My question was/is
If insulin resistance theory is valid, then why taking insulin injections will lower blood sugar?
Forgot what the answers I got in the past, also not able to find the thread, but I remember I was not satisfied with answers which could be me.
thanks
Insulin still works, it just doesn’t work as well. Supposedly, T1 (type 1) diabetics experience insulin resistance, having to increase the amount of insulin they use over time. This is true for T2 too, which is why mainstream medicine assumes diabetes for T2 is a progressive disease – it gets worse over time.
Both T1 and T2 are helped by eating low carb/keto, because the diet limits the increase in insulin resistance. For T2, they may also reverse diabetes. For T1, they help regulate insulin injections so that there is little or no increase in insulin needed over time.
Type one produce NO insulin. They do need insulin to live. Insulin resistance. Your car used to get 30 mile per gallon, now on get 20. Body same way, it’s takes MORE INSULIN to do the same work.
Consider the biology: insulin is necessary to life; that is why Type I diabetics, who produce no insulin, starve to death, no matter how much they eat. They can also die from hyperglycaemia, which is why a low-carbohydrate, high-fat ketogenic diet was standard treatment for Type I diabetes before the discovery of insulin. Type I diabetes is an auto-immune disease, in which the immune system kills off the β-cells in the Islets of Langerhans in the pancreas. 
Type II diabetes, on the other hand, is a metabolic disease, caused by excessive intake of glucose (also known as carbohydrate). The reason they are linked together in the medical mind is that when insulin-resistance (hyperinsulinaemia) gets bad enough, the blood sugar starts to rise. So although the disease is not one of too much glucose (hyperglycaemia is the symptom, not the cause), entrenched medical thinking believes it is, so insulin injections are given to assist the pancreas in lowering hyperglycaemia. It is exactly the wrong treatment for the condition, but there is no money to be made from advising patients to eat differently, and the pharmaceutical companies are profiting greatly from the situation as it is.
Insulin reduces serum glucose by telling cells to take it in and either use or store it. Fat cells store it as fat; muscle cells metabolise it. The brain needs insulin in order to metabolise glucose, but too much insulin, paradoxically, inhibits the brain cells from taking in glucose, thus starving the brain and causing all kinds of problems. Insulin resistance develops when cells are overwhelmed by glucose and have to defend themselves by down-regulating their insulin receptors.
So while insulin injections save the lives of Type I diabetics, they only make the problems of Type II diabetics worse. However, the injections do help Type II diabetics lower their serum glucose, at least until so much damage is done that the body starts to fall apart.
Not a theory, metabolic fact. Receptor down-regulation happens to more than Insulin receptors.
“Insulin Resistant” is in reality a stupid term, nobody is “resistant” to it, if we were, we’d be dead. But resistant is used as a sliding scale, so ok. Being resistant means it just takes more to accomplish the same thing. That’s why things like Semaglutide are huge now, not only does it make the body secrete more Insulin when it’s supposed to, it also makes you Insulin sensitive at the same time, which is why it’s shaving weight off people and lowering A1C’s in people that could never catch up before. Which seems counterintuitive since A1C’s are dropping by making more insulin, in an Insulin resistant person! But it’s also sensitizing them to it so does actually make sense.
Thanks everyone.
I just want to clarify that I am on Keto since 2017. And I am not about to convince my self to take insulin injections.
Just trying to understand.
MORE
But why the “more” is accepted by the cells from external source, and not from the internal source (If I understood correctly the pancreas still functioning and can deliver sufficient amount of insulin for people with insulin resistance)
It’s the “resistance” part. It’s like you are using your key (your internal insulin) to open a door. The landlord put on a extra lock (resistance). Your 400 lb friend (external insulin) comes along and now together you can bust it open.
If I continue the analogy, the problem is that the landlord is going to continue putting on bigger and bigger locks. More resistance. The alternative would be paying the rent - that is, changing your diet - so the resistance is reversed and your own key now works all by itself.
It doesn’t, it has nothing to do with exogenous vs endogenous supply, only the volume that’s needed. That’s why when it’s your own supply, your Insulin levels are higher. Somebody that’s Insulin sensitive will release 20 units of Insulin to bring their blood sugar back down from a slice of Pizza in 30mins, where the Insulin ressitant person will need 40 units and 3hrs to accomplish the same thing.
Correct, it’s not a supply issue, it’s an acceptance issue.
If you’re going deaf, I can say something across the room, the guy beside you hears me just fine, because his hearing is working correctly, and I’m speaking loud enough to hit that side of the room, but for you, I gotta raise my voice almost to the point of yelling, that’s insulin resistance. The volume is fine, it’s just you not hearing it, so it needs to be compensated for.
so you are saying that even the secreted (endogenous) insulin is sufficient for a normal person, It is not enough for insulin resistance person. So the additional insulin supplemented by the exogenous source (if enough), will overcome the resistance for a while, before it has to be supplemented again with larger delta…
Correct, what literally happens (made up math) is you have 100 Insulin receptors on each cell, but 40% of them are clogged at all times, from constantly being beat up by insulin, so now you’re dealing with 60% acceptance, your liver secretes the correct amount either way, so that other 40% your cells are basically ignoring, is just travelling the bloodstream in circulation, which is why your Insulin levels are higher. After it’s not registered as working, your pancreas will release more at some point the signal gets through, and then because you now have way more than you should than the actual glucose load needed, your blood sugar crashes, and so do you. That’s the I just ate a big meal and passed out on the couch for half an hour effect.
Is that part of insulin resistance? I used to get that and wasn’t sure what it was about…
But anyone can have those after a big meal, right? It’s not specific to people with insulin resistance? Or is it…?
Curious about the answer, it would seem to me that insulin resistance extends the time sugar is in the blood, thereby reducing a sugar crash, but that doesn’t seem to be the case.
I wonder if that hypoglycemic response gets damped down over time? That when one is first heading into Type 2 diabetes they will have that after meal crash but as their cells get more and more resistant that no longer happens.
My diabetes specialist doesn’t have diabetes himself or insulin resistance or anything… I’ve talked to him at length about my blood sugar crashes, which I’ve had all my life - even decades before ever getting anywhere near being insulin resistant (my parents were hugely fussy about us kids eating healthy and there were never sweets or junk food in our house growing up).
He told me that he gets those weird blood sugar crashes too, after a meal sometimes. That blood sugar crashes post a meal doesn’t have to have anything to do with diabetes or insulin resistance. And from my experience, I agree with that.
I wouldn’t call “passing out on the couch for half an hour” after a meal a blood sugar crash tho… For me, a blood sugar crash feels very, very different… I get quite anxious and distressed in a blood sugar crash, to be honest.
When I was a kid, those post meal tiredness slumps used to be explained as “all the blood rushes to your digestive system and away from your brain” - I have no idea whether that’s still considered medically/ scientifically valid or not…
I do know that the body has two states - which has to do with the sympathetic nervous system and the parasympathetic nervous system - the former is like the gas pedal in our body, the latter like the brake pedal… The first is for fight/ flight type stuff, the latter is for “rest and digest” (and also procreating).
Eating food is a known way to trigger your parasympathetic system - ie to set off feelings of wellness, comfort, slowing down, resting, etc. (Which is why we have words like comfort food and why ppl engage in eating as an addictive/ stress-relieving process.)
So, feeling a bit slower and relaxed after a meal is kind of a normal bodily function.
But occasionally after a (normal SAD) meal, I’d get those tiredness crashes, where you just want to sleep…
Again, for me that doesn’t FEEL like a blood sugar crash at all… which is why I was interested to hear if pronounced post meal tiredness is somehow specifically related to insulin resistance…
Would be interesting to know if anyone here has done any BG measurements during a post meal sleepy phase… to see whether it actually is blood sugar going down or not…
I don’t recall having any post meal sleepiness since starting Keto tho, so maybe it’s just not a phenomenon observed much on a Keto forum…?
I was told my a Keto-guide that after-meal crashes are caused by the insulin rush, not the sugar load. And because your body is smart, if you have a habit of eating large meals at a certain time of day, it anticipates and dumps a lot of insulin even if you don’t eat a bunch at that meal.
I have been “strict” keto for just over a year though I have been no sugar/low carb all of my adult life. I was diagnosed T2 at 17. As I got older, even on a low-carb diet, I had to start taking meds. At 58, I had to start on insulin when my A1C was 8.3.
After doing Keto on and off for several years, I was still having to increase my insulin amount. I decided enough is enough. I went strict Keto (under 20 gms/day), and within 1 year, I was off all meds, including insulin and my A1C is done just under 6.0 for the first time in my life! I am now 64 yrs old and never felt more energetic and clear-headed. Though I wasn’t trying to lose weight, I lost 35 lbs.
I still have the occasional sugar spike, but it comes back down immediately, within 30-45 minutes, rather than 3-4 hours. So I know enough cells have been replaced with new insulin receptors, so my resistance is way down. I still wear a CGM to keep me honest…
Now I can eat a huge meal any time of the day and NEVER need a nap.
Yes, I was thinking about this issue more today and I’m 90% certain that tiredness directly after a meal can’t be low blood sugar.
Cos directly after, we’re still digesting - food is still being broken down and nutrients, including carbs, are entering the blood stream - so in this phase, blood sugar is still rising…
It’s only AFTER that phase, that the body may “over-correct” the high blood sugar and end up with low blood sugar…
Any idea why an insulin rush would cause tiredness?
@PaulL do you have any scientific insights into this issue?
Not really, you can eat yourself a little tired, but it’s the blood sugar crash that takes you out and makes you pass out, that doesn’t happen in insulin sensitive people. They secrete a little insulin, lower there BG to the correct amount and keep on going.
It extends the time the sugar is in the blood yes, because your body is releasing more and more Insulin to lower, until enough has been released to get the point across, then you have way too much in there, hence the fast drop and the nap!