The science behind weight-loss can be a little intimidating! Every time I try to research the bits I don’t understand; the explanations uncover 50 more things I’ve yet to learn! The terminology is often complex & confusing; and the experts all disagree in their viewpoints. Never more so than with cholesterol.

This blog attempts to relay my own understanding of the science. It relates the basics from my own personal perspective & reading. I preclude the below with the statement that I have no medical or scientific training. If I’m wrong on any of this, then readers’ corrections will help improve my knowledge and are gratefully received!

So here goes…

Cholesterol is a fat (or lipid, to use the scientific term!). It’s present in all cells, in the form of cell-membranes. It also helps make vitamin D, hormones & bile acid for use in digesting fat in the intestines.  To reach all the places it’s needed, it travels around in the body’s own ‘high-speed motorway’; the bloodstream.

If you’ve ever tried to combine oil & water, you’ll have noticed that the two don’t mix. Because cholesterol is a fat & your blood is water-based; the very same principal applies. Fat would just be floating around in your blood-stream in lumps. We couldn’t utilise it for it’s purpose (the construction of cell-membranes, hormones & intestinal bile-acids) & I suspect our blood would become a little bit messy! (I’m picturing washing-up water, after pans have been soaking overnight).

To allow the fat to cohesively travel through the blood, the body encapsulates it in protein. This makes it a definitive ‘particle’, rather than just a blob of free-flowing oil. These particles of fat in ‘protein-wetsuits’ are called ‘lipoproteins’. The proteins which form the wetsuit have a rather pleasing name: apolipoproteins. The same process is applied to all fats in the bloodstream.

The protein-wetsuit should potentially be termed a ‘submarine’, because it’s made to carry more than just cholesterol. Along for the ride are 2 other things: triglycerides (produced from the food we eat) & phospholipids (the ‘glue’ which holds the whole lot together).

Our lipoproteins contain varying ratios of fat to protein. Some have more, some have less. It’s the ‘density’ of this fat-to-protein which determines the type of cholesterol. There are many different forms of lipoprotein, but the two we shall focus on here are ‘High-Density Lipoproteins’ (HDLs) & ‘Low-Density Lipoproteins’ (LDLs). Particles with more fat and less protein have a lower density. Particles with more protein & less fat have a higher density. It’s therefore the ratio of protein to fat which determines whether the particle is HLD or LDL.

In most people, 60-70% of cholesterol is carried in LDLs. These act as a taxi-service; transporting the cholesterol to where it’s needed. The important part here, is the statement ‘where it’s needed!’. If we have too many LDLs then we effectively have more cholesterol than the body requires. What does it do with the excess? It dumps it in the arteries as plaque, which then builds up and can cause blockages. This is the link between cholesterol & heart-attacks. A blockage in the blood-supply to the heart.

Because of this, LDLs are typically termed the ‘bad cholesterol’. They carry more fat than protein, & therefore pose a risk of blocking arteries if we have more cholesterol than the body can use.

If LDLs are ‘bad’, then why does this post mention ‘good cholesterol’? Is there such a thing?

Every cloud has a silver-lining. The ‘cholesterol silver-lining’ is HDLs.

Because these contain more protein & less fat, the taxi still has room for a few more passengers! HDLs are like a taxi-driver on a sunny Wednesday afternoon. They cruise around, looking for work! When HDLs encounter a bit of excess cholesterol, they pick it up from the cells & tissues, and take it straight back to the liver. The liver then unpacks it and either uses it to make bile or recycles it. It’s a self-perpetuating process where the body conducts its own clean-up exercise. If only my washing-up did the same…

But what’s this got to do with the ketogenic diet?

A high-fat diet will naturally raise cholesterol-levels. What’s important to understand is that a high-fat diet also raises the good HDLs! Raising your HDL-levels increases your body’s ability to scour bad cholesterol from the bloodstream. This makes our bodies more efficient at removing excess fat and bad cholesterol. The higher your HDL level, the less ‘bad cholesterol’ you’ll have in your blood! And that means fewer blockages which cause heart disease.

But what about the bad cholesterol. Doesn’t this just go up too?

Remember our submarine? Cholesterol was not the only thing contained in our lipoproteins. We also have phospholipids & triglycerides.

If you remember from our introduction to ketosis; insulin enables the conversion of food into energy, and stores away what energy we don’t use in the form of fat. Well, that excess energy is derived from glucose. When your body has more glucose than it requires, insulin prompts the liver to convert glucose into triglycerides (the second passenger in our submarine).

If you restrict dietary-carbohydrate (thereby glucose); you decrease insulin-levels.

If you decrease insulin (which converts glucose to triglycerides); you decrease triglyceride-levels.

If bad cholesterol is made up of high fat lipoproteins (LDLs); then lower triglyceride-levels mean less bad cholesterol in the blood!

Restricting dietary-carbohydrate prevents the conversion of glucose into the fatty triglycerides which contribute to bad cholesterol. If you ‘up’ your fat levels & reduce your carbs; you raise HDL levels, which in turn removes bad cholesterol from the blood. LDLs are reduced because you’re not producing fat from glucose.

I hope that about covers it. The process is hugely complicated and I’ve gleaned this from many different sources (all of which seem to contradict one-another). I naturally have a lot more to learn, so any comments which can increase my understanding will be hugely welcome!

Thanks for reading,

Adam.