Six things I think you should know about LDL cholesterol

Does bacon deserve the health halo it now seems to have in light of what is becoming common knowledge about saturated fat? Mm. Good question, and it probably comes down to context. If we were to position bacon against Flora Proactive, then that changes the question somewhat: which is better for your health? I mean, one is designed specifically to lower low density lipoprotein (LDL), aka ‘bad’ cholesterol (something we’ve been told for years to strive for) and is ridiculously expensive; the other is … well, bacon. Due to its saturated fat content (or perceived saturated fat, it contains less than 50% of its fat from saturated sources), it is always the second food which people think of when it comes to elevating cholesterol levels and causing heart disease – the first being butter.

Many clients come into my clinic with a total cholesterol above 5 mmol/L and are told by their GP that they should bring their cholesterol level down by way of eating low saturated fat, low total fat and reducing animal protein in their diet. OR (worse) go on cholesterol lowering medication (why is medication worse? Check out here and here). There are many things contributing to a higher cholesterol level, and the risk this poses to you is based on many factors. I’ve covered some of these (and what you can do about it) previously.

Here are 6 things I found useful to know about LDL cholesterol. I’m not talking about particle size, particle number, patterning of particles or Apo A or B, reverse transport cholesterol etc. Keeping it kind of simple. If you know more than your average Joe about cholesterol this will likely be a bit elementary. Otherwise:

  1. Most studies and media reports that report a reduction of risk of heart disease when taking cholesterol lowering medication focus on the relative risk. Relative risk – takes a small effect and it amplifies it. This makes the medication look far more effective than it actually is. Let’s explore what this means:

If you have a clinical trial whereby 100 people are given a placebo drug* and 100 people are given the experimental drug, you might find that 2 people in the placebo group go on to have a heart attack (2%), 98 have no adverse events. In the drug-treated group, 1 person has a heart attack (1%), and 99 people have no adverse events. The difference is 1%, however the relative risk reduction is 50% and a much more impressive number, don’t you think? Those reporting in the media certainly do.

  1. We need cholesterol to synthesise naturally occurring steroids in our system. It is necessary for life. It is the substrate for every sex steroid, for vitamin D, to make new neurons and new synapses to consolidate memories. Many people think cholesterol is in our body solely to clog arteries, and the lower the better. This is not the case. For example, in some populations a low total and LDL cholesterol are linked to higher incidence of depressive symptoms. A low cholesterol level may also result in less synthesising of vitamin D in the body, lower hormone production and an impaired immune system.
  2. LDL is an innate part of the immune system. When there is damage to the artery, you have susceptibility to infection, and there is evidence of pathogens present in plaques. When there is damage to the artery and artery wall, resulting in atrophy, there is an infusion of white blood cells as well as LDL cholesterol which work together to promote inflammation (for healing purposes). Blaming LDL for creating damage is like blaming the fireman for creating a fire.
  3. There is NO level of LDL that is unhealthy. There is an assumption that LDL cholesterol is inherently atherogenic and that above a defined level it is dangerous – there is something about the LDL packaging of cholesterol that causes heart disease. That’s not the case, and some experts in the field believe there is no level of LDL that should be treated with a statin. Researchers reviewing the literature have found people with high LDL with no heart disease. The cut-off of 4mmol/L or 5mmol/L depending on your reference point is an artificial distinction that has been created to suggest LDL is inherently toxic to the heart and cardiovascular system. Now there are people who have a genetic predisposition to storing cholesterol, so they have an increased risk? Actually research looking at the lifespan of people with familial hypercholesterolemia (FH, a mutation in the LDL receptor whereby the end result is elevated LDL cholesterol) have found that, aside from a subsection of the population, there is normal lifespan, with just a small number of these people going on to develop heart disease. There are people who have other genetic variants which do result in build up of LDL cholesterol, and we don’t know enough to say that a very high LDL level is NOT dangerous – however the likelihood of harm will be increased with the presence of other risk factors for cardiovascular disease, such as high blood pressure or smoking.
  4. It is not LDL that is causing heart disease. Blood cholesterol (including LDL) is high in people consuming a higher fat diet. However, research shows that other biomarkers are not only fine, but can be improved when transitioning to a higher fat diet from the standard western diet. A recent paper found that people 60 years and older who have the highest LDL live as long or even longer than those with low LDL. They have lower rates of cancer and lower rates of infectious disease.
  5. If it’s not LDL cholesterol, then what is causing a heart attack? A critical trigger factor is coagulation. We rely on the coagulation factors in our bloodstream to create a clot when we become wounded and begin to bleed. However, our blood can clot without there being a wound. High stress, tobacco smoke, high blood sugar all trigger clotting mechanisms. It looks like this:
    1. In our artery wall, there are tiny arteries which feed to the inside of the artery (called vasovasorum).
    2. Vasovasorum are easily blocked or clogged by clots.
    3. If these can’t feed our artery wall, the wall essentially becomes hypoxic and the tissue dies.
    4. When the tissue dies, the LDL cholesterol comes in to repair it, and this happens repeatedly, causing the artery wall to become thicker and thicker until it chokes the artery.
    5. When you combine this thickening of the artery wall with something that might trigger clotting of the blood (such as high blood sugar, smoking or a stressful or emotional event etc), a clot will pass through the narrowed artery,
    6. The clot will eventually block the artery entirely and the result is a heart attack.
    7. None of this is caused by LDL cholesterol.

What really matters is keeping your clotting factors inactive until they are needed. Most people (unless they are haemorrhaging) don’t need their clotting factors on high alert all the time.

So, which is better for your health? IMO – while bacon may not be a health food, I’d choose it over the Flora (preferably free range, minimal added preservatives, along with an abundance of vegetables). Flora doesn’t have a lot going for it, TBH, and while it may lower your cholesterol level, how important is that really? If your cholesterol levels are high and you’re not sure of your risk, get in contact with someone like me who can work with you to address the lifestyle factors that might be driving up your cholesterol levels and contributing to health risk.

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This bacon isn’t preservative free, however it’s the only one I could see that had less preservatives and was free-farmed, so using it as an illustration. Henderson’s is free of preservatives but only select supermarkets carry their free-farmed variety FYI

 

Peter on cholesterol….pt 2

Following on from last week…. and trying to summarise Peter Attia’s cholesterol talk at AHS12 to illustrate why the cholesterol reading you get from Medlab doesn’t give you a good indication of your risk of atherosclerosis and subsequent heart disease. Cholesterol. The internal regulatory process responsible for cholesterol involves both the production of cholesterol and absorption of it. There are a few reasons why some people have higher cholesterol levels, and broadly speaking there are people who are good at producing cholesterol, and people who are good at absorbing it. The absorption of cholesterol is governed by a receptor in the gut which is responsible for allowing the movement of sterols in and out of the gut. There is also a receptor in the gut that is responsible for getting rid of all unwanted sterols (and excess cholesterol) from the gut to be excreted (called ABCG5 and ABCG8). It’s only ‘free’ sterols that are able to get in – esterified cholesterol (i.e. that which is delivered through food) is not able to enter the gut. For this reason there is very little, if any, relationship between cholesterol in food choices and our total blood cholesterol level. Health professionals have been aware of this for a few years now, however the general public is still confused and I can’t tell you how often I get asked the question of whether there is a limit on eggs. However some may have a defect with the receptor in the gut letting too many of the sterols in, or a problem with the ABCG5/G8 getting rid of the unwanted sterols. The effect this has on overall cholesterol homeostasis is not clear at this stage.

 I can't get enough of eggs, even the grumpy ones. (image from chelseacrockett.com)

I can’t get enough of eggs. (image from chelseacrockett.com)

While we hear a lot about LDL-cholesterol, the lipoproteins responsible for carrying HDL and LDL also carry triglycerides and phospholipids. These are produced by the liver and are known as Apo-A (HDL cholesterol) and Apo-B (LDL cholesterol). Apo-B lipoproteins contain more triglycerides than Apo-A lipoproteins, and include very low density lipoprotein (VLDL), which (when it sheds its triglycerides and phospholipids) converts to IDL (intermediate density lipoprotein) and LDL. VLDL contains more triglycerides than cholesterol (5:1 ratio) compared to LDL which is more in the vicinity of 4:1. When the VLDL are transported from the liver they release triglycerides and phospholipids and triglycerides to be used for energy by the muscles or stored in the adipose tissue. In people that are metabolically healthy, the triglycerides are delivered to the muscles by VLDL to be used for energy – however in those that have metabolic health problems, the triglycerides are more likely to be stored as fat. In addition, as they contain a lot of triglycerides, when we have high levels of processed carbohydrate we are going to have a lot more VLDL in our bloodstream as these excess carbohydrates are converted to triglycerides and packed up in the VLDL. Research has shown that the number of VLDL particles increases risk of athleroschlerosis. In addition, there is a lipoprotein Apo-E which is found in Apolipoprotein E (ApoE) is a class of apolipoprotein found in the chylomicrons (carriers of dietary fat after we eat) and Intermediate-density lipoprotein (IDLs) that is essential for the normal breakdown  of triglyceride-rich lipoprotein constituents such as VLDL, and there exists three main forms – E2, E3 and E4. These differ in the position of certain amino acids in the structure, but alters the function of the Apo-E lipoprotein significantly. Those people with the E2/E2 and E4/E4 expression have been found to be at greater risk of atherosclerosis.

The whole cholesterol issue is confusing. I spent about 3 hours writing that last paragraph and its very rough and actually probably didn’t mention 18 other ‘must knows’ in order to understand it properly. However, I think that, really, the most important thing to understand is that JUST knowing your LDL number (or total cholesterol number) is not going to provide you with a good idea of your risk of atheroschlerosis. Firstly – in NZ we aren’t able to quantify LDL – instead it is a calculated number based on the direct measurement of total cholesterol and HDL cholesterol. That’s an issue. However, moreso, there are certain conditions which can increase risk associated with cholesterol. The Apo-B lipoproteins can get into the sub endothelial space in the artery wall and can spark an immune response, causing inflammation. This inflammation can then increase the number of particles being delivered to the site (as LDL is released in response to inflammation) thus further particles get into the artery wall. The Apo-A lipoproteins, responsible for delivering HDL don’t.

Of course, inflammation is not just caused by one factor – and I bang on about this a lot in pretty much every health related post I write here and on my facebook page. The oxidation and glycation (binding of a glucose molecule to a protein) of the particles can change the functionality of the lipoproteins which causes them to damage the endothelial cells I mentioned above. These processes are caused by an overload of stress in the system: dietary, activity, toxins and the like. Result? Increased likelihood of atherosclerosis. Oxidised LDL can’t be measured in New Zealand but people can send their results to a laboratory in Australia to get this measured.

Another important factor is the size and the number of LDL particles in our system. There are two different patterns – and those with fluffy LDL particles (bigger) are less likely to get stuck in the artery all compared to the smaller (pattern B) particles, which are more atherogenic. It’s not just size that matters, though – it’s overall particle number. And when the size of the LDL particles have been controlled for, it suggests that overall the number of particles is more important. The greater the number of particles, the less able they are to move efficiently around the bloodstream, the more likelihood of being oxidised and subsequent inflammation.

Also important to consider that LDL cholesterol is used as a patch to help with inflammation in the body – if you have high LDL then that could very well be indicative of an underlying issue that needs to be addressed. Interestingly, while we’ve understood that a high HDL is a good thing and the higher the better, in fact a high HDL is not a get out of jail free card either. Indeed, trials that increase HDL levels through therapeutic means have been stopped before their planned end dates due to the lack of clinical benefit in people who have established cardiovascular disease. If HDL is high, then there may well be a reason outside of just eating a good quality diet. There are different forms of HDL and, its primary role is a carrier to remove excess cholesterol away from the blood vessel wall to be excreted, if it is not functioning correctly then that in itself can increase risk of heart disease (depending on other risk factors). If we use the car analogy (as people tend to do when it comes to cholesterol, quite useful), then if the car breaks down, then the cholesterol is not going anywhere – this is double-whammy bad actually, as it is unable to break down the plaque at the artery wall and in itself can cause inflammation.

Yeah. Cholesterol. So how useful are your own cholesterol readings? First – there are a couple of good ‘proxy’ measures that can be gleaned from your results to give you an idea of risk. Triglyceride/HDL can give you an indication of particle size. The smaller the ratio, the larger the particle size, the less risk. You need to calculate this as it’s not given to you. However, this may not be as important as total cholesterol/HDL, which can give you an indication of particle number. The smaller the ratio better and this is likely to be a better indicator of overall risk. Finally, and most importantly, is the context. As I said last week, our cholesterol readings are nowhere near as important as we once thought with regards to atherosclerosis and heart disease – and can’t be looked at in isolation of other risk factors. The context matters, so evaluate them in light of your current lifestyle to get a better understanding of their usefulness.