Overview of the rationale for dietary fat guidelines

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Eddy Edson

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Relationship to Diabetes
Type 2
Detailed review of the evidence for fat quality => LDL-C => CV risks.

https://www.atherosclerosis-journal.com/article/S0021-9150(23)05354-6/fulltext

Highlights

  • LDL particle concentration, usually estimated by LDL-C, causally affects ASCVD.
  • Dietary fat quality is the main environmental determinant of plasma LDL-C.
  • Fat quality affects the risk of ASCVD risk mainly by modifying plasma LDL-C.
  • Dietary guidelines for fat build on the totality and strength of the evidence.
  • There is low probability that they will fundamentally change in the future.

Abstract

The scientific evidence supporting the current dietary recommendations for fat quality keeps accumulating; however, a paradoxical distrust has taken root among many researchers, clinicians, and in parts of the general public. One explanation for this distrust may relate to an incomplete overview of the totality of the evidence for the link between fat quality as a dietary exposure, and health outcomes such as atherosclerotic cardiovascular disease (ASCVD). Therefore, the main aim of the present narrative review was to provide a comprehensive overview of the rationale for dietary recommendations for fat intake, limiting our discussion to ASCVD as outcome. Herein, we provide a core framework – a causal model – that can help us understand the evidence that has accumulated to date, and that can help us understand new evidence that may become available in the future. The causal model for fat quality and ASCVD is comprised of three key research questions (RQs), each of which determine which scientific methods are most appropriate to use, and thereby which lines of evidence that should feed into the causal model. First, we discuss the link between low-density lipoprotein (LDL) particles and ASCVD (RQ1); we draw especially on evidence from genetic studies, randomized controlled trials (RCTs), epidemiology, and mechanistic studies. Second, we explain the link between dietary fat quality and LDL particles (RQ2); we draw especially on metabolic ward studies, controlled trials (randomized and non-randomized), and mechanistic studies. Third, we explain the link between dietary fat quality, LDL particles, and ASCVD (RQ3); we draw especially on RCTs in animals and humans, epidemiology, population-based changes, and experiments of nature.
Additionally, the distrust over dietary recommendations for fat quality may partly relate to an unclear understanding of the scientific method, especially as applied in nutrition research, including the process of developing dietary guidelines. We therefore also aimed to clarify this process. We discuss how we assess causality in nutrition research, and how we progress from scientific evidence to providing dietary recommendations.
 
Very very many thanks. As I've immersed myself in reading about various low carb diet approaches I've run into all manner of confusing statements - for example that saturated fat is entirely fine, that total cholesterol as an indicator of future cardiovascular issues has long been debunked, that a diet high in saturated fat doesn't raise LDL levels, that dairy is absolutely fine because it's 'natural'... I could go on.

A roundup of all the available evidence with a nice simple concluding statement at the end is exactly the tonic I needed.
 
Very very many thanks. As I've immersed myself in reading about various low carb diet approaches I've run into all manner of confusing statements - for example that saturated fat is entirely fine, that total cholesterol as an indicator of future cardiovascular issues has long been debunked, that a diet high in saturated fat doesn't raise LDL levels, that dairy is absolutely fine because it's 'natural'... I could go on.

A roundup of all the available evidence with a nice simple concluding statement at the end is exactly the tonic I needed.
A large portion of the low carb stuff you find on the Internet is total bilge, particularly when it comes to lipids.
 
Very very many thanks. As I've immersed myself in reading about various low carb diet approaches I've run into all manner of confusing statements - for example that saturated fat is entirely fine, that total cholesterol as an indicator of future cardiovascular issues has long been debunked, that a diet high in saturated fat doesn't raise LDL levels, that dairy is absolutely fine because it's 'natural'... I could go on.

A roundup of all the available evidence with a nice simple concluding statement at the end is exactly the tonic I needed.

I remember as a kid being told not to eat eggs as they contained cholesterol. Now it seems to be OK to eat eggs as dietary cholesterol isn't a problem.

The British Heart Foundation has some stuff about this on their website, which doesn't help with the confusion:


The reason for the shift in focus is that although we know that saturated fat, which is the type of fat in dairy, can raise our levels of ‘bad’ cholesterol, this doesn’t appear to be the full picture when it comes to our heart and circulatory health.

Studies are suggesting that, despite their saturated fat content, dairy foods like milk, cheese and yoghurt have a neutral or even positive effect. They could also help reduce your risk of type 2 diabetes and blood pressure, which can both increase the chances of having a heart attack or stroke.

My GP surgery stopped using total cholesterol last year and now use ratios.
 
I remember as a kid being told not to eat eggs as they contained cholesterol. Now it seems to be OK to eat eggs as dietary cholesterol isn't a problem.

The British Heart Foundation has some stuff about this on their website, which doesn't help with the confusion:




My GP surgery stopped using total cholesterol last year and now use ratios.
A classic egg thread from the great Deirdre Tobias:
 
Detailed review of the evidence for fat quality => LDL-C => CV risks.

https://www.atherosclerosis-journal.com/article/S0021-9150(23)05354-6/fulltext

Highlights

  • LDL particle concentration, usually estimated by LDL-C, causally affects ASCVD.
  • Dietary fat quality is the main environmental determinant of plasma LDL-C.
  • Fat quality affects the risk of ASCVD risk mainly by modifying plasma LDL-C.
  • Dietary guidelines for fat build on the totality and strength of the evidence.
  • There is low probability that they will fundamentally change in the future.

Abstract

The scientific evidence supporting the current dietary recommendations for fat quality keeps accumulating; however, a paradoxical distrust has taken root among many researchers, clinicians, and in parts of the general public. One explanation for this distrust may relate to an incomplete overview of the totality of the evidence for the link between fat quality as a dietary exposure, and health outcomes such as atherosclerotic cardiovascular disease (ASCVD). Therefore, the main aim of the present narrative review was to provide a comprehensive overview of the rationale for dietary recommendations for fat intake, limiting our discussion to ASCVD as outcome. Herein, we provide a core framework – a causal model – that can help us understand the evidence that has accumulated to date, and that can help us understand new evidence that may become available in the future. The causal model for fat quality and ASCVD is comprised of three key research questions (RQs), each of which determine which scientific methods are most appropriate to use, and thereby which lines of evidence that should feed into the causal model. First, we discuss the link between low-density lipoprotein (LDL) particles and ASCVD (RQ1); we draw especially on evidence from genetic studies, randomized controlled trials (RCTs), epidemiology, and mechanistic studies. Second, we explain the link between dietary fat quality and LDL particles (RQ2); we draw especially on metabolic ward studies, controlled trials (randomized and non-randomized), and mechanistic studies. Third, we explain the link between dietary fat quality, LDL particles, and ASCVD (RQ3); we draw especially on RCTs in animals and humans, epidemiology, population-based changes, and experiments of nature.
Additionally, the distrust over dietary recommendations for fat quality may partly relate to an unclear understanding of the scientific method, especially as applied in nutrition research, including the process of developing dietary guidelines. We therefore also aimed to clarify this process. We discuss how we assess causality in nutrition research, and how we progress from scientific evidence to providing dietary recommendations.
How is it defining good quality fats ? Is this the old good fats/ bad fats distinction and the Mediterranean Diet ?
 
How is it defining good quality fats ? Is this the old good fats/ bad fats distinction and the Mediterranean Diet ?

There’s a detailed discussion in the paper linked above. These tables attempt to condense that somewhat.

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Interesting that sugars and refined carbs get a mention too.
 
There’s a detailed discussion in the paper linked above. These tables attempt to condense that somewhat.

View attachment 28904

View attachment 28905
View attachment 28906

Interesting that sugars and refined carbs get a mention too.
Wow ! It's Ancel Keys recommendations from his 1959 book, 'Eat Well and Stay Well' and his 1972 book, 'Eat Well and Stay Well the Mediterranean Way'. Decrease Transfats and Saturated Fats and increase Unsaturated fats for heart health. Keys also drew distinctions between Brown Fat from wild animals and White Fat from farmed animals.
 
Wow ! It's Ancel Keys recommendations from his 1959 book, 'Eat Well and Stay Well' and his 1972 book, 'Eat Well and Stay Well the Mediterranean Way'. Decrease Transfats and Saturated Fats and increase Unsaturated fats for heart health. Keys also drew distinctions between Brown Fat from wild animals and White Fat from farmed animals.
Just leaving this here as a prophylaxis in case somebody drops by to repeat the usual slanders against Keys:
 
I remember as a kid being told not to eat eggs as they contained cholesterol. Now it seems to be OK to eat eggs as dietary cholesterol isn't a problem.

The British Heart Foundation has some stuff about this on their website, which doesn't help with the confusion:




My GP surgery stopped using total cholesterol last year and now use ratios.
....and everybody else has stopped using ratios and gone back to absolute level of LDL and the other important measure, Total minus HDL. So Total Cholesterol is back in importance as it's an essential component in the calculation of 'bad cholesterol' i.e. the stuff that's transporting cholesterol into the linings of the arteries.
 
....and everybody else has stopped using ratios and gone back to absolute level of LDL and the other important measure, Total minus HDL. So Total Cholesterol is back in importance as it's an essential component in the calculation of 'bad cholesterol' i.e. the stuff that's transporting cholesterol into the linings of the arteries.
Side note - I was curious about this so I dug out my last fasting blood test results - a printout of the results straight from a regional lab in Ireland.

It includes one ratio - total cholesterol/HDL - and this, I assume, is what my GP was paying most attention to as he went on to enter this number into the QRISK3 risk calculator and deliver onto me some ominous omens about my risk of heart attack and stroke. The lab was not able to calculate my LDL cholesterol level. I looked into this further and found that LDL is not directly measured in a typical blood lipid panel, it's calculated using a formula that is based on total cholesterol, HDL and triglycerides. My triglyceride levels were so high that the formula the lab uses doesn't work, and as no number is given I can't tell which formula the lab is using.

I'd be curious to learn which formula the labs in the UK are using at present, and which ratios appear on the lab results, if any.

Links:
Calculators based on Friedewald (old) and Martin (newer) equations for estimating LDL cholesterol (in the Endocrine and metabolic section).

Unit converter that enables the calculators above to be used. For some reason the units for triglycerides have their own special calculator? I don't get that at all.

Paper that compares the accuracy of currently used equations with a shiny new one:

QRISK3 calculator, which uses total cholesterol to HDL ratio.
 
Side note - I was curious about this so I dug out my last fasting blood test results - a printout of the results straight from a regional lab in Ireland.

It includes one ratio - total cholesterol/HDL - and this, I assume, is what my GP was paying most attention to as he went on to enter this number into the QRISK3 risk calculator and deliver onto me some ominous omens about my risk of heart attack and stroke. The lab was not able to calculate my LDL cholesterol level. I looked into this further and found that LDL is not directly measured in a typical blood lipid panel, it's calculated using a formula that is based on total cholesterol, HDL and triglycerides. My triglyceride levels were so high that the formula the lab uses doesn't work, and as no number is given I can't tell which formula the lab is using.

I'd be curious to learn which formula the labs in the UK are using at present, and which ratios appear on the lab results, if any.

Links:
Calculators based on Friedewald (old) and Martin (newer) equations for estimating LDL cholesterol (in the Endocrine and metabolic section).

Unit converter that enables the calculators above to be used. For some reason the units for triglycerides have their own special calculator? I don't get that at all.

Paper that compares the accuracy of currently used equations with a shiny new one:

QRISK3 calculator, which uses total cholesterol to HDL ratio.
Here are NICE Guidelines from 14 December 2023 ....absolute level of LDL and Total minus HDL are key indicators ...obviously NHS hasn't caught up with them yet and is still reporting obsolete ratios on test results ....

Nice Guidelines


14 December 2023



Cardiovascular disease: risk assessment and reduction, including lipid modification​

NICE guideline [NG238]Published: 14 December 2023


Full lipid profile​

This involves taking a blood sample to measure total cholesterol, HDL cholesterol and triglyceride levels and then calculating non-HDL cholesterol and LDL cholesterol (a fasting sample is not mandated). LDL cholesterol results may not be reported in participants with triglyceride levels more than 4.5 mmol per litre or 9 mmol per litre depending on the formula used by local laboratories.
 
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