#033 Does Saturated Fat Cause Heart Disease?

Feb 10, 2017 Episode Page ↗
Overview

This episode explores the complex link between saturated fat and heart disease, concluding that refined sugar and individual genetics play a more significant role. It highlights the dangers of refined sugar and trans fats, offering insights into personalized dietary approaches.

At a Glance
14 Insights
24m 37s Duration
15 Topics
7 Concepts

Deep Dive Analysis

Revisiting the Link Between Saturated Fat and Heart Disease

Observational Studies vs. Randomized Controlled Trials

Impact of Refined Sugar on LDL and Inflammation

Understanding Large Buoyant vs. Small Dense LDL Particles

The Role of Apolipoprotein B (APOB) in LDL Uptake

Atherogenic Dyslipidemia and Heart Disease Risk

Importance of Genetic Variation in Dietary Response

Specific Genetic Polymorphisms Affecting Saturated Fat Response

FTO Gene and Obesity/Diabetes Risk with Saturated Fat

PPAR-alpha Gene and Lipid Metabolism

PPAR-gamma Gene and Fatty Acid Storage/Glucose Metabolism

APOE4 Gene and LDL Cholesterol Recycling

Negative Repercussions of Saturated Fat Reduction Guidelines

Broader Harms of Refined Sugar Consumption

Key Takeaways: Saturated Fat, Genetics, and Refined Sugar

Small Dense LDL Particles

These are a type of LDL cholesterol that tends to be dangerous. Unlike large buoyant LDL, small dense particles circulate longer, are less easily endocytosed by cells, and are more prone to oxidative stress and inflammatory transformations, which can lead to plaque formation in arteries.

Apolipoprotein B (APOB)

APOB is a protein found in LDL particles that acts as a ligand for LDL receptors on cells, facilitating the uptake of LDL particles into cells. In smaller LDL particles, the receptor recognition site on APOB can be partially obscured, hindering their proper utilization and removal from circulation.

Atherogenic Dyslipidemia

This is a pattern of lipid abnormalities strongly associated with heart disease. It is characterized by elevated levels of triglycerides, increased small dense LDL particles, and low levels of large buoyant HDL cholesterol.

Genetic Polymorphisms

These are variations in genes that cause them to operate slightly differently from similar versions in other individuals. These variations can significantly influence how a person's body responds to specific foods and nutrients, such as saturated fats.

FTO Gene

This gene encodes for the 'fat mass and obesity associated protein.' Certain polymorphisms in the FTO gene can increase obesity risk, particularly when combined with a high saturated fat and low polyunsaturated fat intake, and may negatively affect blood glucose and insulin levels.

PPARs (Peroxisome Proliferator Activated Receptors)

These are nuclear receptor proteins that function as transcription factors, regulating genes involved in metabolism of carbohydrates, lipids, and proteins. Specific PPAR genes, like PPAR-alpha and PPAR-gamma, are relevant to how individuals respond to saturated fats.

APOE Gene

The apolipoprotein E gene has different versions, with APOE4 being a common one. APOE4 is associated with the liver not recycling LDL cholesterol very well, leading to higher concentrations of LDL particles circulating longer, increasing their chance of inflammatory transformations and forming small dense or oxidized LDL.

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Does saturated fat cause heart disease?

The link between saturated fat and heart disease is not straightforward; while some observational studies found a link, randomized controlled trials suggest that a diet high in saturated fat but low in refined sugar and processed foods may not cause heart disease and can even improve risk factors.

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What is the difference between large buoyant LDL and small dense LDL?

Large buoyant LDL is considered beneficial as it transports fatty acids and cholesterol for cell repair and creation, while small dense LDL particles are dangerous because they circulate longer, are less easily utilized by cells, and are more prone to inflammatory transformations that lead to plaque formation.

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How does refined sugar impact LDL and heart disease risk?

Refined sugar consumption can lead to an increase in small dense LDL particles and systemic inflammation, creating a state known as atherogenic dyslipidemia, which is strongly associated with heart disease.

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Can I find out my LDL particle size?

Yes, you can ask your doctor for an advanced test like the ion mobility test, which measures the particle size of LDL and HDL, though it is not yet part of standard care.

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How do genetics influence an individual's response to saturated fat?

Genetic polymorphisms can significantly alter how an individual's body processes and responds to saturated fat, affecting factors like obesity risk, blood glucose, insulin levels, and the risk of developing small dense LDL particles.

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What were the negative consequences of the guidelines to reduce saturated fat intake?

The guidelines led people to increase their intake of refined carbohydrates and processed foods, and also resulted in the widespread appearance and consumption of deadly hydrogenated oils (trans fats), which significantly increase heart disease risk by making cell membranes rigid.

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What are the broader health impacts of refined sugar consumption beyond heart disease?

Refined sugar consumption is linked to increased risk of cancer, changes in brain reward pathways similar to drugs of abuse, altered neuron structure, brain atrophy (even in prediabetes), impaired brain repair, shorter telomeres, and contributes significantly to daily caloric intake for many adults.

1. Eliminate Refined Sugar

Make a significant dietary change by eliminating refined sugar, as it is a ‘mess’ and its removal is one of the best ways to quickly achieve major health improvements for everyone.

2. Avoid Trans Fats

Strictly avoid hydrogenated oils (trans fats) like margarine, as they are deadly and significantly increase heart disease risk by stiffening arteries.

3. Reduce Refined Sugar & Processed Foods

Prioritize a diet low in refined sugar and processed foods, as this combination has been shown to reduce fat storage, improve triglycerides, blood sugar, insulin sensitivity, and lower blood pressure.

4. Avoid Sugar-Sweetened Beverages

Do not consume sugar-sweetened beverages, as they can significantly increase small, dense LDL particles and systemic inflammation (60-100% increase in C-reactive protein), leading to negative biological consequences.

5. Get Genetic Test for Diet

Obtain your raw genetic data from a service like 23andMe and analyze it with tools like Promethease.com or foundmyfitness.com/genetics to understand your specific gene polymorphisms and personalize dietary choices.

6. Request LDL Particle Size Test

Ask your doctor for an ‘ion mobility test’ (available from Quest Diagnostics) to determine your LDL particle size, as small, dense LDL particles are dangerous and strongly associated with heart disease risk.

7. Tailor Fat Intake to FTO

If you have FTO gene polymorphisms that increase obesity risk, prioritize a higher intake of polyunsaturated fats (e.g., fatty fish, nuts) and a lower intake of saturated fat.

8. Tailor Fat Intake to PPAR-alpha

If you have a PPAR-alpha gene polymorphism linked to lower activity and higher disease risk, consume more polyunsaturated fat and less saturated fat, especially if on a ketogenic diet.

9. Tailor Fat Intake to PPAR-gamma

If you have certain PPAR-gamma gene polymorphisms, increase your intake of monounsaturated fats (e.g., avocados, olive oil) and polyunsaturated fats while lowering saturated fat intake.

10. Moderate Saturated Fat with APOE4

If you have the APOE4 gene variant, it is wise to moderate your saturated fat intake, as it’s associated with less efficient LDL recycling and increased risk of harmful small, dense LDL.

11. Consume Saturated Fat Wisely

While saturated fat can increase large buoyant LDL, it’s crucial to avoid consuming refined sugars alongside it, as sugars convert large LDL into dangerous small, dense LDL and increase inflammation.

12. Consume Whole Fruit

Differentiate between fructose from whole fruit and added high fructose corn syrup; consumption of whole fruit is not considered a vice and is different from consuming added sugars.

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Support FoundMyFitness’s efforts by contributing any amount through their pay-what-you-can crowdfunding subscription at foundmyfitness.com/crowdsponsor.

Not all LDL cholesterol is created equal and specifically not all LDL confers the same risk of heart disease.

Host

By staying around in the circulatory system longer, the particle is able to undergo transformations as a consequence of oxidative stress and inflammatory processes. And this is ultimately the beginning of the formation of a plaque in the artery.

Host

The variability of the glucose response shown in this study, on the whole, undermined the entire concept of a glycemic index.

Host

While refined sugar makes for a nice scapegoat for these observational studies linking saturated fat perhaps more directly to heart disease than it should be, I believe that genes play a significant enough role that population biasing may be a part of this problem of observational studies blatantly contradicting each other.

Host

These are deadly, quite literally. They significantly increase the risk of heart disease in small amounts.

Host

All of us should do everything that we can to avoid refined sugar. That stuff is a mess and removing it is one of the best big dietary changes each of us can make if we're coming into this healthier living thing, cold turkey, and trying to make some big improvements quickly.

Host

How to Learn About Your Genetic Polymorphisms

Host
  1. Obtain a genetic test from a company like 23andMe, ensuring you get access to your raw data (even their most minimal package should include this).
  2. Run the raw data through a third-party report service like Promethease (Promethease.com) to analyze against thousands of single nucleotide polymorphisms.
  3. Alternatively, for curated, actionable genetic information focusing on specific polymorphisms like FTO, PPAR-gamma, and PPAR-alpha, use the genetic tool on foundmyfitness.com/genetics.
60% to 100%
Increase in C-reactive protein (inflammation biomarker) after consuming sugar-sweetened beverage Observed in healthy, normal weight young men after 3 weeks of daily 20 ounces of a sugar-sweetened beverage.
around 70%
Percentage of LDL removed from circulation by the liver Primary mechanism for LDL particle uptake.
up to 2.76 fold
Increase in obesity risk due to some FTO gene polymorphisms Particularly in the context of high saturated fat and low polyunsaturated fat intake.
two-fold higher
Higher risk of type 2 diabetes due to a PPAR-alpha polymorphism Associated with lower PPAR-alpha activity, increased triglycerides, total cholesterol, LDL cholesterol, and small dense LDL particles in the context of high saturated fat and low polyunsaturated fat intake.
35% greater risk
Increased risk of heart attack and fatal heart disease from sugar-sweetened beverages For those consuming the equivalent of one to two servings per day.
fourfold increase
Increase in heart attacks for highest intake of refined sugar Compared to those with the lowest intakes, in a study including over 400,000 people.
10%
Percentage of adults getting 25% of daily calories from added sugar A whopping 10% of adults.
over 70%
Percentage of adults getting at least 10% of daily calories from added sugar Over 70% of adults.