Insulin (part 3): Don’t wait for diabetes
You have heard quite a bit about insulin and its actions, so today I have a gift for all of you. This gift is knowledge, and I hope you'll use it to take care of your health proactively. It is hard when you learn something different, especially when it seems like no one else in the world knows what you are talking about. On the other hand, if you want something to benefit your health today, you might not want to wait for everyone else to catch up, as the latter may or may not ever happen.
Most people's insulin resistance can be picked up early and relatively easily. The ALT we discussed in the previous blog is only really present in the liver cells, meaning it does not reside in the bloodstream unless there has been liver cell breakdown. It literally is the liver cells opening up and spilling the ALT into the bloodstream, if you want to be that visual. When you have a blood test, your ALT result is interpreted against the range, normally between 5 and 45 U/L.
A degree of liver breakdown is necessary for optimal function; otherwise, you would never get rid of the old and senile cells which are holding your precious organ back. That means your ALT will never reach 0 U/L, or if it does, you should be extremely concerned. The upper limit, which is more of our focus here, differs depending on your gender and the testing provider. If you are a female and had your bloods taken with SNP, your upper limit is 30 U/L. If you are a male and have been to QML, your upper limit is 45 U/L. Unfortunately for everyone who believes in the ranges they are offered, neither of these are backed by solid evidence.
When you look at your liver's health on a blood test, I assume you want to spot its digression from health long before the liver is halfway through its journey in the toaster oven. By the time you reach the upper limit of these ranges, this is exactly where your liver is going to be. I can say this with confidence as there are so many studies which have demonstrated that fatty liver disease starts at a much lower limit, with one study demonstrating this in an ALT of 17 U/L in women and 25 U/L in men. As is often the case, our Japanese counterparts are ahead of the curve; this knowledge has come from their dedicated research as far back as 2012. My concern is that if NAFLD (non-alcoholic fatty liver disease) can be firmly seen and diagnosed at these lower ALT levels, then we should have a lower cutoff for when the disease starts to unfold. In my clinical experience, this is 15 U/L in women and 20 U/L in men. I remember telling a patient recently with an ALT in the low 30s that I have no doubt he has fatty liver. He wanted to see it for himself, so we did an ultrasound scan, and there it was, staring back at us. The lowest ALT in a fatty liver I have encountered is indeed 17 U/L, which was before I read the Japanese study. In fact, that led me back to the medical journals as I realised that I was staking my patients' health on the wrong reference range.
Sometimes, again due to individual variation, the first sign of insulin resistance on lab testing is in the cholesterol panel instead of the liver marker ALT. Recall our little lesson on insulin physiology, where it stimulates fat cell growth instead of breakdown? When the fat cells are resistant or stubborn to the message of insulin, they refuse to grow further. Therefore, your blood becomes a storage hub for this excess energy when it should only be used for transit. This excess energy is triglycerides - the name comes from three (tri) fatty acids being attached to a glycerol (glyceride) backbone.
When triglycerides are high, they will use up the HDL as these are the boats that try to get rid of excess triglycerides in the bloodstream. If this persists, the liver may end up making more VLDL to store up the excess energy. These VLDLs are turned into your notorious neighborhood criminal - LDL - unless there is so much excess energy / triglycerides, in which case there will be a lag in the process. I refer to this entire process as a metabolic traffic jam.
The first sign of your traffic jam is that in a fasting sample, the HDL is not more than double the amount of triglycerides. This normally happens for years, if not decades, until your liver has to use the next strategy of making more VLDLs (which the test doesn't report) which are then turned into LDLs (which the test does report). At this stage, your LDL and total cholesterol on the lipid panel will cause your doctor to raise alarm bells. When this VLDL-LDL mechanism also fails, again after years of putting up with it, your fasting triglycerides count will eventually shoot up. Believe it or not, sometimes I see people at this stage, where the fasting triglycerides are high and the liver is shot - but with a 'normal' blood sugar level.
So the two earliest signs are ALT and the triglycerides / HDL ratio. Keep an eye on these, and I guarantee you will see this problem long before your sugar caves in. You will spot insulin resistance way before your doctor suspects it happening. You will find answers to your fatigue, brain fog, irritability, weight gain, inflammation, chronic pain, and many other problems whilst your doctor still says everything is in range (and it may be like so for years). You can start planning on what actions to take to work on improving your insulin sensitivity right now. You can wave goodbye to metabolic diseases and welcome health and healing.