For the hard core science minded amongst us, I would love to find some data regarding the effects of berberine and Metformin on insulin levels in non diabetics. This is difficult information to find!! If anyone has some resources I’d love to read them…thanks in advance!
Effect of berberine and Metformin on insulin
PetaMarie
(squirrel-kissing paper tamer)
#3
I just want to thank you for asking the question which prompted me to do some digging. I have Multiple Myeloma and found a study about metformin for use in MGUS (pre myeloma). I sent a letter to my oncologist asking him if we can do a trial run and see what it does to my numbers (which are always rising) at my next appointment in March. Because I can’t afford the thousands of dollars a month chemo, this may be something that helps!
In case anyone else is interested:
BeStill
#4
One big plus to Metformin (if It brings healing to any condition) is the affordability! I was never officially diagnosed with type II diabetes, but was put on Metformin several times. The 3rd attempt it caused crazy swelling and weight gain, doctor took me off it immediately when I was re-weighed in office about 5 days into taking it and had swelling in my ankles and was up about 9lbs. It worked great for my mom, she felt it took about 6 months before she could see a discernible difference in blood sugar readings and then weight loss/control, has been on it for years now and believes it kept her from having to try other diabetes meds. I think it was $3/mo at Sam’s Club pharmacy.
charlie3
(charlie3)
#5
Broaden the question, is there any pill that out performs diet and exercise for addressing the chronic illnesses discussed on the forum?
atomicspacebunny
(Bunny)
#6
BUNNY HARDCORE:
What is Metformin: A glorified sugar/glucose blocker or beta blocker!
What I know about Berberine and Metformin is it can mimic fasting but only if taken in the tiniest possible dose which is some thing I would do if I were to experiment with it.
But “…whole-body glucose oxidation is reduced in response to oral administration of metformin…” Metformin simply blunts the absorption of glucose (and thus levels of insulin) in the intestinal tract and probably why it mimics fasting?
The problem is when muscle tissue becomes more fatty than muscle like, it quits oxidizing glucose into carbon dioxide and why we get fat.
Skeletal muscle tissue and bone work like a steam engine, you have all this coal (glucose) built up or coming in and no way to burn it because there is no way to generate a spark with the bodies chemical to electrical blast furnace (amino-isometric-butyric-acid) in the free floating mitochondria inside adipocytes to turn the extra glucose into carbon dioxide rather than be stored as lipid droplets into the adipocyte. Healthy lean non-fatty skeletal muscle tissue controls this process NOT INSULIN, period.
So when you take Metformin or natural sister compounds it is actually blunting your ability to oxidize carbohydrates so you get stuck in this never ending loop the same as you do with the ketogenic diet, you become more and more resistant to oxidation of glucose? The more you try to restrict glucose within a certain range (maybe we could call it a natural range or parameter?) it could be doing more harm than good?
Dr. Attia talks about progressive resistance training (PRT) below for seniors, (JUST SENIORS, REALLY?) here is where I want to scream it from the roof tops: EVERYONE SHOULD BE DOING THIS? that is how you get rid of the fatty deposits in the muscle tissue that causes the diabetes and expansion or inflammation of adipose tissue from lipid storage (why your fat?) to begin with (and what also caused a fatty liver and pancreas or visceral adiposity besides HFCS; processed sugars where the liver turns this specific non-insulin engaging sugar into visceral fat), restricting your carbohydrate intake to nothing, is a band-aid not the cure?
References:
[1] “…Though the etiology of T2DM is unclear and likely multifactorial, a considerable body of evidence has identified dysfunction in both skeletal muscle and bone in T2DM. People with T2DM display insulin resistance in skeletal muscle [3], characterized by buildup of intramuscular triglyceride [4, 5], and impaired mitochondrial function [6], and this dysfunction has been implicated in the etiology of T2DM. …” …More
[2] “…Insulin resistance is the reduced response of a target tissue (including skeletal muscle, adipose tissue, etc.) to insulin as compared to a healthy control. In essence, insulin is ineffective despite elevated concentrations. Skeletal muscle is the primary site for insulin-mediated glucose uptake in the postprandial state. Insulin binds the receptor in skeletal muscle, which causes the phosphorylation of tyrosine molecules on the insulin receptor. This causes the insulin receptor substrate-1 (IRS-1) to move to the cell membrane and become phosphorylated on adjacent tyrosine molecules. Next, phosphatidylinositol-3 kinase (PI-3 kinase) is activated, causing the downstream activation of Akt (also called protein kinase B) and the phosphorylation of Akt substrate 160 (AS160), which ultimately facilitates the translocation of GLUT4 to the sarcolemma. GLUT4 is responsible for the transport of glucose into skeletal muscle cells (TANIGUCHI CM 2006 7). Skeletal muscle in people with T2DM typically displays some degree of insulin resistance, characterized by a disruption in the signaling cascade described previously, specifically defective tyrosine phosphorylation of IRS-1 and defects in PI-3 kinase and Akt activation (KROOK A 2000 49; CUSI K 2000 105). DeFronzo et al. [16] found that insulin-stimulated leg glucose uptake is reduced by 50% in people with T2DM. …” …More
Dr. Peter Attia writes about Metformin here:
He states “… A few months ago, I wrote about a study that showed metformin diminished improvements in skeletal muscle mitochondrial respiration, cardiorespiratory fitness, and whole-body insulin sensitivity after a 12-week aerobic exercise training (AET) program compared to a placebo in participants at risk for type 2 diabetes in their early 60s. I have also spent the last year doing endless self-experiments with and without metformin, examining the relationship between mitochondrial performance and metformin, using lactate testing at zone 2 (more on this topic another day).
Today, I want to cover a more recent study, that looked at the effects of metformin on the response to progressive resistance training (PRT) in relatively healthy seniors. A question you may be asking yourself is: why would you give relatively healthy people a drug for diabetes in the first place? …”
Here is a recent Email from Dr. Rhonda Patrick and a fascinating Metformin webpage.
Hello, friends!
News to share today – our team has two new great topic articles to pass along!
The first is about metformin, a drug commonly used to treat type 2 diabetes. Metformin is the fourth most commonly prescribed medication in the United States, with more than 80 million prescriptions for the drug written yearly.
But why are we talking about a diabetes drug? In the last few years, some very interesting observations have been made about metformin. Namely…
A TON of evidence indicates that metformin modulates the aging processes to improve healthspan and extend lifespan in multiple organisms.
How it works isn’t fully understood, but evidence suggests that pathways involved in cellular energy and protective responses may be responsible for the drug’s actions.
For example, metformin activates AMPK and inhibits mTOR. It also switches on endogenous antioxidant responses. Collectively, metformin’s actions reduce the accumulation of oxidative damage and chronic inflammation – key drivers of the aging process.
The effects of metformin on healthspan and longevity in animals are mixed, however.
For example, metformin improves lifespan in worms, but not in fruit flies. And its lifespan-enhancing effects in mice varies according to strain and sex of mouse studied, time of initiation of the drug, and length of exposure.
But does metformin modulate the risk of age-related diseases in humans? Observational and clinical studies in humans suggest that metformin slows age-related cognitive decline, reduces the risk of cancer, and may reduce mortality among people who have type 2 diabetes. Sounds pretty awesome, right?
Well, there might be a downside.
Metformin appears to counter some of the health benefits associated with exercise. Some studies have shown that metformin inhibits mitochondrial adaptations and diminishes improvements in whole-body insulin sensitivity after aerobic exercise. Other studies have shown that the diabetes drug impairs muscle hypertrophy after resistance exercise.
Metformin is safe, however, even at high doses, and is readily bioavailable in humans. But the evidence regarding dosing recommendations for slowing aging in humans is limited. Metformin doses used in animal studies lead to blood concentrations of the drug that are markedly higher than those used to treat diabetes in humans.
Interestingly, metformin’s physiological and antiaging effects closely resemble those associated with caloric restriction.
What’s caloric restriction? We’re glad you asked! That brings us to the second new topic page…
Our other new article gives the low down on caloric restriction – everything from the early discoveries in animals to findings from the most recent human trials.
Caloric restriction is, in some ways, an early cornerstone of aging science: It’s one of the oldest and most consistent ways demonstrated to extend healthspan in nearly every lab model of aging tested.
In fact, it’s the only known non-genetic method that demonstrates the capacity to prolong lifespan in multiple organisms. The intervention is simple: a 20 to 50 percent reduction in the amount of food a species consumes in an environment of unfettered free feeding, called ad libitum.
Long-term calorie restriction induces global biochemical and molecular changes in humans.
Long-term trials of caloric restriction demonstrate that study participants’ core body temperature, fasting insulin levels, bone mass, muscle size and strength, and markers of oxidative stress and DNA damage decrease, and their insulin sensitivity and mitochondrial DNA synthesis increase.
The mechanisms that drive these health improvements involve the inhibition of key nutrient-sensing and inflammatory pathways and the regulation of multiple molecular, cellular, and metabolic pathways.
But caloric restriction is hard to do and also hard to test in humans, which is one reason why aging science continues to try to tease out the molecular mechanisms to see how we might get the benefits without the herculean effort of never-ending voluntary starvation.
And there’s good news: Some evidence suggests that other forms of restrictive eating practices may offer the same (or greater) benefits associated with caloric restriction but are more sustainable.
I just know you’re going to love reading these two articles!
You can read about metformin here.
You can read about caloric restriction here.
You can hear a brief mention of metformin from Dr. David Sinclair in this recent podcast.
Enjoy!
Rhonda and team
Emacfarland
(Erin Macfarland )
#7
@atomicspacebunny ahhhhh…you always pull through in the most incredible ways!! Wonderful info!! Thank you!
PetaMarie
(squirrel-kissing paper tamer)
#8
Quick update. I wrote to my oncologist who I am seeing in March for multiple myeloma labs asking his thoughts on trying metformin until then. He agreed to try it and called in a once daily 500 mg extended release tab which was generic for Glumetza. (extended release can decrease GI side effects, is just once a day, etc).
In the US, without insurance, it’s around $840 a month. So…I asked my doc for the regular, old fashioned, not extended release capsuled metformin which my pharmacist says is $11 a month.
PetaMarie
(squirrel-kissing paper tamer)
#9
Good news! I just took my first Metformin for reduction of cancer cells. I’m having my labs rechecked in March so that will give me 4 months trial to see if it has any effect on things. Fingers crossed because it’s affordable compared to chemo which is out of the question and I’m not sick enough yet to be on disability so I’m in that middle place where I can’t afford treatment. Yay (maybe) metformin!
KetoCancerMom
(Cancer Fighting Ketovore :))
#10
I’m interested to see your results. I’m taking 250mg once a day (the directions say 2x) with my one meal. I haven’t seen any significant results with regards to my insulin, although it does look like it is having a positive effect on my glucose! I started the Metformin on Feb 6th.
| Feb 12 | Feb 5 | 1/31 | |
|---|---|---|---|
| Insulin | 22.7 | 19.6 | 10.9 |
| Glucose | 108 | 120 | 100 |
PetaMarie
(squirrel-kissing paper tamer)
#11
I’ve seen a change in my BMP lab results which measures glucose. It’s usually around 116-125 even since I’ve been doing keto. This last result was 106, the lowest it’s been in quite a while. I had coffee with cream before the appointment, so it wasn’t fasting. Other than that, I keep telling myself I’m going to pull out the meter, but I haven’t been testing or recording.