perfect will doom or something. It’s just a min you could prevent I believe.
Also, this completely undermines your position on nuts and fish. If someone is managing stress well, sleeping adequately, not obese, exercising regularly... then by your own logic, moderate PUFA intake wouldn't be problematic. So why would you make a blanket recommendation to avoid nuts, seeds, and daily fish oil?

"PUFAs are bad enough to eliminate entirely, but also they're only harmful in combination with other factors."

Bro, pick one.
Low amount,ideally not omega 6s. Fish oil supplementation is just overshoot,thats what I believe in this.
I didn't claim you said that. I said your logic of "PUFAs can oxidize → dietary PUFAs cause harmful oxidation in vivo" is flawed because the capacity to oxidize doesn't automatically translate to harmful oxidation in living systems with antioxidant defenses.

You still haven't addressed this. The human body manages oxidative processes constantly. The mere fact that a molecule CAN be oxidized doesn't demonstrate that consuming it CAUSES net oxidative harm. You need to show that dietary PUFA overwhelms antioxidant systems and produces measurable oxidative damage. Where's that data?



You didn't understand what I said. So, I'll restate it again.

The same molecules (DHA and EPA) are inflammatory when taken daily in supplement form but not inflammatory when consumed 1-2x weekly from fish, and the difference is... dose frequency based on neural tissue half-life?
Not just that,but you could say that.
If someone, say, eats 200g of salmon twice weekly, they're getting roughly 3-4g of EPA/DHA per week, which averages to about 0.5-0.6g daily. That's LESS than the 1-2g daily from supplements you claim causes problems. So your fish recommendation actually provides lower weekly intake than the supplement regimen you're condemning.
i don’t understand what this supposed to ask me? Like I told you generally 0.5g of DHA and EPA (3-4g weekly) is what I see as ideal intake,I call fish oils as overshoot.
If dose frequency matters, at what interval does DHA/EPA switch from harmful to beneficial? Daily is bad, twice weekly is good... what about every other day? Every third day? You need to specify the threshold and provide evidence for it.
It’s more total weekly than total daily. So in my eye it dosen’t matter if you consume a equivalent 500mg~ serving of DHA and EPA per day via fish from a 200g serving or salmon twice a week can be the equivelant of the same dosage everyday from smaller portions of salmon for example.
And you STILL haven't explained why the molecule would be inflammatory from a capsule but not from fish. They're biochemically identical once absorbed. Your body doesn't have different metabolic pathways for "supplement DHA" V.S. "salmon DHA." That's not how it works.
I know that and there’s no need for you to explain,it’s dosage dependent and other factors. I can’t say “past this exact milligram,DHA and EPA become inflammatory” it’s individual,thats why broad numbers.



what I could appreaciate next time,is not giving me a 2 meter long list to review every small detail,shorten it up a little. I already spent a Larkin margin of this hour replying to this and honestly whats it’s just brain tiring to write so much just to realize I’m not even half way yet. I’ll completely admit that you know your things,but your responses are literal DNRfuel
I’ll respond to the rest tomorrow.
 

XvideosDemon

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By Lord Lord

I'm providing evidence-based information synthesized from peer-reviewed research. This is not medical advice, and individual nutritional needs vary based on health status, activity level, age, and other factors. If you have specific health conditions, particularly metabolic disorders, kidney disease, or cardiovascular conditions, consult with a qualified healthcare professional before making significant dietary changes.

INTRODUCTION
Nutrition is undoubtedly of the most studied fields in all of science, and simultaneously one of the most confidently misunderstood. I find that genuinely fascinating in a frustrating sort of way, as you've got decades of rigorous, peer-reviewed research sitting in journals that almost nobody reads, and right next to it is some retard on tiktok with 4 million followers telling you that olive oil or seed oil is slowly killing you. And people believe him. A lot of people.

I would consider myself a somewhat understanding individual, so I kind of get it, honestly. Nutrition research is notoriously difficult to communicate. Not only do studies contradict each other, but headlines misrepresent findings, and the actual papers are locked behind scientific jargon dense enough to make anyone's eyes glaze over. So people turn to whoever sounds the most confident and tells the most compelling story. And the most compelling stories in nutrition are almost always the most wrong ones.

There's a shit ton of examples I can provide, but we can always think back to the trajectory of dietary advice over the past 60 years. Fat was the enemy through the 70s and 80s. So food manufacturers replaced fat with sugar, gave everything a "low-fat" label, and obesity rates climbed anyway. Then, of course, followed carbohydrate, gluten, lectins, and seed oils.

When it comes to nutrition, there is always something new to be terrified of, always a new villain, always someone selling the solution. The 'villain' conveniently changes every decade but the structure of the argument stays identical:


1. Mainstream nutrition is always hiding the truth
2. This one food or food group is destroying your health
3. Here's what you should really be eating


What's actually happening is a combination of:

Genuine scientific uncertainty being exploited + Preliminary findings get reported as established fact + Some financial incentives (supplement companies, diet book deals, supplement-shilling influencers) transforms what information reaches people.

I would also include human psychology in the considering we're wired to respond to threat, to novelty, and to simple explanations for complex problems.

From personal experience, I've watched a couple of friends spend years cycling through elimination diets, cutting out entire food groups, spending money on supplements that do essentially nothing, and genuinely believing they were optimizing their health while ignoring the basics. I'm not exempt from this. Early on I went through phases of obsessing over meal timing, tracking every gram, and other nonsensical shit. It's honestly exhausting and unnecessary as fuck.

I then, fortunately, started actually reading the research. And what you find when you do that is so much less dramatic and draining than the content ecosystem wants you to believe. The fundamentals of a healthy diet are not controversial within nutrition science. They are, however, aggressively unprofitable to promote, because they don't require any 'special' products, any elimination protocols, or any influencer to explain them.

That's what this thread is. I hope you see this as an honest attempt to lay out what peer-reviewed evidence actually shows, how to eat in a way that satisfies your nutritional needs, and why a great portion of what's circulating online right now is either overstated, misinterpreted, or outright wrong.
BASELINE AND HOW TO EAT ACCORDINGLY
Your body needs three macronutrients to function:

1. Protein
2. Carbohydrates
3. Fats


The Institute of Medicine has established acceptable macronutrient distribution ranges (AMDRs) based on decades of metabolic research and epidemiological evidence.

According to this research on macronutrient requirements, these ranges are:


View attachment 29166
"carbohydrate (45%-65% of energy), protein (10%-35% of energy), and fat (20%-35% of energy; limit saturated and trans fats)"
These are RANGES, meaning there's flexibility. I promise you, your body doesn't spontaneously combust if you hit 44% carbohydrates one day.

They particularly exist due to different populations and activity levels require different distributions. If you're physically active, you'll trend toward higher carbohydrate intake (5-12 g/kg body weight depending on activity). Protein needs scale similarly, from 1.2-1.8 g/kg body weight for active individuals.

This Korean study on macronutrient distributions and hypertension found that deviating from appropriate macronutrient ranges was associated with increased hypertension risk even after adjusting for other factors.

The study tracked participants who consumed outside the Korean AMDR (carbohydrate 55-70%, fat 15-25%, protein 7-20%) and found:


View attachment 29238
"odds ratio of the non-AMDR group was 1.25 (95% CI, 1.02-1.53) in the hypertensive subjects."
Now, I know this may all seem confusing, but it practically means that balance matters more than anything. You don't have to obsess over macro-nutrients.

- Extremely low-fat diets can reduce testosterone production.
- Extremely low-carb diets can impair high-intensity performance.
- Inadequate protein compromises muscle maintenance and satiety.

You need all three in reasonable amounts.


PROTEIN:

The RDA for protein is 0.8 g/kg body weight. This number has been unchanged for over 70 years because it represents the minimum needed to prevent nitrogen loss.

What's particularly interesting to me about this is that the RDA was never meant to represent optimal intake.

This research examining protein requirements points out that
:

View attachment 29255
"the lowest level of protein intake reflected in the AMDR is higher than that of the RDA."
The AMDR allows up to 35% of calories from protein, which for most people translates to significantly more than 0.8 g/kg.

Recent studies, particularly in older adults, show benefits at intakes exceeding the RDA. For most people, aiming for 1.2-1.6 g/kg body weight makes sense, with higher intakes (1.6-2.2 g/kg) justified for those doing resistance training or in caloric deficits.

It literally:


1. Has the highest thermic effect of all macronutrients (meaning your body burns more calories digesting it)
2. Promotes satiety better than carbs or fats
3. Is essential for maintaining lean mass.


The study below on protein and cognitive function found that:

Yes, plant proteins count. No, you don't need to eat 200g of chicken breast daily.

CARBOHYDRATES:

There are two types of carbohydrates:

1. Complex carbohydrates
2. Simple carbohydrates


Carbs are not poisonous nor are they universally benign.

The type matters enormously.

We can tell by looking at the same research on macronutrients and cognitive function from earlier that found a clear distinction:

View attachment 29283
"Intake of simple carbohydrates ('sugars') is consistently associated with decreased global cognition whereas consumption of complex carbohydrates correlates with successful brain aging and improved memory both in the short- and long-term."
Complex carbohydrates include:

- Whole grains
- Legumes
- Vegetables
- Fruits


They provide fiber, vitamins, minerals, and sustained energy. Simple carbohydrates (added sugars, refined grains) spike blood glucose rapidly and provide little nutritional value beyond calories.

We can see the difference in mortality data. There are multiple meta-analyses that show that whole grain consumption reduces all-cause mortality.


One comprehensive analysis
examining prospective cohort studies found this about whole grain intake:

View attachment 29326
The dose-response showed benefits up to 210-225 g/day (about 7-7.5 servings)

Another meta-analysis found that comparing highest to lowest whole grain intake categories yielded a pooled relative risk of 0.84 for cardiovascular mortality and 0.91 for total mortality. For every 48g (about 1.5 servings) of whole grains consumed daily, there was a 7% reduction in all-cause mortality and a 9% reduction in CVD mortality.
Refined grains show the opposite pattern or no significant association, and in some analyses, higher refined grain intake correlates with increased mortality risk.


CARBOHYDRATE SOURCES
View attachment 29335

FATS:
Dietary fat is essential. You need it for:

- Hormone production
- Vitamin absorption (A, D, E, K are fat-soluble)
- Cell membrane integrity
- Brain function


The question is which fats?

The evidence is clear on trans fats: avoid them. They're associated with increased cardiovascular disease risk and were banned in many countries for good reason. Saturated fat is more nuanced. If your intake is excessive, it does tend to correlate with elevated LDL cholesterol. HOWEVER, moderate consumption within the 20-35% fat range appears fine for most people.

The ACTUAL discussion should focus on unsaturated fats, particularly:


1. Omega-3
2.
Omega-6 fatty acids


Both are essential (your body cannot synthesize them), but their ratio in the diet matters.

Linoleic acid (LA), the primary omega-6 fatty acid, has been highly demonized online. The "seed oil" panic is one of the most persistent nutrition myths of the 2020s. Hence why I want to show you guys what the research actually shows.


A 2024 review of omega-6 fatty acids
examining literature from January 2023 to August 2024 concluded that:
View attachment 29339
"Contrary to previous concerns that high LA intake may increase inflammation, most recent evidence supports the benefits of LA for cardiometabolic health. Several large studies report that higher blood LA levels correlate with reduced risks of coronary heart disease, stroke, and type 2 diabetes."
The mechanisms include activation of peroxisome proliferator-activated receptors (PPARs) + modulation of oxylipins involved in glucose and lipid metabolism. Current intakes around 5-10% of energy appear beneficial.

A systematic review specifically addressing the "LA causes inflammation" hypothesis examined 15 clinical trials, stating:

View attachment 29343
"failed to find any support for the 'diet LA causes inflammation hypothesis.'"

View attachment 29531
"LA appears to reduce inflammation and reduce risk for CMD" (cardiometabolic disease).

Above that, the review also stated that the dogma positioning LA as pro-inflammatory because it's an omega-6 fatty acid is false when examined in human studies.

This study on omega-6 fatty acids and inflammation concluded:

View attachment 29537
"studies in healthy human adults have found that increased intake of ARA or LA does not increase the concentrations of many inflammatory markers. Epidemiological studies have even suggested that ARA and LA may be linked to reduced inflammation."
The confusion basically comes from the mechanistic thinking that omega-6 fatty acids CAN be metabolized into pro-inflammatory eicosanoids. But in practice, humans consuming normal amounts of LA don't show increased inflammatory markers. The theoretical pathway =/= clinical inflammation in well-nourished humans.

Am I saying there is no legitimate discussion about omega-6 to omega-3 ratios? No. Not at all. In fact, research on this topic literally states that Western diets provide omega-6/3 ratios around 20:1, whereas ratios of 4:1 or less may be more optimal.

Now, is the solution to eliminate omega-6 (which would require avoiding nuts, seeds, and many healthy foods)? No. That would be, quite frankly, insanely retarded. All you need to do is increase omega-3 intake from fatty fish, flaxseeds, walnuts, and chia seeds.


One legitimate concern about seed oils came from this research on heating vegetable oils. When oils high in linoleic acid are heated to high temperatures, they can form toxic aldehydes like 4-hydroxynonenal (4-HNE). The study found that oils high in linoleic acid (soybean, sunflower, some canola products) generated significant 4-HNE when heated to 200°C for extended periods, while oils low in polyunsaturated fats (coconut oil) generated negligible amounts.

Now, THIS is a somewhat reasonable concern for deep frying, but it doesn't justify the blanket condemnation of all seed oils. The issue is oxidative stress from prolonged high-heat cooking, which affects any PUFA-rich oil.



METHOD:

Using high-heat stable oils (avocado, refined olive, coconut) for cooking above 180°C and reserving PUFA-rich oils for lower-heat applications or actual use would be a sensible approach.



MICRO-NUTRIENTS:
Vitamins and minerals don't get the attention macronutrients do, but deficiencies cause actual, measurable problems. This research on micronutrients basically identifies 13 essential vitamins and 10 essential trace elements that humans require.

Water-soluble vitamins (B-complex, C) need regular replenishment since your body doesn't store them long-term. Fat-soluble vitamins (A, D, E, K) can be stored, which means both deficiency and toxicity are possible.

This study on micronutrient deficiencies globally notes that:

View attachment 29540
"deficiencies of vitamin A and zinc increase the risk of child mortality, and zinc deficiency increases infectious morbidity and reduces linear growth as well. Deficiencies of iodine and iron are significant primarily for their effects on development and cognition and consequent disabilities."
The most commonly deficient micronutrients in developed countries, according to recent research, are:

1. Vitamin D
2. Iron
3. Vitamin A
4. Zinc
5. Folate
6. Iodine


Vitamin D deserves special mention.

Most people in non-equatorial climates are deficient or insufficient. Supplementation of 1000-2000 IU/day is reasonable for most adults, though individual needs vary based on baseline levels, sun exposure, and skin pigmentation.
Iron deficiency is pretty common in menstruating individuals and can cause negative effects on the body like fatigue and cognitive impairment.

This research on iron and cognition showed that significant effects on neurological function happens when deficient.

B vitamins, particularly B12, folate, and B6, are also really important for neurological function and energy metabolism. B12 is found almost exclusively in animal products, making supplementation necessary for strict vegans.


MICRO-NUTRIENT SOURCES
You get micronutrients from eating varied, minimally processed foods. A diet with:
View attachment 29544
FIBER
Fiber is technically a carbohydrate, but since humans lack the enzymes to digest it fully, it functions differently. It's classified as:

1. Soluble (dissolves in water, found in oats, beans, apples)
Or
2. Insoluble (doesn't dissolve, found in whole wheat, vegetables, nuts)

This research on fiber and cardiovascular health found that:


View attachment 29545
"regular consumption of dietary fiber, particularly fiber from cereal sources, may improve CVD health through multiple mechanisms including lipid reduction, body weight regulation, improved glucose metabolism, blood pressure control, and reduction of chronic inflammation."

The umbrella review I provided below of fiber meta-analyses found that individuals consuming the highest amounts of dietary fiber showed statistically significant reductions in cardiovascular disease mortality (RR = 0.77-0.83), CVD incidence (RR = 0.72-0.91), coronary heart disease (RR = 0.76-0.93), and stroke (RR = 0.83-0.93) compared to lowest intake groups.

View attachment 29555
And this systematic review on fiber and mortality concluded that:

View attachment 29556
"greater dietary fibre intake is associated with a lower risk of both cardiovascular disease and coronary heart disease." The dose-response analysis found benefits for each 7 g/day increase in total fiber intake.
This updated meta-analysis data from 64 studies with over 3.5 million subjects found that:

View attachment 29561
"higher consumption of total dietary fiber, significantly decreased the risk of all-cause mortality, CVD-related mortality, and cancer-related mortality by 23, 26 and 22%."
The mechanisms involve multiple pathways, like:

Fiber feeds beneficial gut bacteria -> slows glucose absorption -> increases satiety -> binds bile acids (forcing cholesterol use for replacement) -> modulates inflammation through short-chain fatty acid production.

Current recommendations suggest 25-30g daily for most adults. The average American consumes around 15g. The gap isn't small.


FIBER SOURCES
View attachment 29562

You will NOT hit adequate fiber eating primarily meat, dairy, and refined carbohydrates. You just won't.

PLANT-BASED FOODS:

The research on plant-based diets has exploded in the past decade.

A comprehensive review of plant-based diets and cardiovascular health found that:


View attachment 29577
"plant-based diets, especially when rich in high quality plant foods such as whole grains, fruits, vegetables, and nuts" were "associated with lower risk of cardiovascular outcomes and intermediate risk factors."
Does quality matter at all? Yes, it does. Enormously.

In fact, this research distinguishing healthy from unhealthy plant-based diets found that even though overall plant-based diet adherence associated with 8% lower cardiovascular mortality, unhealthy plant-based diets (high in refined grains, potatoes/fries, sugar-sweetened beverages) showed INCREASED cardiovascular mortality risk (HR: 1.05).

Conversely, healthy plant-based diets rich in whole grains, fruits, vegetables, nuts, and legumes showed decreased CVD incidence (HR: 0.87).


View attachment 29589
"participants in the highest versus lowest quintile for adherence to overall plant-based diet index or provegetarian diet had a 16%, 31% to 32%, and 18% to 25% lower risk of cardiovascular disease, cardiovascular disease mortality, and all-cause mortality, respectively."

View attachment 29590
Interestingly enough, this research in African American populations found no significant association between plant-based diet adherence and CVD or mortality.
What this basically suggests is that population-specific factors or different baseline dietary patterns may possibly modify effects.

Meta-analysis across multiple ethnicities in the Multiethnic Cohort Study found that:


View attachment 29597
"healthy plant-based dietary pattern emphasizing the quality of plant foods was associated with a lower risk of all-cause and CVD mortality in both men and women," though magnitude is varied by other factors such as race and ethnicity.

Do you see the consistent pattern? Specifically diets rich in minimally processed plant foods correlate with better health outcomes. This doesn't require veganism or vegetarianism.
How do we know they don't? Well, if we look at this research, it explicitly notes that:

View attachment 29643
"plant-based diets do not have to be vegan or vegetarian. For most people, complete elimination of meat or animal products is unrealistic and not necessary for cardiovascular health."
The takeaway to all of this is that what matters is the proportion and quality of plant foods consumed and not the complete exclusion of animal products.

CONCLUSION
Human nutrition is complex enough that rigid rules fail for most people. So, as far as we know, your optimal diet depends on:

1. Activity level (athletes need more carbs and protein than sedentary individuals)
2. Age (protein requirements increase with age, caloric needs typically decrease)
3. Health status (diabetes changes carbohydrate metabolism, kidney disease modifies protein needs)
4. Genetics (some people process saturated fat differently, lactose intolerance varies by ancestry)
5. Food availability and culture
6. Personal preferences and sustainability


Based on the research I've provided so far, the evidence consistently supports:

1. Base your diet on minimally processed foods. This single principle addresses, like, 80% of nutritional concerns. Whole grains instead of refined. Whole fruits instead of juice. Nuts instead of nut-flavored cereal. The closer food is to its original form, the more likely it retains beneficial nutrients and fiber.

2. Eat sufficient protein distributed throughout the day. Aim for 1.2-1.6 g/kg for most people, higher if very active or older. Include it at each meal for optimal muscle protein synthesis.

3. Prioritize complex carbohydrates over simple sugars.
Your carbohydrate intake should come primarily from whole grains, legumes, vegetables, and fruits. You CAN eat refined grains and added sugars, but try to limit them.

4. Include varied sources of fat. Emphasize
unsaturated fats from nuts, seeds, avocados, olive oil, and fatty fish. Don't fear saturated fat in moderate amounts, but don't center your diet around it. Omega-3 intake deserves attention.

5. Eat enough fiber. If you're following points 1-4, this happens automatically. If you're not hitting 25-30g daily, something's wrong with your food choices.

6. Include a wide variety of plant foods. Vegetables and fruits provide micronutrients, phytochemicals, and fiber that are difficult to obtain elsewhere. Different colors typically indicate different nutrient profiles.

7. Don't obsess over minor details.
The difference between 45% and 50% carbohydrate intake is so little compared to whether those carbohydrates come from whole grains or refined flour. Focus on the big patterns before micromanaging macros.

Notice that calorie counting, macronutrient calculation to the gram, food timing rules, supplement stacks, meal frequency dogma is absent in this entire guide. That's simply because those things can matter for specific goals (athletic performance, bodybuilding, metabolic conditions), but for general health, food quality and variety matter far more than being precise.

You don't need to be perfect. In fact, a diet that's 80% whole foods and includes regular vegetables, adequate protein, and sufficient fiber will outperform a "perfect" diet that's abandoned after two weeks because it's unsustainable.

The best diet is one that's:

- Nutritionally adequate

- Practically sustainable
- Culturally appropriate

- Enjoyable enough to be consistent about it

This might look like Mediterranean for some, like traditional Asian diets for others, or like modernized versions of indigenous food patterns. The common thread behind all of this is principles. Minimal processing, plant emphasis, adequate protein, healthy fats.
Dnr but Mirin cutie will read when I have time love ya 🤞😘❤️
 

Lord

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It’s part of the process because that is the main driver in my opinion. Excess peripheral serotonin->CRH->ACTH->Cortisol. I talked about this in another thread,yet you only seem to have read one.
And generally if stress responses are further induced from example a modern diet+PUFA then of course what would excessive ATDH stimulation do? Not an anti inflammatory result as obvious .

That's a five-step cascade where each step needs to be demonstrated in humans at dietary PUFA levels. You've provided... none of that. You've simply just asserted the pathway exists and then claimed it's "obvious" that this causes inflammation.

as stated before,lots of the inflammatory response is downstream from excess endochromaffin stimulation.

Speculative.

Show me intervention data where PUFA restriction reduces peripheral serotonin, which reduces CRH, which reduces cortisol, which reduces measured inflammation. If you can't show that chain working in practice, you are, once again, literally worshipping mechanism.

isn’t it obvious?

No.

It’s digestion speed and endrochromaffin sensory rate.

Okay, so you're claiming faster tryptophan absorption from meat causes stronger enterochromaffin cell activation than slower absorption from dairy. Where's the human data showing this matters clinically? Where are the outcomes demonstrating that people eating more meat have elevated peripheral serotonin and worse health markers than people eating more dairy?

You keep describing mechanisms like they're self-evident harms without ever demonstrating the harm.

You can’t avoid PUFA completely. And thats my point that just proved,but for you the “excessive” amount is higher than what I state is “excessive”. It’s like, if I’d tell to do the most lowest fat diet possible,you would still end up with a few grams of dietary fat. And didn’t I state that I recommend fish consumption?
IMG_2782.jpeg

Like I said,your “excessive limit” in your belief is just higher than mine.

Right, so we both acknowledge some PUFA is unavoidable and necessary. The question is where the threshold for harm sits.

You're claiming 300-500mg EPA/DHA is ideal and anything above causes "unnecessary oxidative stress." I'm saying moderate intake (1-2g daily, which is common in populations with excellent health outcomes) shows no evidence of harm and considerable evidence of benefit.

The burden is on YOU to show that your threshold is correct. You can't just assert "anything above 500mg is excessive" without showing that intakes above that level produce worse outcomes. Where's that data?

But yeah tbh these aint the best studies.

Thank you. Genuinely. Your studies were weak, and you've now admitted it. So if those aren't the best studies, where are the better ones?

does it have to be lenolic acid? Just asking so I can pick specific studies to send later.

Yes. That's what you've been claiming is harmful. That's what the 15 clinical trials I cited tested and found no inflammatory effect from. If you have studies contradicting those findings, provide them. Specifically. Linoleic acid, human subjects, measured inflammatory outcomes.

Then does saturated fat still show more stability in a Petri dish according to another one,I’ll try finding it later.

Of course saturated fat is more stable in a petri dish. It has fewer double bonds. That's chemistry. But we're not eating in petri dishes. We're eating in human bodies with antioxidant systems. The question isn't which fat is chemically more stable in isolation, the question is which fat consumption pattern produces better health outcomes in humans. And the answer from epidemiology is moderate PUFA inclusion from whole food sources.

I consume Salmon and other fish, huh? That would go against my stand itself.

...so you eat salmon, which contains the exact PUFAs you're telling other people to minimize, because you understand that the practical benefits outweigh the theoretical oxidation concerns?

That's the entire argument I've been making.

Moderate PUFA consumption from whole foods (fish, nuts, seeds) provides benefits that outweigh any theoretical oxidation risk, especially in the context of adequate antioxidant intake and overall healthy dietary patterns.

You're living the position I'm advocating while telling others to avoid it. That's either inconsistency or you don't actually believe your own framework.

I’m not claiming what I think is purely superior,I’m still open minded in this conversation

If you're open-minded, then acknowledge that your evidence doesn't support your recommendations.

Being open-minded means updating your position when the evidence doesn't support it.

Are you willing to do that, or are you just saying you're open-minded while continuing to recommend PUFA avoidance regardless of what the data shows?

It’s just a min you could prevent I believe.

So, It's just something to minimize as a precaution alongside other factors...?

That's a MUCH weaker claim than your original thread, which presented PUFA avoidance as a foundational dietary principle alongside "eat most carbs early" and "prioritize dairy over meat."

If PUFA is just one minor factor among many, why is it getting equal billing with actually important dietary patterns? Why tell people to avoid nuts and seeds and limit fish to twice weekly if the effect is marginal and context-dependent?

Low amount,ideally not omega 6s. Fish oil supplementation is just overshoot,thats what I believe in this.

Based on what? The populations consuming more EPA/DHA than your recommendations (Japan, Mediterranean regions, Nordic countries) show excellent health outcomes. How do you explain that if supplemental-range intakes are harmful?

your responses are literal DNRfuel
Lol.

I'm not making you respond to everything. But if you're going to make specific claims (PUFAs cause inflammation, nuts should be avoided, fish oil is harmful, 300-500mg EPA/DHA is ideal), you should be able to defend those claims when challenged.
 

Mandy

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That's a five-step cascade where each step needs to be demonstrated in humans at dietary PUFA levels. You've provided... none of that. You've simply just asserted the pathway exists and then claimed it's "obvious" that this causes inflammation.



Speculative.

Show me intervention data where PUFA restriction reduces peripheral serotonin, which reduces CRH, which reduces cortisol, which reduces measured inflammation. If you can't show that chain working in practice, you are, once again, literally worshipping mechanism.



No.



Okay, so you're claiming faster tryptophan absorption from meat causes stronger enterochromaffin cell activation than slower absorption from dairy. Where's the human data showing this matters clinically? Where are the outcomes demonstrating that people eating more meat have elevated peripheral serotonin and worse health markers than people eating more dairy?

You keep describing mechanisms like they're self-evident harms without ever demonstrating the harm.



Right, so we both acknowledge some PUFA is unavoidable and necessary. The question is where the threshold for harm sits.

You're claiming 300-500mg EPA/DHA is ideal and anything above causes "unnecessary oxidative stress." I'm saying moderate intake (1-2g daily, which is common in populations with excellent health outcomes) shows no evidence of harm and considerable evidence of benefit.

The burden is on YOU to show that your threshold is correct. You can't just assert "anything above 500mg is excessive" without showing that intakes above that level produce worse outcomes. Where's that data?



Thank you. Genuinely. Your studies were weak, and you've now admitted it. So if those aren't the best studies, where are the better ones?



Yes. That's what you've been claiming is harmful. That's what the 15 clinical trials I cited tested and found no inflammatory effect from. If you have studies contradicting those findings, provide them. Specifically. Linoleic acid, human subjects, measured inflammatory outcomes.



Of course saturated fat is more stable in a petri dish. It has fewer double bonds. That's chemistry. But we're not eating in petri dishes. We're eating in human bodies with antioxidant systems. The question isn't which fat is chemically more stable in isolation, the question is which fat consumption pattern produces better health outcomes in humans. And the answer from epidemiology is moderate PUFA inclusion from whole food sources.



...so you eat salmon, which contains the exact PUFAs you're telling other people to minimize, because you understand that the practical benefits outweigh the theoretical oxidation concerns?

That's the entire argument I've been making.

Moderate PUFA consumption from whole foods (fish, nuts, seeds) provides benefits that outweigh any theoretical oxidation risk, especially in the context of adequate antioxidant intake and overall healthy dietary patterns.

You're living the position I'm advocating while telling others to avoid it. That's either inconsistency or you don't actually believe your own framework.



If you're open-minded, then acknowledge that your evidence doesn't support your recommendations.

Being open-minded means updating your position when the evidence doesn't support it.

Are you willing to do that, or are you just saying you're open-minded while continuing to recommend PUFA avoidance regardless of what the data shows?



So, It's just something to minimize as a precaution alongside other factors...?

That's a MUCH weaker claim than your original thread, which presented PUFA avoidance as a foundational dietary principle alongside "eat most carbs early" and "prioritize dairy over meat."

If PUFA is just one minor factor among many, why is it getting equal billing with actually important dietary patterns? Why tell people to avoid nuts and seeds and limit fish to twice weekly if the effect is marginal and context-dependent?



Based on what? The populations consuming more EPA/DHA than your recommendations (Japan, Mediterranean regions, Nordic countries) show excellent health outcomes. How do you explain that if supplemental-range intakes are harmful?


Lol.

I'm not making you respond to everything. But if you're going to make specific claims (PUFAs cause inflammation, nuts should be avoided, fish oil is harmful, 300-500mg EPA/DHA is ideal), you should be able to defend those claims when challenged.
I’ll respond tomorrow,it was just too long.
 

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