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Type 2 diabetes does not start with BEING TOO FAT
The diabetes timeline is always written like this….
You ate too much, moved too little and ended up FAT. Your bad.
These extra pounds, created “stress”, leading your cells to become insulin resistant.
Since your cells stopped listening to the insulin, more insulin had to be produced (hyperinsulinemia).
All this extra insulin kept the sugar levels in the normal range……
?Until, the beta cells in the pancreas gave up the ghost i.e. they started to fail.
?Their failure caused sugar levels to rise, particularly after meals, leading to glucose intolerance.
More and more beta cells succumbed to the stresses and strains of mass insulin production.
Culminating in a diagnosis of type 2 diabetes.
It is a simple story, but what if this diabetes timeline is WRONG ?
How diabetes begins
A team of researchers from the University of British Columbia, provide compelling evidence that the story has a different beginning……………
Instead of starting with you being FAT, it starts with you being INSULIN RESISTANT.
Let me explain…..
The insulin gene
When it comes to genes, mice and men, have a lot of similarities – this is why scientists study them. They’re certainly a lot more “human” than fruit flies, worms and yeast.
But there are differences.
One such difference involves the insulin gene or should I say GENES.
Mice have two versions of the gene. INS1 and INS2. Humans only have one version – INS.
The team of researchers set about “exploiting” this difference, along with the fact, that designer models i.e. mice with specific versions of a gene, can be created.
Engineering mice to be insulin deficient
They “engineered” mice that had
- one working copy of the INS1 gene, the other copy was a dud and
- two “bad” copies of the INS2 gene
Remember from high school biology, you always have two copies of a gene, one comes from Mom and one comes from Dad.
This created mice with an interesting insulin profile……
Insulin production in mice
You see, the INS1 gene, is responsible for making insulin in the pancreas, the INS2 gene, is responsible for making insulin, everywhere else. For the record, the everywhere else, includes the brain and thymus.
But, when it comes to diabetes, it’s the insulin in the pancreas that matters……….
This little genetic tweak, created mice that were a little low on insulin – they could make it, just not so much. Kinda like someone with type 2 diabetes, but without the insulin resistance.
The next step…
Fattening the mice up
The mice, along with a group of “ordinary” mice, sporting two copies of the INS1 gene, were offered an opportunity to live the good life, with lots of feasting, on a high-fat diet.
So, who got fat ?
The mice with two copies of the INS1 gene.
Yup. Producing MORE INSULIN caused obesity.
The mice that were “low” on insulin, munched away………. but never got fat. In fact, they were the same weight as animals being maintained on a “low” fat diet.
It was the MORE INSULIN, that made the animals fat.
When insulin was missing, what happened ?
Fat cells behaved differently.
In a nut shell – THEY BURNED MORE FAT.
This is not really a big surprise, insulin’s job description is the CHIEF CALORIE STORER.
What was the “surprise”, was the timeline……..
The diabetes timeline
This research demonstrated, the diabetes timeline looks like this….
You must have hyperinsulinemia, TO GET FAT.
You don’t get fat and then get hyperinsulinemia.
It’s a subtle difference, but the implications are HUGE.
The take home message, too much insulin or hyper insulin secretion, is at the route of the problem and THIS is the issue, that needs to be tackled in the management of type 2 diabetes.
A good place to start, is to do a little CANDY FLOSSING,Download our free report to learn more.
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