What Exactly Is Adipose (Fat) Tissue, And How Does It Matter In Ageing? Part 3: ‘Good Fat’ Vs ‘Bad Fat’

Getting your Trinity Audio player ready...

We often hear fat, or sometimes cholesterol, being described as either ‘good’ or ‘bad’. This can be confusing, because as we discussed in part 1, the word fat can mean a lot of different things. Adipose tissue can, as we discussed in the previous part, be white or brown, but white fat is not inherently bad. Rather, white fat becomes a problem when we have too much of it. In addition to the type of adipose tissue, its location within the body is also important for determining its impact on health. The lipids packed within the adipose tissue also have many variations, some of which are more beneficial or detrimental to health than others. Finally, the lipoproteins that transport cholesterol and triacylglycerol via the blood can determine whether those lipids are removed from the body, or end up trapped in the walls of arteries to cause atherosclerosis.

Saturated, Unsaturated, And Trans Fatty Acids

Fatty acids are the primary lipid fuel source for our cells. They are stored within adipocytes as triacylglycerol – a molecule composed of three fatty acids joined to a glycerol molecule. Triacylglycerols are broken back down into their constituent parts to be released from the adipose tissue and metabolised by other tissues as required. The glycerol component of triacylglycerol is always the same, but fatty acids are very diverse, and each triacylglycerol can have any combination of three fatty acids, meaning there is a vast variety of different triacyclglycerols with different properties. To understand what distinguishes fatty acids from one another, let’s take a closer look at these molecules.

Here’s the molecular structure of palmitic acid. The bulk of the molecule is made up of a chain of carbon atoms (C), each of which is joined by a molecular bond (represented by a line) to its neighbouring carbon atoms, and to a number of hydrogen atoms (H). For our purposes, we can ignore the left-most carbon atom and its bonds, since this does not change between fatty acids. Each carbon atom is able to form a maximum of four molecular bonds, and in palmitic acid, each carbon atom shares a bond with the maximum possible number of hydrogen atoms. This fatty acid is saturated with hydrogen, and we therefore refer to it as a saturated fatty acid.

It’s possible for some carbon atoms within the fatty acid molecule to form two bonds with a neighbouring carbon atom, leaving one fewer bond available for linking a hydrogen atom – such a fatty acid is unsaturated. If there is more than one such carbon-to-carbon double bond within the fatty acid, it is referred to as polyunsaturated. The presence of one or more double bonds causes the fatty acid to ‘kink’ at the site of each double bond. Depending on whether the double bond is cis or trans, the shape of the carbon chain changes as depicted below. We end up with cis unsaturated fatty acids or trans fatty acids. Omega-3 fatty acids are a subgroup of unsaturated fatty acids that have a double bond three atoms away from the carbon atom at the tail end of the chain.

While most fatty foods contain a mixture of different types of fatty acids, saturated fatty acids are found in higher concentrations in certain meat and dairy products, while unsaturated fatty acids are more common in fatty fish, nuts, seeds and vegetable oils. Because they are straight molecules, saturated fatty acids pack together well and are usually solid at room temperature, while unsaturated fatty acids are liquid. Most dietary trans fats are not naturally occurring, but are created in a process called hydrogenation, which converts regular unsaturated fatty acids into trans fats. This makes the molecules straighter, making them solid at room temperature, and prevents them from becoming rancid.

While there is still some uncertainty about the exact health consequences, it is generally agreed among experts that unsaturated fatty acids are better for health than saturated fatty acids, while trans fats are considered particularly dangerous for health and are becoming increasingly rare in our food. Both trans fats and saturated fatty acids increase the ratio of ‘bad cholesterol’ to ‘good cholesterol’ (more on those shortly), which increases the risk of heart disease. Eating more trans and saturated fatty acids also increases the risk of insulin resistance, a precursor to diabetes that promotes most diseases of ageing.

While trans fatty acids should be avoided as much as possible, there is some debate over how bad saturated fatty acids are for health. They’re still worse than unsaturated fatty acids, but may not be as bad as the refined carbohydrates with which they are often replaced, so saturated fats that have been cut from the diet should be exchanged for unsaturated fats. Most health organisations suggest that no more than 10% of one’s calorie intake should come from saturated fatty acids, while 20-30% should come from mono/polyunsaturated fatty acids.

High Density vs Low Density Lipoproteins (‘Good Cholesterol’ vs ‘Bad Cholesterol’)

As discussed in part 1, cholesterol is an essential molecule, forming a key structural component of cell membranes and acting as a precursor for the production of vitamin D and steroid hormones. We discussed how cholesterol is transported in the blood together with triacylglycerol within special particles called lipoproteins. To better understand the different types of lipoprotein and why some are considered more desirable than others, let’s take a closer look at how these particles are composed:

The above image shows the general structure of a lipoprotein, using low density lipoprotein (LDL) as an example. The outer layer of the particle is composed mainly of phospholipids (see part 1), with the addition of some structural cholesterol molecules. Embedded within this layer are apolipoproteins (such as ApoB shown here). These are proteins that act ‘address tags’ that determine the destination of each lipoprotein. Within the outer layer lies a core containing cholesterol esters (cholesterol molecules joined to fatty acids). Though not shown here, larger particles will also contain triacylglycerols.

You may know that marine mammals tend to have a lot of fat. One of the functions of this fat is to help them float, since lipids have a lower density than most other tissue components. Because of this low density, the larger the lipoprotein particle (and therefore, the more lipids it contains), the lower the overall density of the lipoprotein particle. We therefore refer to the smallest lipoproteins as high density lipoprotein (HDL), followed by low density (LDL) and very low density lipoproteins (VLDL), while the lowest density lipoproteins are called chylomicrons.

So, what do all these different lipoproteins do?

• Chylomicrons: In the gut, cholesterol and triacylglycerols absorbed from food are packaged into chylomicrons to be transported to the liver.
• VLDL: In the liver, the contents of the chylomicrons can be combined with cholesterol or triacylglycerols that the liver has stored or synthesised itself. These pooled lipids are packaged into VLDL particles, which are then released into the blood. As VLDL circulates, cells throughout the body (primarily adipocytes and muscle cells) extract triglycerides from the VLDL particles
• LDL: As triacylglycerols are removed from VLDL particles, they become enriched in cholesterol and their density increases, and they become LDL particles. These LDL particles can be taken up in their entirety by cells that need the cholesterol contained within.
• HDL: Cells with leftover cholesterol can export it into HDL particles that circulate in the blood. Most of this HDL is made and released into the blood by the liver. It then returns to the liver carrying the cholesterol it has picked up from peripheral cells. The liver uses this cholesterol to make bile, which is secreted into the intestines to help break down fat.

Having too much circulating LDL is an important risk factor for cardiovascular disease. This is because in order to deliver their cholesterol contents to cells within the arteries, LDL particles must cross the inner lining of the artery called the endothelium. Some of these LDL particles become trapped underneath the endothelium, and immune cells come to absorb them and clear them out. However, some of the lipids and proteins within LDL undergo a reaction called oxidation, which makes it impossible for the immune cells to break it down. This leads to a vicious cycle in which the immune cells trigger inflammation, which leads to more cholesterol being oxidised and summons more immune cells, which trigger more inflammation and so on. Over time, cholesterol and dying immune cells accumulate within the artery wall and form a fatty plaque, which narrows the artery, increases blood pressure, and risks breaking and causing a clot to form and block the artery. This condition is called atherosclerosis and is the most common cause of cardiovascular disease, which accounts for more global deaths annually than any other disease (18.5 million in 2019).

HDL is considered ‘good cholesterol’ because it removes cholesterol from tissues (including the walls of blood vessels) and returns it to the liver, which secretes it in the bile. Thus, having higher levels of HDL protects against the harmful effects of LDL.

Effective ways of lowering LDL and increasing HDL include:

• Consuming fewer saturated fats in favour of unsaturated fats and avoiding trans fats. As discussed previously, saturated and trans fatty acids increase VLDL synthesis by the liver, while unsaturated fats promote HDL synthesis.
• Exercising regularly. VLDL production decreases during moderate exercise and during recovery. Regular moderate exercise increases HDL synthesis.
• Losing weight. As discussed in the previous article, carrying too much adipose tissue leads to some lipids being stored in the liver, which may disrupt liver metabolism and lead to the production of more VLDL.
• Avoiding smoking. Smoking elevates LDL and reduces HDL.
• Taking statins. Statins are drugs that lower LDL by making the liver absorb LDL particles from the blood. Statins can also increase HDL synthesis. Statins are generally given to people who are at elevated risk of developing cardiovascular disease, and there is ongoing debate about whether low-risk people should take them.

Visceral vs Subcutaneous Adipose Tissue

In the previous article, we discussed why having too much white adipose tissue can be a problem. Yet when it comes to health, it’s not just how much adipose tissue you have, but where it is located that matters. Adipose tissue that lies beneath the skin is called subcutaneous adipose tissue (SAT), while adipose tissue that is located near vital organs in the abdomen is called visceral adipose tissue (VAT). While these tissues look similar under a microscope and both fulfil the role of storing excess lipids, their other properties have important health implications.

SAT acts as an insulating layer of the skin that helps us retain heat and stay warm. Humans have far more SAT than any other primate, possibly because it evolved as a replacement for fur. It’s also the preferred site of lipid storage: research suggests that excess lipids get stored as subcutaneous fat first, only overflowing to visceral fat when the capacity of the SAT is exceeded. Normally, 10–20% of total fat in men and 5–8% in women is visceral adipose tissue. VAT may serve as protective cushioning for organs, but it also appears to be more involved in signalling and controlling energy balance (see part 2) when compared to subcutaneous adipose tissue.

Adipocytes within SAT are smaller, more sensitive to the hormone insulin, and absorb lipids from the blood more avidly, which is why excess lipids are preferentially stored there. VAT adipocytes are larger, have a richer blood supply, are better connected to the central nervous system, and are more sensitive to a variety of hormones that control energy balance. VAT adipocytes are also more metabolically active, with a greater tendency to break down their stored lipids, and VAT also contains higher numbers of immune cells. These qualities make having too much VAT problematic because:

• VAT is less sensitive to insulin, which makes it harder to get excess glucose into the adipose tissue to be stored as triacylglycerol.
• VAT doesn’t hold on to its lipid stores as well as subcutaneous fat: it tends to break down its lipids and release fatty acids into the blood. Remember that these fatty acids are thought to be what causes insulin resistance in muscle and liver cells.
• VAT is a more potent driver of inflammation than SAT.

What determines how fat is distributed within the body? Genetic studies suggest that genetic variants account for 30-40% of variations in visceral fat between individuals. These studies generally agree that genetics play a stronger role in determining fat distribution in women than in men. Genetic variants interact with environmental factors in a complex manner to influence which fat stores are favoured. Factors that may promote visceral fat include:

• Ageing: Ageing is associated with increased VAT deposition (more on this in part 4).
• Overeating: Lipids are preferentially stored in SAT, so gaining a large amount of VAT usually requires an excessive caloric intake. VAT is also easier to lose by dieting than SAT.
• Dietary components: Some studies suggest that trans fatty acids and fructose can promote the expansion of visceral fat.
• Lack of exercise: A sedentary lifestyle is associated with increased visceral fat. Exercise promotes weight loss, prevents visceral fat gain and reduces stress.
• Stress: Cortisol, a hormone released during stress, has been shown to increase visceral fat deposition.
• Lack of sleep: Some studies suggest that lack of sleep promotes visceral fat gain.

---

We hope this article has helped you understand the different things people can mean when they refer to fat as being good or bad. Limiting the consumption of ‘bad’ dietary fats helps to improve the balance of HDL and LDL, avoid the expansion of visceral fat and weight gain in general, and protects against heart disease. Unfortunately, maintaining a constant weight becomes harder in old age. In the fourth and final part of this series, we’ll discuss how adipose tissue and lipid metabolism change during ageing.