METFORMIN KAUFMANN NUMBER: 3.1.3.2.2.2.3
General Information
Earlier use of the base plant, Galega officinalis or the French Lilac, was documented in Medieval Europe as an herbal remedy for diabetic symptoms.
Metformin was officially discovered in 1922. Human studies didnât begin until the 1950s, however. It was then that the French physician Jean Sterne introduced the substance to her countrymen as a prescription medication in 1957. The compound debuted in the United States in 1995. Presently, up to 150 million people are on the agent.
Interest in the medication as an anti-aging agent was peaked by a study released in 2014. Type 2 diabetics on either metformin or sulfuronureas (a different type of glucose controlling agent) were retrospectively compared with non-diabetics on neither of these drugs. Comparing 150,000 people, the type 2 diabetics on metformin had higher survivability. Let me rephraseâŚThe diabetics did better than non-diabetics. In fact, among patients in their 70âs, mortality was reduced by 15% in the metformin group.
Composition: Metformin is a biguanide (N,N-Dimethylimidodicarbonimidic diamide), also known by the trade name Glucophage.
Stats
Prescription medication: Oral bioavailability: 50-60%.
Peak plasma concentrations: 1 to 3 hours immediate release / 4-8 hours with extended-release formulations.
Uptake can be delayed 30 minutes if taken with food.
Protein binding in plasma: Minimal.
Half life: 1.7 to 4.5 hours
Categories
1 DNA Alteration: 3
â˘Epigenetic modular; it induces genome-wide DNA methylation
â˘Modulates the activity of S-adenosylhomocystein hydrolase, an enzyme in the methylation cycle.
â˘Decreases genomic instability.
â˘Stimulates telomeric length
2 Mitochondria: 1
â˘Activates endogenous antioxidants: heme-oxygenate-1, glutamate cysteine ligase, glutathione S-transferase, glutathione peroxidase, SOD, catalase, sulfiredoxin and thioredoxin.
â˘Works through the Nrf2-ARE pathway (nuclear factor-like 2 - Antioxidant Response Elements).
3 Aging Pathways: 3
â˘AMP KInase activator.
â˘Depresses MTOR pathway.
4 Quality control: 2
â˘Increases DNA repair efficacy.
5 The Immune system: 2
â˘Blocks the activity of the transcription factor nuclear factor-kB (NF-kB).
â˘Inhibits the differentiation of monocytes to macrophages.
6 Individual cell requirements: 2
â˘Boosts the formation of new nerve cells.
7 Waste management: 3
â˘Reduces blood glucose.
â˘Reduces AGE formation.
â˘Slows lipofuscin accumulation.
â˘Benefits the Cardiovascular system.
â˘Cancer reduction.
â˘Delays menopause in female mice.
Side Effects
â˘The side effects are generally not too bad; GI upset, transient diarrhea, abdominal pain, cramps and excess gas.
â˘Worst case scenario: Lactic acidosis. 3 cases/100,000 patients.
â˘Factors that increase this risk include age greater than 60, decreased liver, kidney or cardiac function, diabetic ketoacidosis, surgery, respiratory failure, ethanol intoxication and fasting.
â˘The drug blocks the metabolism of a few vitamins, so long term therapy should be accompanied by the addition of supplemental B12 and folate. (Take your vitamins).