part 1 as well as part 2 of this serial on insulin, as well as you’ve come upward dorsum for more, thank you! It is ane of my biggest flaws as a writer: brevity is non my rigid suit. (But at to the lowest degree I acknowledge I receive got a problem. That’s the commencement step, right?) This postal service is no exception. In fact, it's in all probability longer than the commencement 2. So go catch a cuppa joe, or tea, or whatever yous like, as well as hunker downward for a nice, long read.
Okay. So I left off last time pointing out that, inward roofing the effects of elevated insulin as well as glucose on the cardiovascular system, reproductive function, the brain, kidneys, eyes, as well as inner ear & repose mechanisms, I had non said ane discussion virtually obesity. I hope we’re all on the same page as well as tin give notice concur that insulin resistance is non something express to people who are carrying some a few—or a duet hundred—extra pounds. Obviously, at that topographic point are millions of non-overweight people who are infertile, receive got pump disease, kidney disease, vision problems, dementia, as well as more. (I receive got written virtually this before. One of my personal favorite posts on this entire blog is the ane where I explained that obesity is but ane to a greater extent than effect of metabolic derangement, rather than its cause.
Nevertheless, we’d live missing a substantial slice of the insulin puzzle if nosotros didn’t speak virtually the role of insulin inward regulating torso weight. Before nosotros acquire to that, however, nosotros commencement demand to expect at the actual functions of insulin, as good as the pancreas. It is an unfortunate byproduct of our epidemic of “diabesity” that nosotros automatically think of blood glucose when nosotros listen the discussion insulin. And there’s no doubtfulness insulin does receive got an of import role inward regulating—or, to a greater extent than specifically, lowering—blood glucose (BG). But that’s non insulin’s only function. In fact, I would struggle it’s non fifty-fifty the primary function. We will acquire to weight, I promise. But exactly similar nosotros did in the cancer series, we’ve got to trudge through a lot of biochemical weeds before nosotros get to the skillful stuff. So hither goes.
Physiological Actions of Insulin &
Insulin-Counter-regulatory Hormones
Insulin-Counter-regulatory Hormones
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| Chart courtesy of Charles Saladino, PhD, Misericordia University |
As yous tin give notice see, at that topographic point are iii hormones—three—whose labor is to raise blood glucose (BG), as well as exactly one—one—whose labor is to lower it. Right off the bat, this hints at something: the human torso may receive got been conditioned inward an surround inward which at that topographic point was probable a frequent and/or immediate & crucial demand to heighten BG, as well as much less of a demand to lower it. This suggests that our BG wasn’t running super-high all that often, considering at that topographic point is a triplicate redundancy inward mechanisms for raising it, but exclusively a unmarried signal of failure for lowering it. (Hormonally speaking, that is. I’m non forgetting virtually non-insulin-mediated glucose disposal, which is a dainty do goodness of intense exercise.)
I’m non claiming that the evolutionary/ancestral wellness perspective is right 100% of the time, nor that it is the only thing nosotros should consider when trying to brand feel of things. I do believe, though, that it provides a handy framework to guide us inward assessing things logically as well as intelligently, as well as that nosotros tin give notice expect to the anthropological tape to endeavour as well as notice answers for some of our modern ills. For example: our ancestral diets were probable far less insulinogenic than our modern, grain-heavy ane is. Even if Paleolithic man—or whoever you want to expect dorsum to as your private ethno-geographic dietary ancestors—ate some little amount of grain inward add-on to a generous render of tubers as well as seasonal fruit, overall, the glycemic charge as well as insulin-raising effects of the total diet were in all probability real small. And these hominid ancestors may receive got had a need—not constantly, but ofttimes enough—to run away from predators or to chase prey, which would receive got necessitated an immediate way to heighten blood glucose. And because the raising of BG at a critical instant would receive got literally been a thing of life or death, it makes feel that the triple redundancy is there. It is exclusively inward the modern world, where cortisol as well as adrenaline (epinephrine) are high all the time inward some people, where this constant flooding of the blood with glucose gets us inward trouble—particularly when combined with a high-carbohydrate diet. Back inward the day, getting BG upward at the appropriate fourth dimension was lifesaving. Today, however, keeping BG (and insulin) upward all the fourth dimension is quite literally killing us.
Okay, so at that topographic point are iii hormones that heighten BG, piece insulin lowers it. And the blood glucose lowering final result of insulin is quite important. Ask a type 1 diabetic if insulin is “toxic,” as well as you’ll in all probability acquire a real dissimilar reply than if yous inquire a nutritionist inward the LCHF/keto camp. Insulin is non toxic. It is a damn handy hormone to have—when your torso responds to it properly. In fact, insulin, itself, is a lifesaving hormone. The evolution of synthetic insulin to assist type 1 diabetics was null curt of a miracle. People who were at death’s door could similar a shot atomic number 82 long, healthy, productive lives. There is most definitely a role for a low-carb diet for type 1 diabetics, but fifty-fifty those next a LCHF diet volition silent require some insulin. (Just far, far lower doses than they typically demand on a high-CHO diet.)
Because insulin injections were null curt of lifesaving for T1 diabetics, nosotros tin give notice forgive the early on pioneers of treating diabetes for assuming they would live every bit beneficial for T2 diabetics. After all, if insulin lowers blood glucose inward T1 diabetics, as well as T2 diabetics receive got high BG, as well as then it stands to argue that insulin volition assist T2 diabetics as much as it does T1s. Problem solved, illness cured, right?! Unfortunately, as nosotros now know, the therapeutic exercise of insulin for type 1 diabetes does non interpret to type 2 diabetes.
What mainstream endocrinologists don’t appear to realize is that BG is elevated inward T1 diabetics as well as T2 diabetics for completely dissimilar reasons. In T1Ds, it’s because they arrive at fiddling to no insulin. In contrast, T2Ds arrive at plenty of insulin. They’re awash inward it. Their cells are practically drowning in it. The work is, their cells receive got stopped responding properly. It’s similar the story of the man child who cried wolf: do it over as well as over as well as over again, as well as eventually the villagers halt paying attention. In T2D, insulin is knocking, but no one’s home. T1 is insulin deficiency, piece T2 is insulin resistance in the facial expression upward of insulin excess. (There may come upward a time, when someone has very advanced, real longstanding T2D, that their pancreatic beta-cells truly telephone band it quits as well as they don’t arrive at much insulin. This is called “beta prison theatre cellular telephone burnout.” Obviously, that’s non the scenario we’re focusing on here. I exactly desire to acknowledge that it tin give notice happen. Also, it is as yet undetermined whether chronic hyperinsulinemia causes insulin resistance, or if cells acquire insulin resistant first, resulting inward hyperinsulinemia. Which is the cart, as well as which is the horse?)
Another clue that T1D as well as T2D are dissimilar pathologies is that an untreated T1 diabetic volition receive got sky-high blood glucose along with sky-high ketones. (Sky-high ketones are the final result of the uncontrolled catabolism of their adipose tissue. This is ketoacidosis, which is a completely dissimilar solid ground from diet-induced nutritional ketosis.) T2 diabetics, on the other hand, volition receive got sky-high blood glucose without sky-high ketones. Why? Because they arrive at tons of insulin, as well as insulin inhibits lipolysis. Let’s say that again: Insulin inhibits lipolysis. (With lipolysis existence the primary rootage of ketones.) We’ll come upward dorsum to this side past times side time, when nosotros speak virtually torso fatty regulation. T2 diabetics can experience ketoacidosis, but it's far to a greater extent than mutual inward T1s.
Giving insulin to a type 2 diabetic who already secretes likewise much insulin is similar the misguided prescribing of antacids to individuals who receive got low stomach acid. If doctors would stair out the HCl activity of patients who complain of GERD, heartburn, as well as full general indigestion, they would encounter that the bulk of these folks don’t receive got excess stomach acid; they truly receive got too little! And if doctors would stair out a T2 diabetic’s insulin levels, the way Dr. Kraft did with so many patients, they would encounter that they receive got too much. And, inward next the anointed touchstone of care, they would receive got to reconcile the wisdom of giving these people fifty-fifty to a greater extent than insulin. Maybe making the insulin assay a component division of a regular checkup would finally wake modern medicine upward to the sentiment that type 2 diabetes is non an insulin deficiency.
The Pancreas:
Endo-, Exo-, as well as Paracrine
Okay. Now that we’ve entered the territory of lipolysis as well as ketosis, it’s fourth dimension to dive a fiddling deeper into the physiological mechanisms of insulin as well as other blood glucose regulating hormones, as good as accept a closer expect at the pancreas.
With all this blood glucose talk, it would live slow to think that your pancreas has ane job, as well as ane labor only: to secrete insulin. On the contrary, this is exactly ane of many functions this precious organ performs. The pancreas is an endocrine, exocrine, as well as paracrine organ. As an endocrine organ, it secretes hormones into the blood. As an exocrine organ, it secretes substances into a duct. As a paracrine organ, it secretes substances that human activity on itself. (Specifically, sure cells of the pancreas secrete hormones that act locally, i.e., on other cells of the pancreas.) Here’s how this works:
(1) Remember from way dorsum inward the serial I did on digestion, that the pancreas is a major thespian inward helping your torso suspension downward food so yous tin give notice absorb all those swell nutrients from your caramel pecan cheesecake grass-fed ribeye as well as organic asparagus. The pancreas, itself, doesn’t digest anything. What it does is it is the little intestine that truly does the piece of work of digestion. Pancreatic digestive enzymes (which include enzymes that suspension downward protein, carbs, and fat) brand their way to the intestine via the pancreatic duct. This is the exocrine business office of the pancreas.
(2) The specialized beta cells of the pancreas secrete insulin into the blood, as well as the alpha cells secrete glucagon into the blood. This is the endocrine function.
(3) Insulin as well as glucagon move through the bloodstream to exert their effects on target cells all over the body, but they also human activity locally, on the pancreas itself. This is the paracrine function. This is a large deal. Bigger than big. It’s huge, inward fact, as well as I didn’t fifty-fifty realize how huge until virtually 2 weeks ago. More on this at the cease of the post.
The digestive/exocrine business office is non relevant to the topic at hand, so we’ll leave of absence it aside. Let’s expect at the endocrine function. When a healthy, non-metabolically derailed somebody consumes carbohydrates, their blood glucose goes upward a fiddling bit, as well as insulin is secreted to convey it dorsum down. On the other hand, if it’s been a piece since this somebody has eaten anything, the pancreas secretes glucagon. Recall from the hormone chart inward a higher identify that glucagon maintains blood glucose levels during fasting—or, really, exactly betwixt meals, afterwards insulin has returned to its low-ish baseline. Glucagon is what keeps blood glucose from plummeting to dangerously depression levels if it’s been, say, xiv hours since your finally meal.
Glucagon:
Totally Underappreciated
Glucagon is a fascinating hormone. It’s the Rodney Dangerfield of hormones; it gets no respect. And that is a shame. The truth is, glucagon is such a huge thespian inward all this that, upon learning to a greater extent than virtually it, I was worried I had done yous all a disservice, because I should receive got called this serial “It’s the Glucagon, Stupid.” But then, when I learned even more, I felt reassured, because it is truly virtually the insulin. (Shut up, Amy. No ane cares. Get dorsum on topic.)
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| Insulin, glucagon, as well as blood glucose: the ultimate balancing act. |
Something else that stimulates glucagon is ingestion of protein. This is where things acquire interesting. The seasoned low-carbers alongside yous know that poly peptide stimulates insulin. (This is a skillful thing. This is a large component division of how nosotros create musculus mass; insulin helps escort amino acids into the cells. It’s also why yous don’t absolutely need carbs post-workout. The poly peptide volition heighten insulin all past times itself.) Some of yous low-carbers who aren’t quite as familiar with the ins as well as outs of all this powerfulness receive got heard somewhere that poly peptide “spikes blood glucose.” You powerfulness receive got also heard people maxim that, inward damage of blood glucose regulation, for some people, a large whack of poly peptide is as bad as chocolate cake, as well as for this reason, people on low-carb diets for the specific purpose of keeping blood refined saccharify depression should live careful non to overconsume protein.
I am non argument that ingesting poly peptide doesn’t heighten blood glucose. (It does.) And I’m non argument that sure amino acids aren’t strongly glucogenic. (They are.) BUT: let’s encounter how this truly works, because steak as well as chicken are not chocolate cake, okay?
Let’s expect at this through our evolutionary lens. Let’s say your tribe has exactly had a skillful kill. And let’s say you’re somewhere downward toward the middle of the tribal hierarchy. Maybe the higher ranking males as well as females receive got commencement dibs, as well as they chow downward on the organs, the entrails, as well as some of the other prized pieces of this prey. By the fourth dimension it’s your plough to lop a slice off with your handy rock tool, perchance all that’s left is a large ol’ slice of musculus meat—and a relatively lean one, at that. But this isn’t 2015 inward the U.S., as well as there’s no baked potato, buttered roll, as well as soda to go with your meat, so your repast is meat, as well as null else. Lots of protein, a fiddling combat of fat, as well as virtually null carbohydrate.
If yous were to eat this slice of meat, as well as the poly peptide raised insulin (as it does), non exclusively would the amino acids go from your bloodstream into your cells, but plenty of glucose would go along with them. Now, existence that yous are a Paleolithic “person,” let’s say your blood glucose is cruisin’ somewhere some 75. But now, thanks to your slice of meat, yous receive got an insulin rising in the absence of dietary carbohydrate. Without a counter-regulatory hormone, your blood glucose could acquire too low. (Assuming you’re non overtly ketogenic, that is. You tin give notice receive got what would otherwise live considered freakishly depression BG but experience completely fine if your ketones were high enough.) So give thanks goodness at that topographic point is a counter-regulatory hormone, inward glucagon. Sorry for this fiddling digression; I exactly figured that, for some of the lay readers out there, who powerfulness non know virtually all this, this would live a skillful way to explicate why dietary poly peptide stimulates both insulin and glucagon. It’s quite nifty, how nature does this. SO: I don’t think it’s right to say that eating a large whack of poly peptide “spikes blood glucose.” I think what it does is stimulate glucagon, which raises blood glucose inward gild to counteract the glucose lowering effect of insulin. This is totally normal, as well as no work whatsoever—FOR Influenza A virus subtype H5N1 METABOLICALLY HEALTHY PERSON. (And it's why plenty of low-carbers don't need to deliberately boundary poly peptide intake.) But let’s encounter what happens inward a metabolically UNhealthy person—specifically, someone who is insulin resistant.
It could live the glucagon, stupid,
but really, it’s silent the insulin
Insulin resistance occurs when cells no longer respond to the presence of insulin. We know for sure that musculus cells tin give notice acquire insulin resistant. But you know what other kinds of cells tin give notice acquire insulin resistant? THE GLUCAGON-SECRETING ALPHA CELLS OF THE PANCREAS. Yes! Now we’re getting somewhere.
It’s fourth dimension to examine the paracrine business office of the pancreas. Recall from the hormone chart way inward a higher identify that glucagon mobilizes fuels. It activates gluconeogenesis, glycogenolysis, and lipolysis. We know glucagon does this. This is how it keeps blood glucose at a rubber (i.e. high enough) degree betwixt meals or during a longer fast – it catabolizes existing musculus tissue to acquire at some glucogenic amino acids, as well as it stimulates the breakdown of downward glycogen into private glucose molecules. It also stimulates lipolysis—that is, the breaking downward of stored torso fat, the glycerol percentage of which tin give notice live used to brand glucose. Now that nosotros encounter what glucagon does, nosotros tin give notice receive got a much ameliorate agreement of type 1 diabetes. T1D is glucagon run amok in the absence (or deficiency) of insulin. Untreated, type 1 diabetics rest inward a perpetual solid ground of catabolizing their ain bodies inward gild to live fueled. They suspension downward their muscles, they suspension downward their adipose tissue, and, eventually, they’ll suspension downward their organs. You tin give notice encounter why, inward the absence of insulin to counteract the glucagon, T1 diabetics powerfulness live emaciated.
Here is something absolutely fascinating virtually the paracrine pancreas. Before entering the full general blood circulation, the insulin that is secreted past times the beta cells plant direct on the alpha cells. The alpha cells are insulin’s first stop before it travels to the repose of the body. Basically, insulin tells the alpha cells to halt churning out glucagon. BUT: the amount or concentration of insulin that hits the alpha cells is much, much greater than the concentration of insulin than the repose of the torso responds to. It’s almost like, inward tamping downward the alpha cells, most of the insulin is siphoned off, so a much lower concentration is left for the repose of the body. This is what is supposed to happen. And this explains why it is so hard for type 1 diabetics to deal their blood sugar. If they were to inject themselves with insulin at the strength needed to suppress glucagon, it would completely overwhelm the repose of the torso as well as sure enough receive a life-threatening “low.” In a best instance scenario, the amount of insulin they inject is matched to the amount of refined saccharify (and protein) they eat. But this does non at all accept into work concern human relationship the extremely concentrated amount the alpha cells require inward gild to halt secreting glucagon. So yous tin give notice encounter similar a shot why T1s receive got BG that is all over the map.
Okay, dorsum on message. In a salubrious person, glucagon’s catabolic effects exclusively dominate when insulin is low—between meals as well as during a fast. For someone on a low-carb diet, glucagon volition live somewhat active all the time, but inward the fed state, it volition live by as well as large overridden past times the presence of insulin—yes, fifty-fifty exactly the relatively small amounts of insulin a low-carber would secrete. In a type 1 diabetic, glucagon dominates all the time. This is why they waste matter away without exogenous insulin, as well as also why they receive got concomitantly high glucose and ketones. In a metabolically salubrious person, fifty-fifty little amounts of insulin are plenty to boundary the effects of glucagon. (This is the beauty of a low-carb diet inward a salubrious person: BG that is neither likewise high nor likewise low. I emphasize again: insulin is non toxic. Insulin is great, provided your torso knows what to do with it.)
I said before that T1D is glucagon run amok, because there’s no insulin to closed off that signal. Oddly enough, for many type 2 diabetics, their status is also glucagon run amok, but it’s evidently non because there’s no insulin. There’s a ton of insulin; many cells exactly don’t aid anymore. And remember: alongside the cells that don’t aid anymore are the glucagon-producing alpha cells. Because the alpha cells are insulin resistant, they business office as if at that topographic point is no insulin. That is, they go along to hemorrhage glucagon. So, fifty-fifty when blood glucose is high, such as afterwards a high-carb meal, glucagon tin give notice heighten it even higher. The carbs would receive got raised BG, as well as therefore, insulin, but because the alpha cells no longer sense the insulin there, they volition go along to pump out glucagon as if a high-carb repast had not been ingested. And what volition this glucagon do, but go along to heighten BG even more, by breaking downward existing musculus tissue to acquire at the glucogenic amino acids? (Remember, though, that fifty-fifty with sky-high glucose, hyperinsulinemic T2 diabetics powerfulness non generate lots of ketones, because, inward a fell twist of fate, the adipose tissue still seems to live sensitive to insulin, as well as insulin inhibits lipolysis.)
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| As bad as soda? Come on. |
And remember: poly peptide elevates both insulin and glucagon. THIS is why people who are extremely insulin resistant are well-served non to “overconsume” protein. (Whatever that means, anyway. The threshold is an private thing.) If they are eating “too much” of a nutrient that raises glucagon, and, past times extension, blood glucose, but they cannot clear that glucose out of the blood due to insulin resistance, this is a form of double whammy.
I suspect these forces were at piece of work inward my ain mother, who had poorly controlled T2D. (Read virtually her unfortunate as well as hapless medical aid here.) She was on insulin, as well as her blood refined saccharify was completely unpredictable, regardless of what she ate or her insulin dose.
It’s interesting to authorities annotation that, alongside many overweight T2 diabetics, they are “large,” but they don’t appear to receive got much musculus mass. With what nosotros exactly covered, nosotros tin give notice speculate that perchance they receive got less musculus because their bodies are so skillful at breaking musculus down. As for how they cease upward heavier, when someone is severely insulin resistant (and remember, this goes for their alpha cells), I suspect it plant similar this:
Elevated glucagon --> catabolize muscle
Elevated insulin --> do NOT catabolize stored torso fat
Boy, is that a horrible scenario to notice one’s self in: suspension downward your extremely valuable musculus tissue, but nope, don’t behave on whatsoever of that fat! Leave it right where it is! In fact, brand more!
Okay, since I’ve finally—finally—circled dorsum to the topic of torso fat, this is a skillful identify to cease for now, as well as we’ll start right dorsum hither side past times side time.
Remember: Amy Berger, M.S., NTP, is non a physician as well as , LLC, is non a medical practice. The data contained on this site is non intended to diagnose, treat, cure, or forestall whatsoever medical condition.
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