chronic high glucose > chronic insulin > insulin resistance > hyperglycemia > oxidative stress > disease and reduced longevity
https://insulinresistance.org/index.php/jir/article/view/18/25
If you want to age faster, enjoy your starches… people have had to survive on many things. It doesn’t mean that they’re healthy or long lived.
Dr John McDougall has been spreading the “starch” gospel for years… I’ve listened to his talks and frankly, it’s unsubstantiated by the science.
I’m also running a vegan keto feeding and fast right now… but I will admit that I’m a carnivore most of the year.
so you’re actually arguing that chronic glucose intake, which stimulates chronic insulin release doesn’t cause insulin resistance… a condition where the body’s cells are unresponsive to chronic levels of insulin… wow…
the articles I linked point to the more clear conclusion that excess insulin causes insulin resistance … again:
and here is the causality chain… where do you see the problem of causality:
chronic high glucose > chronic insulin > insulin resistance > hyperglycemia > oxidative stress > disease and reduced longevity
It’s fascinating that you believe that starch is the solution and fat is the problem.
As far as weight loss - that’s not even what I’m talking about. High glucose and high insulin cause oxidative damage and accelerate aging and disease… weight and fat is a symptom of disease, not the cause.
If you do want to talk about weight loss, it’s about satiation and carbs, especially glucose, have an incredibly potent effect on appetite because of insulin. It’s why Keto works in the first place. Fats satiate. Starches don’t because they cause fluctuations in blood glucose causing chronic eating of more carbs, and that drives overeating and weight gain. It’s a sick cycle that is killing people!
It is possible to lose weight by eating starches in a caloric deficit, but if you look at the underlying physiology, the lean mass loss is higher than on a fat based keto diet.
You may really believe that starches are the answer… but the science is pointing in the opposite direction.
I cited several articles that explicitly point to the damage caused by glucose and insulin… you don’t respond to those - if you advocate for starches, then the glucose and resulting insulin should be good for us, right? and the insulin resistance that builds up over time should be good for us too? and it’s also the cause of poor satiation causing weight gain and that should be good for us, right?
Just fascinating … I’m trying to understand why you believe that glucose that spikes insulin isn’t a problem… on every front. Do you have any articles that show that constantly spiking insulin is good for us? that eating starches vs. eating fats results in less lean mass loss?
Bunny - you had a link for the starch based diet… can you share that here? I think it would be useful.
I’ve done that. I’ll let the community review the publications and decide for themselves.
I’ll ask you again to show the break in the causation chain I pointed to.
Here’s the simple way the disease (insulin resistance) and the symptom (fat mass gain) tie back to glucose.
Eat starch … blood glucose spikes… insulin released… triglycerides sequestered in fat cells… repeat… chronically
This glucose fluctuation drives overeating and weight gain… just noting that here.
Eventually the fat cells are incapable of handling the excess and become insulin resistant… in some people, they can be slim and already get there, once they are insulin resistant, glucose levels rise, then insulin levels rise. Both are damaging and cause nerve and organ damage and premature death.
watch the video and skip 16 minutes in to get to the key
watch and skip 6 minutes in
watch and skip 4.5 minutes in and then 7 minutes in … the “overfill adiposite”
skip 10 minutes in
skip 1 minute in
The experts cited here have shown clinical results and they use the term glucose over and over.
I’ll let the forum decide where the science is.
science from 1996
The results suggests that quickly digested starch promotes the development of insulin resistance in rats. The relatively slow time course resembles the normal development of insulin resistance in humans.
Just a note here - misinformation causes harm.
If abstaining from glucose causes no harm - that’s one thing. Don’t eat glucose (or fructose)… noone is hurt.
If endorsing a glucose diet as healthy actually causes harm, that’s another thing entirely… people get hurt.
humility is always important.
Karim
You are a very patient person. It is clear to me you are right. Now go do something more productive. 
I’m wondering what you think the cause is?
Proof is not what you really want, it is obvious your having comprehension difficulties in stitching together anything resembling common sense?
I guess chasing your own tail can be fun!
Have fun!
Me too. Here is the causality chain that @Karim_Wassef laid out. It seemed logical and well supported.
Can you at provide a simple causality chain like the one that Karim laid out that summarizes your theory of what causes type II diabetes? Otherwise, all I’m hearing from your side of the debate is this:
As Dr. Peter Attia eloquently puts it:
”…The biggest single problem with nutrition “science” is that cause and effect are rarely linked correctly. Stated another way, it’s one thing to observe an outcome, but it’s quite another to conclude the actual cause of that outcome. …” - Dr. Peter Attia
Empirical Cross Validation? based on, concerned with, or verifiable by observation or experience rather than theory or pure logic.
Quantifiable? able to be expressed or measured as a quantity.
Observer’s Paradox? In the social sciences (and physics and experimental physics), the observer’s paradox refers to a situation in which the phenomenon being observed is unwittingly influenced by the presence of the observer/investigator.
Placebo Effect? a beneficial effect produced by a placebo drug or treatment, which cannot be attributed to the properties of the placebo itself, and must therefore be due to the patient’s belief in that treatment.
I could cite a plethora of different independent research studies (quantifiable empirical cross-validation) showing (reaching the exact same conclusion) how amyloid plaques gum up the brain (Alzheimer’s, Dementia) because it is always burning glucose and becomes glucose resistant, but who wants to believe (process of elimination) that simple table sugar is the cause and the effect?
@Karim_Wassef
@atomicspacebunny
I think @alexelcu actually does have an interesting claim; fructose creates insulin resistance but glucose does not. It actually is supported by a bit of research. In this study, 1000g of fructose per day quickly elicits insulin resistance, however 1000g of glucose per day for seven days does not.
In this article, 8 weeks of fructose administered at the level of 25% of total daily calories decreased insulin sensitivity by 17% in previously healthy subjects, but a diet of 25% glucose had no effect.
That pretty much exhausts everything I’ve seen about the subject.
@alexelcu, you’ve made an interesting claim, and you seem to have done quite a bit of research on the subject. The two articles above support your claim, but don’t really constitute a etiology of typeII diabetes where glucose is not an important player as well. I’d be interesting to hear your full argument, and I’m sure others would too. Would you mind laying out a basic framework that supports your claim that glucose plays no role in the development of typeII diabetes?
This has to do with visceral adiposity being that high fructose corn syrup (HFCS) DOES NOT trigger insulin and DOES NOT increase blood glucose but the liver coverts it directly into visceral fat which then in turn accumulates in microscopic particles inside the internal organs like the liver and pancreas and around them and by receding the GLUT4 insulin regulated glucose transporter found primarily in adipose tissues and striated skeletal muscle and cardiac tissue, hence a “…17% decrease in insulin sensitivity?
References:
[1] DISCOVERY OF INHIBITOR OF FRUCTOSE TRANSPORTER OFFERS NOVEL TREATMENT FOR DIABETES AND CANCER: “…Fructose is a naturally occurring carbohydrate. Also called fruit sugar, it is found in fruits, most root vegetables and honey and is absorbed directly into the blood stream during digestion. Commercially, fructose is extracted from sugar cane, sugar beets and corn as high-fructose corn syrup and used as a sweetener in numerous processed foods and drinks to enhance taste and browning. It is the sweetest of all the naturally occurring carbohydrates such as glucose and sucrose and cheapest to produce. As a result, many individuals consume extremely high amounts of this carbohydrate every day. Fructose consumption has increased by almost 50% among U. S. adults in the last 30 years. …” …More
Nice one, mind as well ask about studies of probability of death when jumping under a moving train while ur at it. To save karim some time heres an answer to your question u can (again) deflect:
I dunno. I don’t know much about it, and it’s mostly over my head anyway. I find @Karim_Wassef’s argument compelling, but there appears to be a counter-argument to be made.
I think that two studies I cited support the claim that large doses of fructose decrease insulin sensitivity in short term experiments, but large doses of glucose do not. This does not exonerate glucose over longer timespans under different conditions however. If @alexelcu has evidence of the latter, i think it would be interesting to read.
I read that research and I agree that fructose is instrumental in insulin resistance. Even Dr Robert Lustig goes into it in ge video I posted.
This was interesting specifically because fructose doesn’t cause an insulin spike… so why does it cause insulin resistance.
This is because it hits home in the liver with fatty liver disease (bunny said it) with accumulation of visceral fat. The liver is the master controller of metabolism and with it down, insulin resistance follows.
However, Dave Feldman, Ben Bikman, Jason Fung, Paul Mason, Ivor Cummins, among many as well the paper I cited (published back in 1996), all show a second path to the disease. And that goes through the more direct path of adiposite overflow. Basically, the constant (yes chronic) flow of glucose causes chronic insulin and continuous sequestration of triglycerides into adiposites.
There are some people who have the genetic ability to continue to create new adiposites and these people get huge with fat, but do not develop insulin resistance. This is because there are new storage sites constantly being created to absorb the triglycerides with the same level of insulin. Insulin has an epigenetic effect of triggering this new “fresh” fat cell creation here.
But there are other people who are genetically unable to do this. They can be thin and their fat cells are “done”. There is no more room to stuff more triglycerides into the existing adiposites. So they swell. As they do, they resist the body trying to force more triglycerides into them. So the body has to force it in - literally. It issues more and more insulin to drive more into the existing cells … glucose levels rise, insulin levels rise, the fat cells swell and become unhealthy… insulin resistance.
Most of us are somewhere between the two extremes. But the mechanism is the same. Eat glucose… fill adiposite… maximize genetic ability to have adiposite… overfill adiposite to the extreme… unregulated insulin… repeat until insulin resistance…
So you can make the argument that fructose causes fatty liver with is a super accelerator to insulin resistance. Yes. But there is a secondary path to adiposite overfill also causing insulin resistance.
Ignoring this is like saying that standing in front of a fast moving truck kills you but if it’s a moving VW Beatle (car from the 60s for you kids), you should be ok… mmmm no.
As an aside - is it possible to eat starch in moderation and not develop insulin resistance?
The problem here is multi fold… the first is that the cyclic insulin causes by eating glucose, having blood glucose rise, and the insulin bringing it down… intrinsically drives hunger. So we eat again… and again… this hunger cycle can be controlled with discipline … but it’s like saying “it’s ok, I’ll jump out of the way before the car hits me”
Second… In poor countries where food is scarce and they self ration, they may be able to develop a culture where they strictly control their dietary intake of glucose. but in the modern environment with an abundance of cheap starch… this is not likely… starchy food is made to be addictive and the dietary regulations are to eat as frequently as possible.
If one were to control their glucose intake and be very disciplined in their caloric in and out so they are ok being hungry and consciously don’t eat - they can jump out of the way of the car… but what a horrible life of continuous hunger and deprivation…
That’s what the media and “conventional” medicine have been spouting for 50 years… how much destruction must that ideology bring before we wake up and recognize that it’s a trap to keep us sick, addicted, miserable and on drugs?
This is a nice summary, and it’s the one that makes the most sense to me as well.
I’m still curious to hear the counterargument that glucose plays no role in the development of typeII diabetes however. I think it would be fascinating if there is any evidence whatsoever supporting this contention. I can’t imagine how it’s possible.
Starch based diet from a historical perspective but keep in mind the law of cause and effect with the studies cited below, their may have been e.g. a lot of intermittent or extended fasting going on, on top of it?
The other is, everything was organic e.g. bread (grains) eaten within 48 hours* of being milled (turned into flour) and baked?
It would be very difficult to reproduce these antiquated results in todays industrialized world of agriculture and food processing instrumentalities…
Footnotes:
[*] …very nutrient dense, very similar to eating meat and possibly fat (germ oils) or what you would get from eating animal proteins and fats (germ oils)?
”…When a food rationing system during World War I severely restricted the Danish population’s intake of meats, dairy products, fats, and alcohol but placed no restrictions on such foods as barley, bread, potatoes, and vegetables, Denmark achieved the lowest mortality rate in its history [5]. Similarly, the mortality due to diabetes in England and Wales decreased sharply while wartime food rationing in both World War I and World War II limited access to animal-source foods and fats, only to increase after the those foods became available again in peacetime [6]…More
[5] Hindhede M. JAMA. 1920. Vegetarian experiment with a population of 3 million: the effect of food restriction on mortality in Copenhagen during war. [Google Scholar]
[6] Young FG, Richardson KC, Lawrence RD, Himsworth HP, Harris H, Crofton WM, Walker M, Hilton SM. Discussion on the cause of diabetes. Proc R Soc Med. 1949;42:321–330.[PMC free article] [PubMed] [Google Scholar]
A little fructose isn’t going to hurt anything, but the bigger picture is getting energy from a bar that’s really more about the protein than energy. Fructose isn’t going to do anything for workout energy, that’s why people doing TKD use Dextrose. The bars may be fine for the protein, but they’re much better ways for pre-workout energy.
