A related BLOG post by an MD (Hyperinsulinemia: Should You Be Tested?).
My initial target was hacking my diabetes. That was even the subtitle of my original BLOG (Hacking my T2DM). For years, I took the medications that the doctors gave me and my diabetes got worse. In the end I was on 100+ units Insulin delivered via a pump and I was getting worse. I thought there must be a better target since the doctor’s approach wasn’t helping me.
Diabetes and Insulin Resistance
In seeking answers, I found that the diabetes related to Insulin Resistance. So I chased after curing my Insulin Resistance via the Low Carb diet. In doing so my diabetes was apparently cured.
Certainly the low carb diet has greatly helped my Insulin Resistance, but the question remained of whether my diet has cured my Insulin Resistance and there’s indications that I am not completely cured (Insulin Resistance Test).
Aspects of Insulin Resistance
Turned out that Insulin Resistance has a bunch of subtle aspects. There’s hepatic (in your liver) Insulin Resistance, peripheral (in your muscles) insulin resistance, physiological insulin resistance, etc. Each of these play a role in diabetes and each are affected in various ways by the Low Carb diet.
Somebody may have written a good write-up on all of this but I haven’t yet seen it. Everyone seems to have a piece of the story. Perhaps a BLOG post sorting it out would be helpful?
Fatty Liver and Diabetes
Recently, I’ve been circling around a more nuanced view of the problem and have been looking more closely at the role of the fatty liver and glycogen stores.
Your body stores glucose in the liver as glycogen. Once those glycogen stores are filled, excess carbohydrates then fill up the liver fat. . Fat then overflows into other internal organs, particularly the pancreas. Eventually the pancreas isn’t able to make enough Insulin to keep up with the resistant areas. That’s when you end up on insane levels of Insulin.
How Does a Low Carb Diet Work?
Low carb reverses fatty liver quickly by first dropping glycogen stores. It only takes a day or two of eating very low carbs to reduce your glycogen stores to minimal levels. The liver then mobilizes its own fat for energy. This leads to a leaned liver within a week or less. This leads to less fat in the pancreas and restores normal insulin production in the pancreas.
In addition, the reduction in carbohydrates leads to a reduction in blood glucose and insulin levels. The lower glucose load allows the pancreas to keep up. This is part of why the Low Carb diet is effective with diabetes so quickly.
Obesity fits into this in a strange way since increasing insulin sensitivity (decreasing Insulin Resistance) allows cells to take up more glucose. But a low carb diet reduces the glucose from the diet. Under a low carb diet most of the glucose the body needs comes from Gluconeogenesis (GNG) (glucose made by the liver from stuff other than glucose). So GNG which is a problem under a high carb diet because it contributes to the amount of glucose in the body, then becomes what provides the necessary glucose to survive under a low carb diet.
What Causes What?
But all of this raises the question of what causes what. Current dogma mostly blames energy surplus as the problem. You are fat because you eat too much and getting fat makes you Insulin Resistant, diabetic, etc.
Since the Low Carb cure reduces weight it’s hard to tease out which effect leads in terms of the effectiveness of the cure. I know in my own case that I got off all Insulin within two weeks and I hadn’t lost much weight yet.
The Real Target
I’ve come to view Hyperinsulinemia as the central issue in the development of the cluster of issues known as Metabolic Syndrome (hypertension, hyperlipidemia, obesity, Type 2 Diabetes). Others have recently presented the same insight. One crucial paper on the subject is (Erion, K.A. & Corkey, B.E. (2017). Hyperinsulinemia: a Cause of Obesity? Curr Obes Rep (2017) 6: 178.).
Purpose of Review
This perspective is motivated by the need to question dogma that does not work: that the problem is insulin resistance (IR).
The prequel to severe metabolic disease includes three interacting components that are abnormal: (a) IR, (b) elevated lipids and (c) elevated basal insulin (HI). HI is more common than IR and is a significant independent predictor of diabetes.
We hypothesize that
(1) the initiating defect is HI that increases nutrient consumption and hyperlipidemia (HL);
(2) the cause of HI may include food additives, environmental obesogens or toxins that have entered our food supply since 1980; and
(3) HI is sustained by HL derived from increased adipose mass and leads to IR.
We suggest that HI and HL are early indicators of metabolic dysfunction and treating and reversing these abnormalities may prevent the development of more serious metabolic disease.
Not only are high levels of Insulin the key driver in the processes related to the development of Metabolic Syndrome but they are the key drivers in reversing Metabolic Syndrome.
Taking exogenous Insulin drives hyperinsulinemia.
Eating too many carbs drives hyperinsulinemia like nothing else can do.
Reversing hyperinsulinemia via a combination of low carb diets and fasting does the best possible of any treatment.
Another view showing evidences on both sides (Shanik MH1, Xu Y, Skrha J, Dankner R, Zick Y, Roth J. (2008). Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse? Diabetes Care. 2008 Feb;31 Suppl 2:S262-8.).
We examine situations where insulin itself appears to be a proximate and important quantitative contributor to insulin resistance.
1) Mice transfected with extra copies of the insulin gene produce basal and stimulated insulin levels that are two to four times elevated. The mice are of normal weight but show insulin resistance, hyperglycemia, and hypertriglyceridemia.
2) Somogyi described patients with unusually high doses of insulin and hyperglycemia. Episodes of hypoglycemia with release of glucose-raising hormones, postulated as the culprits in early studies, have largely been excluded by studies including continuous glucose monitoring.
3) Rats and humans treated with escalating doses of insulin show both hyperinsulinemia and insulin resistance.
4) The pulsatile administration of insulin (rather than continuous) results in reduced requirements for insulin.
5) Many patients with insulinoma who have elevated basal levels of insulin have reduced (but not absent) responsiveness to administered insulin.
In summary, hyperinsulinemia is often both a result and a driver of insulin resistance.