Personally, I would give rest to my own system I guess for a month or a bit more.
Then I would try a tea or pills of the Herb mentioned above in the chat (Skullcap).
And another obvious approach could be to reduce the dose dramatically and then start building up as needed (guided by a continuous glucose monitor or fingerpricking regularly). All these after giving the system a rest. But yeah, there may be more experienced people with Acarbose and the relief of side effect out there.

Anyways, I would also recommend to reduce your ingest of bread and refined carbs, as those are contrary to what we want to achieve: enhanced health span. I have not seen many other numbers of people here recently but my personal goal is to maintain a regular blood glucose in the morning of 80 mg/dL. (There are so many other biomarkers, but difficult to measure daily at home. Iā€™m planning to get a trigliceride meter too.)

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Actually if I stop for a few days then restartā€¦ the gas is worseā€¦ then subsudes after a day.

I have only heard of people doing 50mg dose with 1st biteā€¦not 100 mg.

Might skip dose when having beer.

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Start slowly. 25mg for a week or two, progress to 50mg when confident and progress to 100mg maybe few months later. When I got my prescription filled pharmacists said that I should take first doses during meal and slowly progress to first bite. She said usually most unwanted side effects should subside in 12 weeks when intestinal flora adjusts. Havenā€™t really checked upon that claim, but my gas is not so bad to begin withā€¦ I have started with 50mg in the first third of the mealā€¦ and will slowly progress to first bite. Yesterday I had pasta dinner and had a bit more gas and uncomfortable filling in my intestineā€¦ but by morning everything was ok.

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I am up to 100 mg tid with meals. After some awful weeks of uncomfortable gas, I started taking a beano with each acarbose. Much better.

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Taking Beano with Acarbose undoes any benefit of Acarbose. Gas and GI distress with Acarbose is just letting you know Acarbose is doing its job, and you are eating too many carbohydrates.

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Not true-as regards ā€œundoes any benefit of Acarboseā€ The below study shows that there is some decreased benefit when combined, but is still beneficial.

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One issue with the mice used in the ITP trials, all trials actually, is that the mice are not genetically diverse. Dr. Miller will readily admit this.

A good point, but keep in mind that lot of humans have metabolic syndrome but only small fraction of them (with genetic weakness in max insulin production) become type II diabetics. However everyone with metabolic syndrome probably suffers damage from either high blood sugar (diabetics) or high insulin levels (required to drive down blood sugar in non-diabetics). With Acarbose the body no longer needs high insulin levels which are suspected of causing inflammation or resulting in high triglyceride levels : Insulin only drives the blood sugar into muscle cells, which then convert the glucose they donā€™t need into fat and dump it back into the blood. Once all the bodyā€™s fat cells are full (when they are around 10x normal size) they stop absorbing much fat and instead send out a signal to raise insulin resistance of muscle cells to drive down blood triglyceride levels. You end up with two of the bodyā€™s systems (Insulin controlling blood sugar and fat cells controlling plasma triglyceride levels) fighting each other.

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From google results: 10.5% of the U.S. population, have diabetes & about 30% have met syndrome, which would suggest that about 1/3 of the people with met syndrome have diabetes. That doesnā€™t seem so small.

The question asked in reverse does turn up an answer: The overall prevalence of MetS among type 2 diabetic patient in this study was 68.3%

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Thanks for your response. I made the mistake to group in the same umbrella T2D and metabolic syndrome (which is really the way I think of it). I you are metabolically ill by diet (usually high in carbs) then you have ā€œdr-spin-T2Dā€. 90% of US population is ā€œdr-spin-T2Dā€ or in better terms is ā€œmetabolically syndromedā€.

I understand that knowing the fact of that huge percentage of the population being illed by diet, then the ITP project and the chosen chow makes sense in that context. But, at the end, you are not studying life-extension molecules but medicine to fight the diet. At least that is what I see.

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Yeah, NIH gives those laughable numbers.
Can you believe that only 10% of the US population has diabetes? I donā€™t.
Now, diabetes/prediabetes/insulin resistance/pre insulin resistance/obesity/high blood preasure are all stages of the same disease: metabolic syndrome. And, in my opinion, should be grouped together into a single number (even if the separated numbers due to ā€œseparationā€ criteria are also reported). And that number is, indeed 92% as of 2018:

(And today should be worse, probably 95%).

But coming back to the numbers reported by the NIH, 10 + 30 =40% which is already huge (but less than half of reality in practice)

And again, just diabetes + prediabetes have been reported higher by others. For example, 52% as of 2012:

(Using that narrow criteria I would estimate 60% today)

So yes, I guess one should not expect that only Rapamycin + Acarbose would solve the problem. Clearly dietary + lifestyle changes should go first. And the ITP should be doing the same which implies necessarily a change in diet and lifestyle for the mice. Unfortunately, ITP is only focused in solving the problem with pills. Iā€™ve heard Richard Miller saying those terrible words himself in the Sheeky Science channel:

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I suspect there is something deeper going on. Yes, diet & lifestyle, but I think people may get moved into a different physiological state, in which their body doesnā€™t use the food they do get correctly. I suspect that people feel hungry & low in energy, so they eat. For some reason, only part of what they eat is available for use.

In other words, if it were as simple as eating well & exercising, it wouldnā€™t be as pervasive & intractable a problem as it is.

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This ā€˜The Driveā€™ episode elucidates the point of the prevalency of insulin resistance: #140 - Gerald Shulman, MD, PhD: Insulin resistanceā€”molecular mechanisms and clinical implications - YouTube

They say that young people especially can be a decade or more away from T2D. You just donā€™t know if you only check blood glucose, because they just stay average glycemic.

(In the background they suffer from hyperinsulemia.)

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I think Lustgarten explains it with the microbial burden. If you inject young healthy people with LPS they get T2D. This means it comes from the microbial burden. Probably coming through the gut. If you donā€™t fix this, it will wreck the whole system over time.

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It is indeed as simple as that to reach the right control group for a longevity test. My complain vs the ITP test is that they have a metabolically ill by diet & lifestyle control group (trying to mimic the US population). And then trying to solve the problem with a pill rather than going to the root cause: diet & lifestyle. With optimal diet and lifestyle, you will get a decent control group on which you can test real longevity molecules rather than ā€œfixersā€ of bad dietary and bad lifestyle patterns. Maybe some real longevity molecules are not being discovered due to the nasty burden of the diet and lifestyle of the mice in the ITP.

Now, for us, of course correct dietary + lifestyle should go first if we are really trying to extend our lifespan. And Iā€™m only saying first. Not only. Secondly, longevity molecules would help to extend further healthspan and deal with real aging-related issues.

Now, of course, another problem is to accept what is the correct diet. Today I think the correct diet is: 2g of protein per kg of ā€œmy ideal/goal body weightā€ per day (which turned into real meat is 2 X 3 = 6g of meat, chicken, fish) + low carbs to enough to keep body feeling right only coming from real fruit and real vegetables + fat enough to keep body feeling right mainly coming from the meat but also from coconut oil + no softdrinks at all and lots of plain water & tea (no sugar of course). All eaten in a 9 hours window. Blood glucose, fasting insulin, triglicerides and weight should all be moving towards the correct marks without any pill. Only with this indeed I reached close to 95% of my ideal marks. Now Iā€™m taking additional Rapamycin + Skullcap and Iā€™m 100% on ideal marks.

And about the ā€œsomething deeperā€ going on, I honestly think it is genetic. This is around the third generation of metabolically ill people (by food and lifestyle). So this generation is suffering the burden of its own bad eating and exercise patterns, but also the burden of receiving sick genes from ~ 2 generations above.

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Exactly. That is why I think the numbers for T2D from the NIH are laughable. Saying that the prevalence of T2D in the US is ~10% in adults is misleading. The real number is: 95% of adults in the US are metabolically-ill, which is really scary but a fact.

Very interesting. Thanks.
And one of the hypothesis for Acarbose is the ā€œfixingā€ of the gut micriobiome.

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Thanks for the link to the article. I hadnā€™t seen it before. Perhaps Beano does not undo all of the benefits of Acarbose (as I apparently mistakenly implied), but the authors of the study (who both worked for Bayer, the manufacturer of Acarbose) were forced to admit that ā€œcoadministration of Acarbose and Beano may lead to a pharmacodynamic interaction, resulting in a decrease in the activity of Acarbose,ā€ ā€¦ ā€œthe effectiveness of Acarbose was generally reduced by Beano,ā€ and ā€œchronic coadministration of these agents may interfere with the long-term efficacy of Acarbose.ā€
Rather than encouraging my patients to continue consuming carbohydrates and taking Beano to reduce Acarbose-induced flatulence, I recommend they limit their carbohydrate intake and take smaller doses of Acarbose to cover themselves when they ā€œfall off the wagon.ā€

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Yes, I get that recommendation, but we all slip up, and beano is there to save you from the disastrous interpersonal implications!
My opinion, is that carbohydrates are awesome, and life without them would be misery :slight_smile:

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Just stumbed upon this paper, which has some interesting information:

Acarbose to reverse Brain Agingā€¦

Chronic acarbose treatment alleviates age-related behavioral and biochemical changes in SAMP8 mice

The administration of maintaining the homeostasis of insulin/insulin-like growth factor 1 (IGF-1) signaling and/or glucose metabolism may reverse brain aging. In the present study, we investigated the effect of acarbose, an inhibitor of Ī±-glucosidase, on age-related behavioral and biochemical changes. The SAMP8 mice were randomly divided into old control group and acarbose-treatment group. The mice in the acarbose group were administered acarbose (20 mg/kg/d, dissolved in drinking water) orally from 3 to 9 months of age when a new group of 3-month-old mice was added as young controls. The results showed that the aged controls exhibited declines in sensorimotor ability, open field anxiety, spatial and non-spatial memory abilities, decreased serum insulin levels, increased IGF-1 receptor and synaptotagmin 1 (Syt1) levels and decreased insulin receptor, brain-derived neurotrophic factor (BDNF) and syntaxin 1 (Stx1) levels in the hippocampal layers. The age-related behavioral deficits correlated with the serological and histochemical data. Chronic acarbose treatment relieved these age-related changes, especially with respect to learning and memory abilities. This protective effect of acarbose on age-related behavioral impairments might be related to changes in the insulin system and the levels of BDNF, IGF-1R, and the pre-synaptic proteins Syt1 and Stx1. In conclusion, long-term treatment with acarbose ameliorated the behavioral deficits and biochemical changes in old SAMP8 mice and promoted successful aging. This study provides insight into the potential of acarbose for the treatment of brain aging.

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