Insulin is so easily villainized for causing metabolic syndrome and diabetes and that’s one of the reasons why low carb diets are all the rage these days.
But is there a possibility that something is being overlooked?
That is what I want to discuss with you in this article.
First, why are people drawn to the ketogenic diet?
To list a few reasons:
- It’s supposedly better for fat loss
- It’s been shown to improve insulin sensitivity
- It’s been thought to enhance metabolic flexibility
- It’s supposedly better for satiety
- Carbs are a poison, so on keto you eliminate it
- On keto, glucose variability is better, which translates to more graceful aging
- Cognition is better
And much more…right?
Those are the most frequent mentioned reasons why people do the ketogenic diet. But the number one reason bar none is that keto is supposedly better for fat loss.
People also do it because they want to feel better, mentally and also physically.
This all stems from many keto proponents that cherry-pick their research and because of a misunderstanding of the research and how the body works.
Let’s start with the number one health and fat villain…insulin.
Insulin: the poor misunderstood hormone
Insulin is a hormone produced in the beta-cells of the pancreas. Insulin is always produced in small amounts during fasted periods or during low carb intake, and then produced in much greater quantities when carbs are eaten.
The main reason why insulin is demonized is because of the following thinking:
“Insulin’s role is to shuttle glucose into your cells where it can be stored as glycogen or be turned into fat and to inhibit the all so important fat burning”
What if I told you that’s not the big picture?
A brief history of insulin
Sir Edward Schafer, who was a Professor of Physiology in Edinburgh, appears to have named insulin and described its actions back in 1913, although insulin hasn’t been discovered yet.
Schafer described insulin as having ‘autacoid’ and ‘chalone’ actions; ‘autacoid’ being a substance with excitatory actions and ‘chalone’ one with inhibitory actions.
Schafer went on to describe how ‘insuline’ had both excitatory and inhibitory actions. His description of how he thought the hypothetical substance ‘insuline’ acted in the body is remarkable because the passage of time has shown him to be correct almost word for word.
Things have been confused, however, by a 20 year ‘black age’ of endocrinology (between approximately 1960 and 1980), where leading scientists—through extrapolating beyond their new discoveries—confused scientific thinking and teaching. They formulated new hypotheses based for the first time on hard scientific evidence but they got it badly wrong through extrapolating (incorrectly) from in vitro experimental data in rat tissues to in vivo metabolism in humans.
The consequence of this error was the (fallacious) concept of insulin being “required” for glucose entry into cells rather than just accelerating glucose uptake. The hyperglycemia of diabetes was interpreted as a “damming back” of glucose in the bloodstream as a consequence of a lack of insulin, which caused hyperglycemia.
This became established teaching and, although the concept was shown to be erroneous in the mid-1970s, the teaching has not changed. Consequently, therapy has been based on a flawed concept.
Glucose entry into a cell
Glucose doesn’t need insulin to enter a cell. Glucose is transported into the cell through various GLUT transporters, for example, GLUT1-6. Only GLUT4 is insulin-dependent, meaning insulin stimulates GLUT4 activity, but not the activity of the other GLUT transporters.
It’s been shown that glucose is taken up into cells perfectly fine even in the absence of GLUT4, which shows that glucose uptake doesn’t require insulin. Research also shows that the rate of glucose uptake is dependent on the amount of glucose in the blood. The more glucose there is in the blood, the more glucose is taken up in the cell – to a degree of course.
Interestingly, in the face of hyperglycemia, tissue glucose uptake is usually increased above normal even when insulin deficiency is severe. This cannot be reconciled with the concept that insulin is required for glucose uptake by insulin-sensitive tissues (Sonksen & Sonksen, 2000).
We now know that even in the fasted state or in a state of absolute insulin deficiency, there are sufficient glucose transporters already in place to allow glucose uptake to exceed that of a normal individual when blood glucose is sufficiently high.
- There are insulin-independent glucose transporters in each cell that can take glucose up from the blood.
- If blood glucose goes high enough, uptake into cells is enhanced even without insulin.
- Blood sugar only goes too high when glucose production in the liver (not dietary glucose) exceeds glucose uptake in the cell.
Insulin’s actions include:
- Excitatory, which include stimulating:
- glucose uptake
- glycogen synthesis
- glucose oxidation
- lipid synthesis (only when very large amounts of glucose is consumed at once)
- amino acid uptake in the muscles
- Inhibitory, which include inhibiting:
- lipolysis (the breakdown of fat in fat tissue)
- proteolysis (the breakdown of protein into amino acids in organs and muscles)
- glycogenolysis (the breakdown of glycogen)
- gluconeogenesis (the synthesis of glucose from amino acids, glycerol and lactate)
- ketogenesis (the generation of ketones from fatty acid oxidation)
At low concentrations, insulin puts a break on lipolysis, protein breakdown, gluconeogenesis and ketogenesis. In large amounts, insulin aids in shuttling glucose into cells.
When insulin starts to drop too low, lipolysis becomes overactive and releases too much fat into the circulation. This overload of fat is then converted to energy in the muscles and the rest than cannot be oxidized is deposited in the cells as fat. Ever heard of fatty liver and the accumulation of fat around the heart and in the muscles? Yes, that is driven by excess lipolysis for one.
Furthermore, when insulin drops too low, the breakdown of protein in muscles and organs are enhanced and this leads to organ shrinkage and muscle wasting. Even a few hours of stress, where cortisol is very high, can shrink the thymus almost completely. Cortisol becomes elevated in a state of low insulin. Insulin is powerfully anti-catabolic as it potently inhibits cortisol.
Lastly, when insulin is low, gluconeogenesis becomes elevated. Research in humans as far back as 1970 shows that high blood sugar is actually not a result of eating too much glucose, but because of overactive gluconeogenesis in the liver. Inhibiting gluconeogenesis normalizes blood sugar even when carbs are eaten.
What causes insulin resistance?
As you can start to see, high blood sugar, insulin resistance and diabetes are not caused by the consumption of carbs, but rather an excess of fat (through the diet or lipolysis) and/or stress hormones.
In the short term, insulin secretion is enhanced to try to manage the elevated blood sugar, which is driven by excess gluconeogenesis, but over time, the beta-cells become damaged and insulin secretion reduces. Inhibiting serotonin synthesis reduces lipolysis and gluconeogenesis and ameliorates hyperglycemia in type 2 diabetic animals (R).
- Helps to regulate blood sugar
- Prevents excess protein breakdown
- Enhances glucose uptake into cells when a large amount of carbs is eaten
- Promotes glycogen storage
- Prevents insulin resistance by inhibiting excess lipolysis
- Lower inflammation, as it’s anti-inflammatory
Interestingly, giving insulin to early and late diabetics can be highly beneficial, much more so than other blood-sugar lowering or diabetic medication.
Check my facebook post about it:
In the next article, I’ll discuss how to improve blood sugar levels and insulin sensitivity.
As always, thanks so much for reading my article. Let me know in the comments below if you have any questions. And if you found this article to be insightful and helpful please like and share so this information can help others as well.
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