Causal effects of relative fat, protein, and carbohydrate intake on chronic kidney disease

Mito

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ABSTRACT​

Background
The effects of specific macronutrients on kidney function independent of total calorie intake have rarely been studied, although the composition of macronutrient intake has been reported to affect health outcomes.
Objectives
We aimed to investigate the effects of macronutrient intake ratios on the risk of chronic kidney disease (CKD) by Mendelian randomization (MR) analysis.
Methods
The study was an observational cohort study mainly based on the UK Biobank and including MR analysis. First, we evaluated the relative baseline macronutrient composition—that is, the number of calories from each macronutrient divided by total calorie intake—of the diets of UK Biobank participants, and we used Cox regression to assess the incidence of end-stage kidney disease (ESKD) in 65,164 participants with normal kidney function [estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m2]. We implemented a genetic instrument for relative fat, protein, and carbohydrate intake developed by a previous genome-wide association study (GWAS) and performed MR analysis. Two-sample MR was performed with the summary statistics from independent CKDGen GWAS for kidney function traits (n = 567,460), including CKD (eGFR <60 mL/min/1.73 m2) and log-transformed eGFR.
Results
The median relative macronutrient intake composition at baseline was 35% fats, 15% protein, and 50% carbohydrates. Higher relative protein intake in subjects with normal kidney function was significantly associated with a lower risk of incident ESKD (HR: 0.54; 95% CI: 0.30, 0.95) in the observational investigation. Two-sample MR indicated that increased relative fat intake causally increased the risk of kidney function impairment [CKD (OR: 1.94; 95% CI: 1.39, 2.71); log eGFR (β: −0.036; 95% CI: −0.048, −0.024)] and that higher relative protein intake was causally linked to a lower CKD risk [CKD (OR: 0.50; 95% CI: 0.35, 0.72); log eGFR (β: 0.044; 95% CI: 0.030, 0.058)].
Conclusions
A desirable macronutrient composition, including high relative protein intake and low relative fat intake, may causally reduce the risk of CKD in the general population.
 

Blaze

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Joined
Apr 25, 2020
Messages
202

ABSTRACT​

Background
The effects of specific macronutrients on kidney function independent of total calorie intake have rarely been studied, although the composition of macronutrient intake has been reported to affect health outcomes.
Objectives
We aimed to investigate the effects of macronutrient intake ratios on the risk of chronic kidney disease (CKD) by Mendelian randomization (MR) analysis.
Methods
The study was an observational cohort study mainly based on the UK Biobank and including MR analysis. First, we evaluated the relative baseline macronutrient composition—that is, the number of calories from each macronutrient divided by total calorie intake—of the diets of UK Biobank participants, and we used Cox regression to assess the incidence of end-stage kidney disease (ESKD) in 65,164 participants with normal kidney function [estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m2]. We implemented a genetic instrument for relative fat, protein, and carbohydrate intake developed by a previous genome-wide association study (GWAS) and performed MR analysis. Two-sample MR was performed with the summary statistics from independent CKDGen GWAS for kidney function traits (n = 567,460), including CKD (eGFR <60 mL/min/1.73 m2) and log-transformed eGFR.
Results
The median relative macronutrient intake composition at baseline was 35% fats, 15% protein, and 50% carbohydrates. Higher relative protein intake in subjects with normal kidney function was significantly associated with a lower risk of incident ESKD (HR: 0.54; 95% CI: 0.30, 0.95) in the observational investigation. Two-sample MR indicated that increased relative fat intake causally increased the risk of kidney function impairment [CKD (OR: 1.94; 95% CI: 1.39, 2.71); log eGFR (β: −0.036; 95% CI: −0.048, −0.024)] and that higher relative protein intake was causally linked to a lower CKD risk [CKD (OR: 0.50; 95% CI: 0.35, 0.72); log eGFR (β: 0.044; 95% CI: 0.030, 0.058)].
Conclusions
A desirable macronutrient composition, including high relative protein intake and low relative fat intake, may causally reduce the risk of CKD in the general population.
Walter Kempner and his rice diet specifically addressed treatment of CKD , high blood pressure, heart disease , diabetes and other conditions in real patients by changing the macro-nutrients way back in the 1940’s and healed almost everyone. In a time where medicine had no other treatment options and you would die. Program ran at Duke Univesity until the 1990’s. Kempner used
A diet of nearly pure carbs reversed CKD. No fat and 5% protein permitted. No salt allowed. So, carbs in near total isolation efffectively reversed CKD and many disease conditions in truly miraculous fashion.

The macro percentages in that study look like it would give a flawed result as no macros were given in isolation or near isolation to determine specific macro effects. Merely altered the intake percentages a little and measured the kidney function. The increase in protein credited with less CKD might really just reflect the decreased fat percentage causing the benefit instead of their conclusion that it was the protein.

So, carbs in isolation according to Kempner had a great benefit.(Carbosis-according to Minger)
I doubt protein in isolation/excess would be anything but damaging to CKD due to the nitrogenous waste products.
Fat in isolation‘s effects on the kidneys if you nearly eliminate carbs (think ketosis) might very well be beneficial or not for some disease conditions.

But A diet of nearly pure protein cannot be ok for CKD. In excess it would only be a burden on the liver and kidneys.

Fat intake in an already metaboloically compromised end stage CKD patient without eliminating carbs interferes with mitochondria energy production due to the Randle effect. A person who is metabolically healthy might be ok with those macros but not someone so close to kidney failure. The kidney has the body’s absolute highest metabolic rate. Even more than the brain. Fat in the presence of carbs inhibits the ability to use glucose for energy.

They should have isolated each macro as much as possible to determine the effect.
 
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Mito

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Walter Kempner and his rice diet specifically addressed treatment of CKD , high blood pressure, heart disease , diabetes and other conditions in real patients by changing the macro-nutrients way back in the 1940’s and healed almost everyone. In a time where medicine had no other treatment options and you would die. Program ran at Duke Univesity until the 1990’s. Kempner used
A diet of nearly pure carbs reversed CKD. No fat and 5% protein permitted. No salt allowed. So, carbs in near total isolation efffectively reversed CKD and many disease conditions in truly miraculous fashion.

The macro percentages in that study look like it would give a flawed result as no macros were given in isolation or near isolation to determine specific macro effects. Merely altered the intake percentages a little and measured the kidney function. The increase in protein credited with less CKD might really just reflect the decreased fat percentage causing the benefit instead of their conclusion that it was the protein.

So, carbs in isolation according to Kempner had a great benefit.(Carbosis-according to Minger)
I doubt protein in isolation/excess would be anything but damaging to CKD due to the nitrogenous waste products.
Fat in isolation‘s effects on the kidneys if you nearly eliminate carbs (think ketosis) might very well be beneficial or not for some disease conditions.

But A diet of nearly pure protein cannot be ok for CKD. In excess it would only be a burden on the liver and kidneys.

Fat intake in an already metaboloically compromised end stage CKD patient without eliminating carbs interferes with mitochondria energy production due to the Randle effect. A person who is metabolically healthy might be ok with those macros but not someone so close to kidney failure. The kidney has the body’s absolute highest metabolic rate. Even more than the brain. Fat in the presence of carbs inhibits the ability to use glucose for energy.

They should have isolated each macro as much as possible to determine the effect.
The study is regarding protein as a possible cause of CKD, not a diet to treat someone who already has it.

PROTEIN AND KIDNEY DAMAGE/DISEASE

You’ve heard it before, you’ll hear it again: protein causes your kidneys to fail. This is a 50+-year-old thesis coined by Brenner that goes something like this. Protein leads to urea production, urea has to be filtered by your kidneys, your kidneys work harder, and this leads to the eventual destruction of the nephron (the kidney’s functional unit). But in humans, there’s no evidence that this occurs (1, 2). The conclusions of these papers (1, 2) are actually also in-line with another meta-analysis of the protein-kidney failure argument (3); however, we showed their methods to be faulty (1). Also, their narrative (3) interpretation of the ‘bad’ effects protein has on the kidney simply doesn’t show the decline in kidney function you would expect IF the Brenner hypothesis is correct!

Yesterday this article dropped: https://academic.oup.com/.../10.1093/ajcn/nqaa379/.... Essentially, the article uses a fancy method of randomization (not really randomization in the traditional sense) called Mendelian Randomization. Mendelian randomization uses genetic variation as a natural experiment to investigate the causal relations between potentially modifiable risk factors and health outcomes in observational data. In the UK biobank sample studied (>65k people), the authors then use Genome-wide Association Study data as a comparator. It’s not the easiest study to understand, but using association (Note: that’s important) they ascribe what they label as ‘causal’ effects (if you believe in Mendelian Randomization then you might accept causal, but it’s still association in my books). Here are the authors’ results and conclusions:

“Higher relative protein intake in subjects with normal kidney function was significantly associated with a LOWER risk of incident ESKD [end-stage kidney disease] (HR: 0.54; 95% CI: 0.30, 0.95)… increased relative fat intake causally increased the risk of kidney function impairment [CKD (OR: 1.94; 95% CI: 1.39, 2.71)… and that higher relative protein intake was causally linked to a lower CKD risk [CKD (OR: 0.50; 95% CI: 0.35, 0.72)… A desirable macronutrient composition, including high relative protein intake and low relative fat intake, may causally reduce the risk of CKD in the general population.”

To me, this is simply another nail in the coffin in which the Brenner thesis should be buried. I realize that the absence of evidence isn’t evidence of absence, but honestly, this thesis has lived in a vacuum of data for too long. People need to stop saying that protein CAUSES [sic] kidney (or liver, which sometimes is thrown in for ‘good measure’) failure/damage. There’s simply NO data to indicate that’s true! The circular logic of renal patients on low(er) protein diets is NOT evidence that protein caused the disease in the first place.
 

Blaze

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Apr 25, 2020
Messages
202
The study is regarding protein as a possible cause of CKD, not a diet to treat someone who already has it.

PROTEIN AND KIDNEY DAMAGE/DISEASE

You’ve heard it before, you’ll hear it again: protein causes your kidneys to fail. This is a 50+-year-old thesis coined by Brenner that goes something like this. Protein leads to urea production, urea has to be filtered by your kidneys, your kidneys work harder, and this leads to the eventual destruction of the nephron (the kidney’s functional unit). But in humans, there’s no evidence that this occurs (1, 2). The conclusions of these papers (1, 2) are actually also in-line with another meta-analysis of the protein-kidney failure argument (3); however, we showed their methods to be faulty (1). Also, their narrative (3) interpretation of the ‘bad’ effects protein has on the kidney simply doesn’t show the decline in kidney function you would expect IF

Yesterday this article dropped: https://academic.oup.com/.../10.1093/ajcn/nqaa379/.... Essentially, the article uses a fancy method of randomization (not really randomization in the traditional sense) called Mendelian Randomization. Mendelian randomization uses genetic variation as a natural experiment to investigate the causal relations between potentially modifiable risk factors and health outcomes in observational data. In the UK biobank sample studied (>65k people), the authors then use Genome-wide Association Study data as a comparator. It’s not the easiest study to understand, but using association (Note: that’s important) they ascribe what they label as ‘causal’ effects

To me, this is simply another nail in the coffin in which the Brenner thesis should be buried. I realize that the absence of evidence isn’t evidence of absence, but honestly, this thesis has lived in a vacuum of data for too long. People need to stop saying that protein CAUSES [sic] kidney or liver failure.
I glad you posted that and , You are correct , of course that the study is on healthy people who do not have CKD yet. They followed a large group to see who got worse kidney function. I am in no way anti protein and a healthy kidney can handle a ton more protein than most people think.

Protein in extreme excess is nothing but a burden ......... and excess phospate also for that matter. It can and will certainly damage organs in excess.
 

Serge

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Good, it seems like we have a full spectrum of opinions :) In short - high blood sugar does this (at least with diabetics)

 

Blaze

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Good, it seems like we have a full spectrum of opinions :) In short - high blood sugar does this (at least with diabetics)

Well, after personally rigorously experimenting for years with every single diet approach under the sun, I now heavily favor a more Peat style diet approach. He repeatedly recommends lower fat intake and not eating way too much protein or phosphate.He favors non starch sugars like fruit and and seems very liberal about large amounts of sugar use and even says it can help to cure diabetics and that they die faster if you withhold sugar. So, on this forum, an approach blaming high blood sugar exclusively for damage done to diabetics would not seem to be in line at all with those recommendations by Ray.
 

Serge

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Well, after personally rigorously experimenting for years with every single diet approach under the sun, I now heavily favor a more Peat style diet approach. He repeatedly recommends lower fat intake and not eating way too much protein or phosphate.He favors non starch sugars like fruit and and seems very liberal about large amounts of sugar use and even says it can help to cure diabetics and that they die faster if you withhold sugar. So, on this forum, an approach blaming high blood sugar exclusively for damage done to diabetics would not seem to be in line at all with those recommendations by Ray.
I definitely agree. But still here's a guy who reached like 86 years old living most of his life with T1D and treating patients with T2D and T1D presumably sucessfully. He doesn't favor high fat, so he must be advocating high protein and is clearly anti-sugar. Go figure. I myself is HCLF, see what happens with my BG in a few months, right now I'm around 8mmol/l average during the day.
 

Blaze

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Messages
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I definitely agree. But still here's a guy who reached like 86 years old living most of his life with T1D and treating patients with T2D and T1D presumably sucessfully. He doesn't favor high fat, so he must be advocating high protein and is clearly anti-sugar. Go figure. I myself is HCLF, see what happens with my BG in a few months, right now I'm around 8mmol/l average during the day.
Lol , we all end up experimenting on ourselves with diet. Sugar is either awesome or a great evil due to location alone. Sugar metabolized properly and used in the cells for energy production—awesome. Sugar that was metabolically prevented from being utilized by the cells for energy or prevented from being stored as fat or glycogen for later use is then found located in the bloodstream at unhealthy levels and is a great evil wreaking havock and damaging everything.

Get back to us and keep us informed on whatever success you have and what works best for you. We all learn from each other on this forum. Best of luck maintaining healthy levels of blood glucose.
 
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Serge

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Get back to us and keep us informed on whatever success you have and what works best for you. We all learn from each other on this forum. Best of luck maintaining healthy levels of blood glucose.
I definitely will! I know for myself that detailed personal experience (better successful:happy:) is valuable for many people.
 
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