17th September 2018
I have headed off into different areas from time to time, but to be frank I never thought I would start looking more closely at albumin. This is a substance that almost always ends up getting measured when you do a general blood screening test for patients – for some reason or other.
Albumin is a protein that floats about in the blood. It is made in the liver and, I suppose, it has some important functions in the body. Although I have never really quite known what. At medical school, silence. In medical journal, silence. It seems to be a ubiquitous substance, like nitrogen in the air. We all know it’s there, but we don’t know how it got there, or what it does.
About the only thing I know about albumin is that as the level drops, fluid leaks out of the blood into the abdominal cavity, due to a fall in osmotic pressure. This causes the stomach to swell up like a balloon and is known as ascites.
Small starving children in Africa have ‘pot bellies’ because they cannot make enough albumin. The syndrome is known as kwashiorkor a.k.a. oedematous malnutrition. Alcoholics often have ascites because their livers start to fail, and they cannot make enough albumin either, so fluid – sometimes many tens of litres – fills their abdominal cavity. I have happily drained bucket’s full from stomachs in my time. Just stick in a wide-bore needle and stand back. The pressure can be quite high.
Other than that, I knew nothing about albumin, apart from the fact that, whenever I request a blood test in the elderly, the albumin is almost always a bit low. I have no idea what to make of such a result, or what to do about it. ‘Tick and file – and forget’ represents my normal action.
However, after writing an article about the glycocalyx, and how important it was for arterial health, I wondered if having a low protein/albumin level in the blood might be a bad thing. In that the protein part of the glycocalyx might need to be replenished from somewhere. Perhaps by albumin? Therefore, a low albumin level might be a bad thing – from a cardiovascular disease perspective.
Following such thoughts, I found myself reading papers such as this one: ‘Degradation of the endothelial glycocalyx in clinical settings: searching for the sheddases.’ I definitely need to get out more. In fact, this paper was fascinating. It discusses the role of the glycocalyx, and things that can damage it. [jargon warning].
‘The endothelial glycocalyx has a profound influence at the vascular wall on the transmission of shear stress, on the maintenance of a selective permeability barrier and a low hydraulic conductivity, and on attenuating firm adhesion of blood leukocytes and platelets. Major constituents of the glycocalyx, including syndecans, heparan sulphates and hyaluronan, are shed from the endothelial surface under various acute and chronic clinical conditions, the best characterized being ischaemia and hypoxia, sepsis and inflammation, atherosclerosis, diabetes, renal disease and haemorrhagic viral infections.’1
Which is pretty much what we already know. Many factors that increase the risk of CVD, damage the glycocalyx, and in atherosclerosis there is clear glycocalyx loss/dysfunction. The bit about haemorrhagic viral infections is fascinating and could be worth a future blog.
However, the information I was looking for was to find out if albumin really did help to maintain the glycocalyx and noticed this. ‘…plasma components, especially albumin, stabilize the glycocalyx and contribute to the endothelial surface layer.’ Something I would never have thought to pay the slightest attention to before now. Anyway, in short, yes, albumin does help to maintain the glycocalyx.
Next question. Is there any evidence that having a low albumin level contributes to CVD risk? Well, of course, there is. Here, in the paper ‘Critical appraisal of the role of serum albumin in cardiovascular disease.’ 2
When they looked at serum albumin levels and patients with stable coronary artery disease, the risk of a major adverse cardiovascular event was raised 368%, and the risk of overall mortality went up 681% (relative increase in risk). In their words…’This study unequivocally confirms the important association between SA (serum albumin) and individuals with chronic stable CAD’.
So, you may ask, can you do anything about your serum albumin level? I am not sure that you can do very much. A high protein diet may help, in that the more protein you eat, the more amino acids are available to make albumin from, and Kwashiorkor is due to a low protein diet – so this could do no harm.
At this point, however, the main point that I want to make here – again – is that, once you start to understand CVD as a process that is triggered by endothelial damage, you can start to look at the research on CVD in a completely different light. You can make associations where, using the LDL hypothesis, none exist. It also makes sense.
I find that it is also like freeing your mind from a tyranny. I find it refreshing, and exciting, and I hope that you do to. ‘The difficulty lies not so much in developing new ideas as in escaping from old ones.’ John Maynard Keynes.
Next, they just fired Peter Gotzsche from the Cochrane Collaboration. This is a bloody outrage.