When it comes to understanding fats (cholesterol in particular), we have grown more and more uncertain around how cholesterol influences heart attacks and strokes. We’re none the wiser when it comes to understanding our ‘good’ cholesterol vs ‘bad’ cholesterol and how to interpret our numbers on a blood test. This is largely due to the complex world that is lipids (fats), which often leaves even doctors unsure about what’s right from wrong.
With heart diseases causing roughly a quarter of all deaths in the U.K. (British Heart Foundation, 2023), it is in our best interest that we understand what to look out for when it comes to our health checks as well as understanding the risk factors that lead to heart disease.
In this article I will be talking about something called Apolipoprotein B or abbreviated as ApoB, which should hopefully help you consolidate your understanding of cholesterol and heart disease.
To understand the relevance of ApoB, we must first refresh our understanding of cholesterol, lipoproteins and atherosclerosis.
Cholesterol is a type of fat which provides essential functions to the body. It gives our cells structure, which then allows things to get in (like nutrients and oxygen), and also for debris and toxins to leave. Cholesterol is also the precursor to all of our steroid hormones, like progesterone, estrogen, testosterone and cortisol to name a few. Finally, cholesterol is important for the formation and synthesis of Vitamin D as well as bile.
Each cell has the ability to make cholesterol however some cannot make enough for its own usage. The liver is the primary organ responsible for manufacturing cholesterol to provide to other parts of the body. Since cholesterol is a fat and fats are not water soluble, they cannot travel freely in our blood and require a chaperone. Enter lipoproteins.
Lipoproteins are structures that are part fat but also part protein which does make them water soluble and therefore acts as the ‘cargo’ ship that onboards cholesterol to take it wherever it needs to go. It is these cholesterol carrying lipoproteins that make up the ‘L’ part of HDL and LDL cholesterol. Something you probably would have seen on a blood test or at least have heard about.
Think of the relationship between cholesterol and lipoproteins like the gooey insides of a crème egg (cholesterol) and the chocolate egg itself (lipoprotein).
On a typical routine blood test, you are generally just getting your LDL-Cholesterol and HDL-Cholesterol levels checked, which is looking at the total amount of cholesterol within all LDL and HDL particles. More on this later.
Now that we have a better sense of cholesterol’s functions in the body as well as how they are transported through the body, we must now understand how and why atherosclerosis happens.
Atherosclerosis is the process whereby the walls of the arteries narrow down which leads to a blockage of blood flow. The coronary arteries carry blood to the heart and the middle cerebral artery carries blood to the brain and when these are blocked, a heart attack or stroke ensues.
This narrowing of the artery walls is usually due to a build-up of plaque, which primarily consists of fatty substances, oxidised cholesterol, and other unused waste products like calcium and fibrin.
High density lipoproteins (HDL) and low-density lipoproteins (LDL) both serve in the human cholesterol trafficking system by taking cholesterol to different cells to be used. But where they differ is that HDLs contain less cholesterol than LDLs and also acts as a ‘pick up’ truck to take any excess cholesterol back to the liver to be recycled whilst LDLs have a tendency to submerge itself and its contents (cholesterol particles and triglycerides) into the gaps of blood vessels which contributes to plaque formation and atherosclerosis. LDLs are therefore considered as ‘atherogenic’ particles.
In normal circumstances, when HDL and LDL levels are within their optimal ranges, the anti-atherogenic functions of HDL will balance out the deleterious effects of LDL but when the amount of LDL particles rise, we are slowly increasing our risk of atherosclerosis. Hence why LDL is classically stated as bad and HDL stated as good.
Along with LDL, there are 4 other atherogenic particles that behave in the same way as LDL and can contribute towards atherosclerosis. Intermediate and very low-density lipoproteins (IDL & VLDL), chylomicrons and Lp(a) (also called lipoprotein little a). These are typically not tested for in routine blood tests. Although, we do routinely test this within many of our Health Assessment Packages.
Apolipoprotein B (ApoB) is a protein structure that sits on the surface of all atherogenic particles including VLDL, IDL, LDL, chylomicrons and Lp(a). Back to the crème egg analogy, this would be like wrapping a ribbon around the egg and then sticking a small sticker on the egg. Looking at the number of ApoB and can therefore be a great indicator of all atherogenic particles present as opposed to just looking at LDL.
Another important reason why ApoB numbers are far superior at detecting risk of cardiovascular disease and atherosclerosis is, whilst on a standard blood panel looks at your LDL-C, which is telling you the total mass of cholesterol within all LDL particles, with ApoB, you are looking at the total number of atherogenic particles present which is thought to be a more accurate predictor of risk (Proitsi, 2021).
This is likely because the more of these atherogenic particles you have (the higher number of crème eggs), the greater exposure you have of them submerging into the gaps of blood vessels depositing their cholesterol content (gooey inside bit).
To complete this thought experiment and analogy, picture two people.
Person A has 100 crème eggs (ApoB) and all the gooey inside bit put together weighs 1kg (total amount of cholesterol)
Person B has 200 crème eggs (ApoB) and all the gooey inside bit put together also weighs 1kg (total amount of cholesterol)
Person B’s rate of developing atherosclerosis is higher than person A because there are more particles floating around which may submerge into the sub-endothelial space of blood vessels.
As discussed, most standard blood panels won’t test for ApoB levels however it is getting more and more commercially available for testing these days and we offer this type of testing as part of our Cardiovascular & Diabetes assessment and our Health and Wellness Essentials and Advanced assessments.
Optimal ranges for ApoB are generally <120 mg/dl however in high-risk individuals such as type 2 diabetics or those who have had previous major adverse cardiovascular events, getting ApoB levels down to 60-70 mg/dl is recommended.
For general population, we like to aim for an optimal level of <90mg/dl
From a nutritional and lifestyle perspective there are a few things to consider but essentially anything that will raise cholesterol synthesis in the body will likely raise ApoB levels too.
Insulin resistance
As well as cholesterol, all ApoB particles contain triglycerides too. When triglycerides levels increase (usually an unwanted sign of insulin resistance), more ApoB particles will have to be manufactured to sufficiently handle the triglyceride and cholesterol burden. Insulin resistance, the earlier stage of type 2 diabetes is therefore something we should be taking effective steps at preventing (Stannard & Johnson, 2004)
Weight management & body composition
Like insulin resistance, careful monitoring of optimal weight should be prioritised. Weight loss of 6-12% was shown to decrease ApoB levels and supports insulin sensitivity as well. (Lamantia et al, 2016).
This suggests that much of the consideration from a dietary perspective should be allocated towards prioritising personal preference, as this will result in a greater chance of staying adherent to the diet for long enough to see weight management results.
In addition to controlling weight, optimising body composition by reducing excess body fat and supporting adequate lean mass levels will be crucial at improving insulin sensitivity.
Exercise & general movement
Both resistance training and aerobic cardio training improves insulin sensitivity through different mechanisms, but there is a growing body of evidence suggesting that utilising both forms of exercises can improve insulin sensitivity greater than just one mode alone (Bird & Hawley, 2016).
Structured physical activity sessions typically only account for roughly 10-15% of our energy expenditure per day which isn’t a huge amount. Therefore, it is important that we are consciously working on our non-exercise activity such as walking and general day to day movement which will help contribute towards the number of calories we burn a day, supporting overall weight management.
Saturated fats
Excess saturated fat consumption is linked to raising blood cholesterol levels and so managing intake becomes a primary way of supporting optimal metabolic health and insulin sensitivity (Weickert, 2012). We recommend no more than 10% of total daily energy intake to come from saturated fat for susceptible individuals.
Dietary Fibre
Dietary fibre can impact your ApoB levels in several ways. Firstly, by adding bulk to your stools, it does a good job at absorbing excess cholesterol in circulation to be excreted out.
As dietary fibre makes its way to the intestines, the bacteria within can ferment on it creating short chain fatty acids, a beneficial substrate for gut health. Short chain fatty acids can have a favourable impact on our gut microbiota and has been shown to decrease the synthesis of cholesterol by the liver (Soliman, 2019). We recommend roughly 14g of fiber per 1000 calories of food intake.
We hope you found the content in this article useful. Our team of practitioners are on hand to assist you with your goal of improving your cardiometabolic health.
Our team use a combination of nutrition, lifestyle, and functional medicine approaches to help our clients meet their health goals. We then use appropriate lab testing and in-house body composition analysis to ensure that you are targeted in your approach and tracking results appropriately, holding everyone accountable.
We are on hand, ready to support you with your health transformation.
- Bird SR, Hawley JA. Update on the effects of physical activity on insulin sensitivity in humans. BMJ Open Sport Exerc Med. 2017 Mar 1;2(1):e000143. doi: 10.1136/bmjsem-2016-000143. PMID: 28879026; PMCID: PMC5569266.
- Stannard SR, Johnson NA. Insulin resistance and elevated triglyceride in muscle: more important for survival than "thrifty" genes? J Physiol. 2004 Feb 1;554(Pt 3):595-607. doi: 10.1113/jphysiol.2003.053926. Epub 2003 Nov 7. PMID: 14608009; PMCID: PMC1664785.
- https://www.bhf.org.uk/what-we-do/news-from-the-bhf/contact-the-press-office/facts-and-figures
- Lamantia V, Sniderman A, Faraj M. Nutritional management of hyperapoB. Nutr Res Rev. 2016 Dec;29(2):202-233. doi: 10.1017/S0954422416000147. Epub 2016 Nov 8. PMID: 27821191.
- Proitsi, P. (2021) ‘The key role of apolipoprotein B in major vascular diseases and longevity’, The Lancet Healthy Longevity, 2(6). doi:10.1016/s2666-7568(21)00120-3.
- Soliman GA. Dietary Fiber, Atherosclerosis, and Cardiovascular Disease. Nutrients. 2019 May 23;11(5):1155. doi: 10.3390/nu11051155. PMID: 31126110; PMCID: PMC6566984.
- Weickert MO. Nutritional modulation of insulin resistance. Scientifica (Cairo). 2012;2012:424780. doi: 10.6064/2012/424780. Epub 2012 Sep 5. PMID: 24278690; PMCID: PMC3820526.
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The above article was contributed by
Danny
Primary Author
