The Secrets Revealed. Finally. Part Two

Insulin. Often when talking to patients, this has happened hundreds not dozens of times, the word ‘insulin’ is heard as ‘glucose.’ So, alert! We are talking about insulin. Some of the principles of tracking objective health markers were laid out in Part One and they all apply here.

There are several intermediate energy storage molecules; triglycerides and glycogen are two commonly known ones. There are dozens, perhaps hundreds, of energy storage and release signalling molecules: insulin, ghrelin, leptin, GIP, etc. Insulin is an easily interpreted, system-wide, energy-storage, signalling molecule that we can benchmark, track and easily modify.

Besides the widely known property of being released by the pancreas and then going to various cells to enable them to take in blood borne glucose insulin has many direct hormone like effects besides this; for example, insulin decreases arteries ability to synthesize and release nitric oxide. I like nitric oxide; they sell little blue pills to help men make more of this useful substance and insulin blocks this healthy wonderful molecule from being made. It does lots of other stuff but more importantly for our use of tracking it is its statistical relationship to stroke, heart attacks, impotence, cancer incidence and, and… well that’s enough. Isn’t it? Oh, one other nifty little thing: it is pretty much inversely related to testosterone. Low insulin, high testosterone, high insulin, low testosterone. add that to the list.

In some measure it is an association, not a cause but in several other ways it is causal. We would die without it but are healthier with as little as necessary to keep our glucose down nice and low. So measure it, track it and make it better.

There are three large scale, important components that determine insulin levels: of course genetics, some are genetically prone to insulin resistance and high insulin, and second, insulin receptor sensitivity which is related to exercise and third is diet; eating an insulinogenic diet, one that stimulates insulin release, will obviously (tautologically) stimulate higher insulin. Now, insulin, like triglycerides. varies wildly from the fasting to the non-fasting state. Further, in some people there is a tight concordance between their fasting and non-fasting insulin and in others there is not and in cases like this the fasting insulin is less accurate as an indicator of non-fasting insulin levels. Well, let’s not let perfect be the enemy of our good and let it be that fasting insulin is a wonderful indicator of overall insulin related metabolic health. If it is high that is bad and if it is low that is good. Adjusting this marker is sometimes a little tricky. Let me explain.

Since, as we will see in detail in a later post, we care very much about fasting glucose, we don’t want to manipulate insulin at the expense of too high a fasting glucose. This is easily done and in fact an almost necessary intermediate state along the path to getting both where you want them.

OK, if you follow my Step One diet, found elsewhere in these blogs, you will see a rapid drop in your fasting insulin, unless your baseline says your insulin is low or too low already in which case don’t use the Step One Diet. Insulin levels around 2-3 microU/dl is ideal unless you are trying to gain mass in which case this is too low. You see, at some level insulin is androgenic; cellular uptake of protein depends on insulin too. As a rule 4 or less is associated with fat loss; again unless the insulin has dropped too fast and the glucose has gone up too much. Hey, I didn’t say this was easy!

The underlying ‘trick’ is that some things adjust more readily than others. You can change your diet in such a way that your diet driven insulin drops more quickly than your insulin receptor sensitivity, genetically and exercise driven, can adjust and then your fasting and even A1c glucose markers will go up more than you would like. There is a time function going on here; some things take longer to change than others and are by various feedback loops interdependent in such a way that following markers will feel like one step forward and two back unless you track things through time and by various iterations determine the rate of change, and rate of change to the better, that your body takes to make positive adaptive changes of the kind your initial testing indicates is needed.

OK, that does it. That last sentence shows that this topic is going to be tougher to explain than I thought, important but tougher. It’s all stuffed in my head so, with your help and forbearance, I will get it out. But for now this will be the end of Part One of Part Two. Huh?

Smile and God Speed,

Dr. Mike

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