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originally posted by: TiredofControlFreaks
a reply to: TiredofControlFreaks
sorry - pressed enter before I finished.
taking 100 aspirin all at once will kill you. Take 1 aspirin for 100 days and you will be fine and maybe experience beneficial effects.
Just because a lot of something causes a problem, does not mean that a little of the same thing will also have an effect.
The poison, as usual is in the dose.
I call this doom porn
originally posted by: Fowlerstoad
a reply to: M4ngo
But ... but .. Metformin slows aging and increases lifespan potentially *see link*, even in non-diabetics. Should not we all be taking metformin? Plus, it is very cheap as far as cost.
www.medicalnewstoday.com...
originally posted by: M4ngo
Yeah, that's a bunch of BS. But by all means load up if that's what ya want to do—lots of ignorance in this thread.
Antidiabetic drug metformin (GlucophageR) increases biogenesis of Alzheimer's amyloid peptides via up-regulating BACE1 transcription.
Biological and biophysics aspects of metformin‐induced effects: cortex mitochondrial dysfunction and promotion of toxic amyloid pre‐fibrillar aggregates
Metformin Facilitates Amyloid-β Generation by β- and γ-Secretases via Autophagy Activation
Metformin increases APP expression and processing via oxidative stress, mitochondrial dysfunction and NF-κB activation: Use of insulin to attenuate metformin's effect
The combined use of metformin and insulin could be a therapeutic strategy for Alzheimer's Disease
The relationship identified between the key pathogenic peptide of AD and metformin/insulin is clearly of great interest and may have important implications for the treatment of T2DM and AD. However, large clinical trials are necessary to confirm and clarify the therapeutic efficacy of these compounds.
originally posted by: Agartha
originally posted by: M4ngo
Yeah, that's a bunch of BS. But by all means load up if that's what ya want to do—lots of ignorance in this thread.
I couldn't agree more! Just look at all the misinformation in the OP!
I have been wondering why you wouldn't post links for the articles you cited as 'real science' on page 5, so I searched for them myself and now I understand:
Antidiabetic drug metformin (GlucophageR) increases biogenesis of Alzheimer's amyloid peptides via up-regulating BACE1 transcription.
This is in vitro, and anything can happen in a petri dish. Let's wait for the in vivo studies and then clinical trials to see if they really are onto something. This study proves nothing.
Biological and biophysics aspects of metformin‐induced effects: cortex mitochondrial dysfunction and promotion of toxic amyloid pre‐fibrillar aggregates
This one was an in-vivo study, but with mice and unfortunately what happens with mice doesn't always mirror humans. We need clinical trials. This study proves nothing.
Metformin Facilitates Amyloid-β Generation by β- and γ-Secretases via Autophagy Activation
Mice again and you know success in a lab doesn't always mean success with humans. Clinical trials needed. This study proves nothing.
Metformin increases APP expression and processing via oxidative stress, mitochondrial dysfunction and NF-κB activation: Use of insulin to attenuate metformin's effect
This was the most interesting article, I really enjoyed reading it but I am surprised you posted it as it shows the benefits of Metformin. A snippet from your article:
The combined use of metformin and insulin could be a therapeutic strategy for Alzheimer's Disease
The study was on mice once again, hence this is in the conclusion:
The relationship identified between the key pathogenic peptide of AD and metformin/insulin is clearly of great interest and may have important implications for the treatment of T2DM and AD. However, large clinical trials are necessary to confirm and clarify the therapeutic efficacy of these compounds.
Hope this was useful!
RESULTS:
In human and mouse organotypic cultures in vitro, metformin decreased testosterone secretion and mRNA expression of the main factors involved in steroid production. In vitro, the lowest observed effect concentration (LOEC) on testosterone secretion was 50 µM in human, whereas it was 500 µM in mouse testis. Lactate secretion was increased in both human and mouse organotypic cultures with the same LOEC at 500 µM as observed in other cell culture models after metformin stimulation. In vivo administration of metformin to pregnant mice reduced the testicular size of the fetal and neonatal testes exposed to metformin during intrauterine life. Although the number of germ cells was not affected by the metformin treatment, the number of Sertoli cells, the nurse cells of germ cells, was slightly yet significantly reduced in both periods (fetal period: P = 0.007; neonatal period: P = 0.03). The Leydig cell population, which produces androgens, and the testosterone content were diminished only in the fetal period at 16 days post-coitum.
CONCLUSIONS:
This study showed a potentially harmful effect of metformin treatment on the development of the fetal testis and should encourage future human epidemiological studies.
originally posted by: M4ngo
Metformin Exposure Effects Human and Mouse Testicular Cells In Vitro and In Vivo
Fact: people die all the time from lactic acidosis caused by Metformin.
Fact: Metformin directly alters gut microbiota and long-term Metformin use causes chronic vitamin b12 deficiency. Do you know what vitamin b12 is used for in the body? Obviously not because if ya did, then ya would not be blindly arguing a drug that causes it. Vitamin b12 is essential in DNA synthesis and red blood cell production.
Metformin causes Alzheimer's, don't give me some smartass remarks when you don't even know what you're talking about.
I included all the links to Metformin being a neurotoxin on Page 1, post 3. You failed to look.
Optimal control of diabetes can reduce the progression of cognitive deficits in patients with AD. The use of drugs such as rioglitazone, pioglitazone has demonstrated to have a positive impact upon cognition and memory in patients with mild to moderate AD. While metformin by itself increases the formation of Β-amyloid, combined with insulin it enhances the effects of insulin in reducing amyloid levels.
While metformin by itself increases the formation of Β-amyloid
Participants with diabetes (n = 126) had worse cognitive performance than participants who did not have diabetes (n = 1,228; adjusted odds ratio 1.51 [95% CI 1.03–2.21]). Among participants with diabetes, worse cognitive performance was associated with metformin use (2.23 [1.05–4.75]). After adjusting for age, sex, level of education, history of depression, serum vitamin B12, and metformin use, participants with diabetes who were taking calcium supplements had better cognitive performance (0.41 [0.19–0.92]).
Metformin use was associated with impaired cognitive performance.
One recent case-control study that included 14,172 participants 65 years of age or older reported that taking metformin over the long term increased the risk of AD
Among participants with diabetes, cognitive performance was worse in patients who were taking metformin
MMSE scores were lower in participants with diabetes who used metformin (mean score ± SD 22.8 ± 5.5) than in those who did not use metformin (24.7 ± 4.4).
In our series, patients with diabetes who were taking metformin had worse cognitive performance than participants who were not taking metformin.
Our observations agree with those previously reported by Imfeld and colleagues (22), in particular that patients who are taking metformin may be at an increased risk for cognitive impairment.
Alternatively, patients who are prescribed metformin may have worse glycemic control or diabetes-related complications than patients with diabetes who are not prescribed metformin
Metformin is a widely prescribed first-line monotherapy for type 2 diabetes but is associated with vitamin B12 deficiency and peripheral neuropathy.
A case-control study of more than 14,000 patients reported that long-term metformin use was associated with an increased risk for AD in those ≥65 years old
Alternatively, metformin also impairs absorption of vitamin B12 via a drug interaction that occurs at the distal ileum. Low serum vitamin B12 levels are associated with AD and other neurodegenerative diseases
While metformin by itself increases the formation of Β-amyloid