How Apob & Visceral Fat Increase Your Risk Of Heart Disease.

Optimising Visceral Fat & ApoB Is Key To Reducing Your Risk Of Heart Disease.

When it comes to cardiovascular disease, two of the biggest risk factors we must consider are:

1. ApoB concentration - A measure of the number of circulating lipid particles.

2. Visceral Fat & Insulin Resistance - The amount of fat in your abdominal cavity and major organs and how it influences your risk of insulin resistance.

It is easy to separate these two factors and attempt to address them independently, but recent studies suggest that there may be a close relationship that we need to be aware of.

ApoB

Atherosclerosis, by definition, is caused by the retention of an ApoB lipid particle in the artery wall.

This retained particle then sets off an inflammatory cascade, which ultimately results in the formation of atherosclerosis¹.

Mechanism of atherosclerosis formation.

The greater the number of particles the artery wall is exposed to over time, the higher the risk of atherosclerosis and a heart attack².

Not all circulating ApoB particles will transition across the artery wall, but some will.

Even more will get through in the setting of other cardiovascular risk factors such as smoking and high blood pressure.

The analogy I use with patients is throwing a tennis ball (ApoB particle) against a glass window.

The more you throw over time, the greater the likelihood one will get through to the other side.

If you have high ApoB, often indicated by a high LDL-C, then there is a greater likelihood one will get through.

If you have high blood pressure, you are just throwing those tennis balls (ApoB) harder.

If you smoke, you’ve just walked up to that window with a hammer and smashed it.

Those ApoB particles are just sailing right through at this point.

It’s not a perfect analogy, but it gets the main point across.

Visceral Fat & Insulin Resistance

While rates of smoking have decreased significantly in recent decades, the rates of obesity and excess visceral fat have increased dramatically³.

Trends in the number of obese and severely obese people by region.

Excess weight, as measured by BMI, is typically considered a measure of excess body fat.

But there are two types of body fat:

1. Subcutaneous Fat (SAT) - Located just under the skin.

2. Visceral Fat (VAT) - Located in the abdominal cavity and major organs.

And the research suggests that it is this excess visceral fat (VAT) that is driving most of the risk.

Excess visceral fat results in a higher risk of insulin resistance, which is the precursor state to diabetes.

In the setting of insulin resistance, a higher ApoB concentration increases the risk of cardiovascular disease dramatically.

If ApoB is the fire, insulin resistance is the gasoline poured on top of that fire.

Yes. I know. 12 is a high cut-off for insulin, and also for an ApoB of >1.05. Comments to the study authors, please.

When insulin levels are low, and there is no insulin resistance, a high ApoB does increase the risk of cardiovascular disease.

But only moderately.

When BOTH Insulin levels and ApoB are high, the risk of cardiovascular disease explodes.

Controlling both then has to be a priority for the prevention of cardiovascular disease.

But what about those of ‘Normal’ weight?

When someone is classified as being of ‘normal’ weight, that typically means they have a BMI of less than 25.

The relationship between excess weight, a high BMI and the risk of severe insulin resistance and diabetes is clear⁴.

Relationship of BMI and Risk Of Diabetes.

For every 1-point increase in BMI, there is a 23% increased risk of diabetes⁵.

Rates of obesity have tripled in the last 60 years.

However, people within a relatively normal BMI range also develop type two diabetes, which is typically considered more a feature of excess weight.

Why?

A recent study looked at first-degree relatives of those with type 2 diabetes who were of normal weight and did not have diabetes.

They then compared their visceral fat levels and insulin resistance parameters to weight-matched controls with no family history of diabetes.

Those with a first-degree relative with type 2 diabetes had⁶:

• More Visceral Fat

• A greater tendency toward Insulin Resistance.

It bears repeating, but this is in individuals who are both normal weight and do not have diabetes.

Even within their ‘normal’ weight range, clearly, genetic factors are at play, increasing their visceral fat and insulin resistance markers, which subsequently increase their risk of type 2 diabetes.

And, by extension, their cardiovascular risk.

So what happens if you take people of ‘normal’ weight with type 2 diabetes and get them to lose weight?

You put their diabetes into remission.

Losing 6.5% of their body weight over a 12-month period induced remission of diabetes in 70% of such patients⁷.

These patients had a normal ‘total body weight’ and BMI but had excess visceral fat.

This means that each individual has what is called a ‘personal fat threshold’, which means that for some people, even modest weight gain can result in significantly more excess visceral fat and all the risks that come with it.

This is also why using ‘weight’ or BMI is often a very poor marker of risk for individuals.

BMI is more of a marker of population-level risk.

Measures of insulin resistance and excess visceral fat are better markers.

These markers include Fasting Insulin, Glucose, HOMA-IR, LPIR score, HBA1c, waist circumference & VAT levels on DEXA.

But is all excess visceral fat bad for cardiovascular disease?

While excess VAT increases the risk of a variety of major medical conditions, a recent study suggests that it might not always be the case for cardiovascular disease.

Certain genes give rise to higher levels of visceral fat.

Of these sets of genes, some⁸:

• Increase ApoB levels

• Make no difference to ApoB levels

• Lower ApoB levels

In the group with a neutral effect on ApoB, there was no long-term impact on future cardiovascular risk.

For the group that had lower ApoB levels, there was actually a reduction in cardiovascular risk.

It was only in the group with higher ApoB levels that cardiovascular risk increased.

In this later group, for every 1% increase in visceral fat, there was a 57% increased risk of cardiovascular disease.

This study suggests that most of the risk of cardiovascular disease is mediated by the excess ApoB and not necessarily the excess visceral fat alone.

Confused?

Don’t be.

Here’s the main takeaway:

Excess visceral fat increases the risk of diabetes. That is not a good thing. Regardless of ApoB levels.

Losing only 6.5% of your body weight can put type 2 diabetes into remission even when you are in a ‘normal’ weight category.

High levels of VAT and ApoB are VERY bad for cardiovascular risk.

High levels of VAT but low levels of ApoB are suggestive of a lower risk of cardiovascular disease - but other diseases are still at increased risk.

Optimising both ApoB and VAT is the key to minimising the risk of cardiovascular disease and other major medical conditions.

ApoB can be lowered with dietary approaches, but if significant reductions are needed, then medication may be required.

Excess visceral fat can be eliminated with even modest weight reduction.

ApoB, Insulin Resistance and Visceral Fat are key markers of cardiovascular risk, but their relationship is complex.

However, if you are not measuring these markers, you are very much in the dark regarding your cardiovascular risk and what to do about it.

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For an accessible and comprehensive overview of understanding and managing heart health, you can check out the best-selling book Heart. An Owner’s Guide.

For those based in Ireland, Dr Barrett works with a small number of clients to provide a comprehensive evaluation of cardiovascular risk and a tactical approach to maximally reducing that risk.

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In Case You Missed Them:

1. Antibody-Based Therapeutics for Atherosclerosis and Cardiovascular Diseases. Int. J. Mol. Sci. 2021, 22, 5770.

2. Dose-Response Associations of Lipid Traits With Coronary Artery Disease and Mortality. JAMA Netw Open. 2024;7(1):e2352572.

3. NCD Risk Factor Collaboration (NCD-RisC). Trends in adult body-mass index in 200 countries from 1975 to 2014: a pooled analysis of 1698 population-based measurement studies with 19·2 million participants. Lancet. 2016 Apr 2;387(10026):1377-1396.

4. Body-mass index and diabetes risk in 57 low-income and middle-income countries: a cross-sectional study of nationally representative, individual-level data in 685 616 adults. Lancet. 2021 Jul 17;398(10296):238-248.

5. Association of body mass index and age with incident diabetes in Chinese adults: a population-based cohort study. BMJ Open. 2018 Sep 28;8(9):e021768.

6. The role of adipogenic capacity and dysfunctional subcutaneous adipose tissue in the inheritance of type 2 diabetes mellitus: cross-sectional study. Obesity (Silver Spring). 2024 Jan 14.

7. Aetiology of Type 2 diabetes in people with a 'normal' body mass index: testing the personal fat threshold hypothesis. Clin Sci (Lond). 2023 Aug 31;137(16):1333-1346.

8. The relationship between genetic liver fat and coronary heart disease is explained by apoB-containing lipoproteins. Atherosclerosis. 2024 Jan;388:117397.