Metformin is the most prescribed drug for diabetics and pre-diabetics.
This is so despite very large studies that show Metformin doesn’t actually help reduce mortality in diabetes at all.
In fact, there are plenty of reasons to question if it is even safe and is Metformin bad for you instead.
In this newsletter, I want to show you two studies on metformin.
The first study is a very large meta-study.
I don’t normally use meta-studies, but in this case, I think it’s quite valuable.
The researchers were honest.
They had a tough time because these kinds of studies are very difficult to do if they are extremely damaging to the prospects of a drug.
There are just too many drug companies clamoring for drug company cash.
It doesn’t make it easy for honest scientists.
So let me give you their conclusion.
Metformin did not significantly affect the primary outcomes all-cause mortality, and cardiovascular mortality.
This is their finding after looking at 13,110 patients.
Some patients took Metformin, and then some patients did not.
All of the patients were diabetic or pre-diabetic.
In other words, Metformin doesn’t work.
As to why metformin doesn’t work, let’s look at a recent study.
The first thing to realize about Metformin is that it accumulates in the energy-producing parts of each cell, the mitochondria.
Mitochondria are responsible for breathing, energy, and life.
There are thousands of mitochondria in some cells.
And virtually all cells in the body require mitochondria to stay alive.
The researchers find that mitochondria
accumulate metformin by 1000-fold in the mitochondrial matrix, relative to in serum.
When the Metformin is in the mitochondria, it has very disturbing effects
ATP hydrolysis is inhibited by metformin.
There is a fabulously complex biochemical chain reaction that produces ATP.
And researchers think ATP is the energy vehicle for the whole body.
Metformin interferes with the production of ATP in the mitochondria.
It also interferes with one of the functions of folate, a B vitamin.
Metformin disrupts folate-related one-carbon metabolic pathways.
Metformin interferes with so many different metabolic processes that often it leads to a vitamin B12 deficiency.
And it can lead to a possible folate deficiency.
Metformin also interferes with the creation of glucose from protein.
If the body is not getting enough sugar, it must make its own sugar to live.
That process of producing sugar in the body is gluconeogenesis.
Metformin stops gluconeogenesis, potentially lowering blood sugar and killing cells.
Recently, mitochondrial glycerophosphate dehydrogenase has also been reported to be inhibited by metformin, and this effect has been proposed as the origin of metformin’s ability to suppress gluconeogenesis.
So, you may be thinking that the point is to lower blood sugar.
But the problem in diabetes isn’t that there is too much sugar, it is that the body doesn’t metabolize it.
Metformin does not solve that problem — frankly, it interferes with so many things but does not help at all.
To solve diabetes, you don’t want to lower your sugar.
You need to solve the problem stopping your body from processing sugar and allowing it to build up in the body.
Now you can see why Metformin has not led to a lower death rate from diabetes.
And why you may want to reconsider taking Metformin in consultation with your doctor.
Effects of metformin and other biguanides on oxidative phosphorylation in mitochondria