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Longbowgilly

Metformin timing question

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Longbowgilly

Hi,

 

I am on 500mg Metformin ER twice a day.

I went to get my prescription reprinted and the Doctor I saw told me that I will get better results taking both tablets together (1000mg) at night rather than the twice a day I had been told to do. She said that it was supposed to work that way as its extended release.

I would love to hear your views on this, as I often forget to take it and if I can just do it once with my evening meal for example I am hoping I would be less likely to forget!:o

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PATRIC

My sis is a CDE and that is what she told me too. I take 1250 with meal about 7pm and 750 about 11. The late one dropped my morn FBG about 8-10 more on average.

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jwags

I take 3 x 850 of metformin. I have exoerimented with all sorts of timing. I get most of my liver dumps at night or in the morning. My latest dosing seems to work best. I take 850 before bed, then another 850 when I wake up to use the bsthroom, 4-5 am. Then the last 850 I take mid morning around 9-10 am. This regimen helps prevent the spikes. Since I eat very low carb I rarely spike with meals. The ER version of met is time released so I don't know if timing is as important as the regular. I take the regular.

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TX_Clint

I take 1000 metformin ER after breakfast and another 1000 metformin ER after diner. I have tried other schedules and have not seen a consistant difference.

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princesslinda

I take metformin-ER 500 mg twice daily as well, taking one dose as soon as I get up in the mornings (around 6 am) before I even think about b/fast (fortunately it doesn't bother my stomach). I take my 2nd dose about 10 pm, just before bedtime.

 

I'd encourage you to try taking it that way for a couple of weeks and see if you notice any difference/improvement.

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jims_forum

As a 30 year+ type 2 and extensive use of metformin and watching on a cgms; I have the following opinions:

 

a) single large doses on my body do not work and for valid medical reasons glossed over by folks.

 

B) ingestion time for standard metformin is 2.5 hours up to full strength an lasts 1 to 3 hours and 2 hours for me.

 

c) I have a dose at 10:00 pm ( 500 mG) and one at 12:00am midnight - this cuts back the excess liver glucose release from 12:30 am midnight through 5:00am.

 

d) loading in a single large dose only lasts for the 2 hours. Taking the way I do and met is being kept up for 4 hours and right over the worst window on Dawn effect from 3:00am to 5:00 am. One single large dose only would last 2 hours - single dose time. The human body does not redistribute large doses over more time - it simply provides a stronger dose over the same short interval of a single dose.

 

e) I also take dose at 6:00am, Lunch and Dinner as well.

 

I can watch the metformin work on my cgms and see the Blood glucose drop as metformin comes up to strength in blood on each and every dose ingested.

 

Also I have attached the latest findings on how metformin actually works!

 

Science News

... from universities, journals, and other research organizations

 

Most-Used Diabetes Drug Works in Different Way Than Previously Thought

Jan. 6, 2013 — A team, led by senior author Morris J. Birnbaum, MD, PhD, the Willard and Rhoda Ware Professor of Medicine, with the Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, found that the diabetes drug metformin works in a different way than previously understood. Their research in mice found that metformin suppresses the liver hormone glucagon's ability to generate an important signaling molecule, pointing to new drug targets. The findings were published online this week in Nature.

________________________________________

For fifty years, one of the few classes of therapeutics effective in reducing the overactive glucose production associated with diabetes has been the biguanides, which includes metformin, the most frequently prescribed drug for type 2 diabetes. The inability of insulin to keep liver glucose output in check is a major factor in the high blood sugar of type 2 diabetes and other diseases of insulin resistance.

"Overall, metformin lowers blood glucose by decreasing liver production of glucose," says Birnbaum. "But we didn't really know how the drug accomplished that."

Imperfectly Understood

Despite metformin's success, its mechanism of action remained imperfectly understood. About a decade ago, researchers suggested that metformin reduces glucose synthesis by activating the enzyme AMPK. But this understanding was challenged by genetic experiments in 2010 by collaborators on the present Nature study. Coauthors Marc Foretz and Benoit Viollet from Inserm, CNRS, and Université Paris Descartes, Paris, found that the livers of mice without AMPK still responded to metformin, indicating that blood glucose levels were being controlled outside of the AMPK pathway.

Taking another look at how glucose is regulated normally, the team knew that when there is no food intake and glucose decreases, glucagon is secreted from the pancreas to signal the liver to produce glucose. They then asked if metformin works by stopping the glucagon cascade.

The Nature study describes a novel mechanism by which metformin antagonizes the action of glucagon, thus reducing fasting glucose levels. The team showed that metformin leads to the accumulation of AMP in mice, which inhibits an enzyme called adenylate cyclase, thereby reducing levels of cyclic AMP and protein kinase activity, eventually blocking glucagon-dependent glucose output from liver cells.

From this new understanding of metformin's action, Birnbaum and colleagues surmise that adenylate cyclase could be a new drug target by mimicking the way in which it is inhibited by metformin. This strategy would bypass metformin's affect on a cell's mitochondria to make energy, and possibility avoid the adverse side effects experienced by many people who take metformin, perhaps even working for those patients resistant to metformin.

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PATRIC

Jim I`m a one year newbie to treatment for the T2 D and always trying to learn something about this disease. I`ve got a question for additonal clarification on your statement in (a) about the "glossed over" part. What have they glosssed over and why.

I`m assuming if you are taking five pills a day you are taking 2500mg (haven`t seen Met in form less that 500...but I may be wrong.?

And since you have CGMS device I would assume that you are also injecting insulin ??

I don`t doubt your experience and accurate monitoring with you CGMS but wonder how precisely you can predict the hour by hour affects of the Met if you are also using insulin as well . It also contradicts some of what I have read about the timing and length of time the Met ,regular and ER, affects your system.

As for the study I`m sure the alphabet soup of researchers and research facilities are legitimate and genuine in their search for better understanding and application of medicines for Diabetes treatment. The general feeling I came away from reading this article is that it is rather self serving and will probably be contradicted by one or more of the multitude of other groups of Researchers of treatment of D. They all have their own agenda and feel their thoughts are the right ones. Met has been around a long time and I would think that most of what they know has been gleaned from a multitude of data gathered over that time.

Not trying to be argumentative , just trying to learn and appreciate your input !

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jims_forum
Jim I`m a one year newbie to treatment for the T2 D and always trying to learn something about this disease. I`ve got a question for additonal clarification on your statement in (a) about the "glossed over" part. What have they glosssed over and why.

I`m assuming if you are taking five pills a day you are taking 2500mg (haven`t seen Met in form less that 500...but I may be wrong.?

And since you have CGMS device I would assume that you are also injecting insulin ??

I don`t doubt your experience and accurate monitoring with you CGMS but wonder how precisely you can predict the hour by hour affects of the Met if you are also using insulin as well . It also contradicts some of what I have read about the timing and length of time the Met ,regular and ER, affects your system.

As for the study I`m sure the alphabet soup of researchers and research facilities are legitimate and genuine in their search for better understanding and application of medicines for Diabetes treatment. The general feeling I came away from reading this article is that it is rather self serving and will probably be contradicted by one or more of the multitude of other groups of Researchers of treatment of D. They all have their own agenda and feel their thoughts are the right ones. Met has been around a long time and I would think that most of what they know has been gleaned from a multitude of data gathered over that time.

Not trying to be argumentative , just trying to learn and appreciate your input !

 

Thank you for responding.

 

When the met has worn off/exhausted; I see my glucose levels drift up ( when no digestion glucose generated. I watch the Bloog glucose and I see the blood glucose start to drop after 2.5 hours on the clock after ingestion. This has gone on reliably. It then lasts the 2 hours for me where my blood glucose flatlines and stays stable - except for digetsion output where in fact blood glucose climbs. I awlways get the nasty liver excess glucose release -dump when the metformin is not up to strength during the times I notice I have clearly seen times when the liver attempts to raise the BG yet that will be stalled at a slight increase. If metformin not there I will see my blood glucose jump 511 peak on Caveman machine and on CGMS because it tends to average out the fast peaks; I will see the cgms show blod glucose shoot up to 311 and average out at 278.

 

There are NO self serving statements Patrick. Much as what has been peddled by many on these posts as how metformin works has been in fact theories and best guesses not FINDINGS. This report i listed was not self-serving but actual findings lab work done and suggested by earlier work by Pits, Salk , John Hopkins Childrens have found as well.

 

The only self serving statements are the peddling of ortodoxy based on guesses, theories and a quiltwork of unverified studies as fact peddled by self-serving lobbyiests. And yes as you noticed that America was late putting metformin to work by many years and has taken another 10 years to catch up with real science.

 

The fact is that many here in this country peddle a story there is no such thing as a liver leak and yet today the biggest use drug used in type 2 diabetes is metformin; a drug that can stop directly excess liver glucose release and directly outside the ampk/glucose control channel in the liver.

 

That effect was found 5 years ago and sat in the Indiana Jones Government warehouse of finds. I am not impressed.

 

On another note; yes I do use humalog lispro to assist meal bolus. I have used Lantus and it works but found I did not need it. In past I have used glyburide/starlix'actos glucotrol and dam glad off them. While extra insulin may be needed due to aging and pancreas islet stallout due to excess glucose pressure/oxidation; Type 2 Diabetes does not start and end as primarily an lack of insulin. If only we could stuff enough insulin in/actos we could stop type 2. A most unfortunate short sighted view not born out by the results and expanding quantities of type 2's at ever increasing rates.

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