A standard lipid panel (blood test for cholesterol) measures three things - the amounts of triglycerides (fat), cholesterol, and the HDL cholesterol particles in the blood. The LDL figure is calculated by the machine in the lab based on these three measurements. LDL is not measured directly by the standard lipid panel blood test.
In the hours after eating the triglyceride in the blood can either be fat coming from the intestine while digestion is underway, or fat that has come from the liver. In the fasted state the triglyceride figure is largely representative of the portion that comes from the liver.
The liver pumps out fat into the blood in the form of VLDL particles, which are little blobs of triglyceride wrapped in cholesterol and proteins. These travel around the body delivering fat to fuel the body or for storage elsewhere and get smaller and smaller as they do so. There are various names for the sizes of these shrinking VLDL particles but the last and smallest stage is an LDL particle - LDL cholesterol. At this stage most of the triglyceride has been depleted and the particle had more cholesterol on it than triglyceride inside it. The triglyceride result on the blood test measures all the triglyceride in the blood and does not directly measure the different sizes of particle or how many of those particles there are. A small number of large particles will look identical on that test to a large number of small ones. Small is bad - more particles banging around in arteries crashing into the artery walls.
If you want the gold standard test you'd need an Apolipoprotein B (Apo B) test which basically counts the 'bad' particles rather than measuring the amount of triglyceride and cholesterol in the blood. Unfortunately that test is difficult to access at this time - the only way I could get one here in Ireland is to get it privately through a heart health screening service which includes a package of blood tests, and which costs €495. I won't be doing that. If you want to dig deep on how it all works this page has links to three video interviews with lipidologist Dr Thomas Dayspring, in which he explains how all the particles and tests work along with a load of other stuff like how a statin works -
Link. It's six and a half hours of interviews - not everyone's cup of tea but you will learn a lot if you're interested.
I know hardly anything about the causes of high triglycerides except for one circumstance - how I came to have high trigs myself. When I was diagnosed this time last year my triglyceride result was 9.11 mmol/L (epic!). From reading pretty much everything written by Prof Roy Taylor on the subject of Type 2 remission and watching several interviews with him since then (I think this one is the most informative -
Link) I would summarise one of his theories as follows:
- If a person puts on too much weight their adipose tissue (fat cells) may become less receptive to taking in more triglyceride from the blood for storage. Taylor calls this the 'Personal Fat Threshold'.
- As adipose tissue becomes less receptive to storing fat then the fat that the liver is pumping out has less places to go. Levels of fat in the liver rise as a result.
- As the liver becomes more and more full of fat it 'tries harder and harder' to pump it out - more VLDL particles in the blood - higher triglycerides.
- A high concentration of triglycerides in the blood increases the rate at which this fat is deposited in other tissues in the body, including the pancreas. In those who are genetically susceptible this ectopic fat causes lipid toxicity in pancreatic beta cells, leading to cell dedifferentiation. Translation: in some people, fat stored inside the cells that produce insulin poisons them and 'switches them off'.
- Over time the effects of lipid toxicity appear to become permanent in most people.
I believe Taylor when he says that a fatty liver is the root cause of Type 2 diabetes (in most people at least) and that elevated triglycerides are the main mechanism by which is gets progressively worse over time.
Losing a lot of weight probably 'empties out' fat cells, probably making them more receptive to taking in triglycerides from the blood, probably enabling the liver to resume exporting fat effectively, probably bringing fat levels in the liver down and probably lowering triglycerides. This probably greatly reduces the rate at which fat is deposited in the pancreas, allowing cells to burn it off over time, and enabling a portion of the beta cells in the pancreas to 'switch back on' and start producing insulin again. This is probably the mechanism by which big weight loss can lead to T2 diabetes remission. From 9.11 mmol/L last October my trigs dropped to 1.6 in January having lost 12Kg, 1.2 in June having lost 33Kg or so, and 1.0 last month at the same level of weight loss. My statin was reduced in that time and I'm on no other meds which might affect triglycerides. I'm still on meds so I can't tell yet whether I'm in true remission territory. What I can say with certainty is that in my case weight loss and exercise brought down my triglycerides. I'm eating more fat today as a proportion of my diet today than I was in January. Experiments with CGMs show I can safely eat quite a bit more carbs in a meal today, after having my Metformin halved from 2000mg to 1000mg daily, than I could in January. It appears that I got some insulin response back some time after I got my triglyceride levels down.
With all that said, your case may well be entirely different to mine. I have no idea how your combination of other illnesses and medications impact on your triglyceride levels. I would suggest though that if you are in a position to lose weight and are able to do so it might be a good idea. Not a bad idea at least. It might also be a good idea to discuss the issue with a doctor who is aware of the current science on Type 2 and grasps the high probability that triglycerides are the primary mechanism by which Type 2 diabetes gets progressively worse over time. My GP doesn't know that. My diabetes specialist nurse didn't know that last time I spoke to her. My diabetologist... shortly after I was diagnosed I had a quick referral as there seemed to be a lack of certainty about what type of diabetes I had (long story). He asked if I knew what caused my diabetes. I answered - 'Visceral fat, in and around the liver and pancreas, probably'. 'Probably is right!' was his response, and he left it there.
I didn't know the word 'ectopic' at that time and I now know that visceral fat, which is fat inside the abdominal wall, which is largely adipose tissue, is an indicator of the problem of a fatty liver and Type 2 diabetes, an indicator that adipose tissue under the skin has become less receptive to storing more fat, but is not the direct cause. The cause is ectopic fat specifically - fat stored in cells that aren't meant to be storing so much fat, a thing that some people are very sensitive to. At this time the science makes all the details I laid out above look very probable but not so well proven that all the doctors in all the lands have received and believed the news just yet, or so it would seem. I will say this though - I have zero faith in my GP at this time when it comes to the issue of cholesterol and triglycerides. The man still goes on about ratios. He tried to refer me to a f*^king pathologist in the early days to figure out why my triglyceride levels were so high. Hasn't the slightest clue how all this works. I believed Roy Taylor, got the weight loss done fast, saw my trigs drop to lovely healthy levels, and I'll be taking one word on my blood test results extremely seriously for the rest of my life. 'Triglycerides'.
