Rapamycin vs Metformin

I've got a supportive MD who runs an aging clinic I'm seeing soon and am considering next steps. So far I've ...

  • Fixed all the basics (hormones, glucose, BP, ...)
  • Taking 2000 metformin daily
  • Did the NAD patches, plus daily booster

 

Canonically the next step would be Rapamycin, however I've heard rumors that if you're good with Metformin activating AMPK that perhaps Rapamycin isn't necessary. If it's still 'a good idea' or at least not a bad idea, thoughts? 

From the March Life Extension magazine page 98

Human Strategies to Suppress Excess mTOR

Rapamycin is being studied in humans to assess its ability to suppress excess mTOR and potentially reverse age-related pathologies. 

The most efficient way for people to suppress mTOR today is to activate cellular AMPK.

This can be done with the drug metformin, intermittent fasting/calorie restriction, and/or AMPK activating nutrients like gynostemma and hesperidia

The interesting thing is that the article is about the Canine Rapamycin project to suppress mTOR, yet at the end seems to be saying that Metformin is the best way to go about it via AMPK 

Further in this article from Feb 2018 by Bill, the sequence is

  1. Living causes cellular waste, which is removed via autophagy
  2. "Recent discoveries show that almost every intervention proven to extend healthy lifespan involves activation of autophagy (removing toxic cellular waste)"
  3. "One of the safest and most effective methods to optimize autophagy is by activating an enzyme in our cells called AMPK"
  4. "AMPK performs its fat-removing process, in part, by regulating a protein called mTOR"
  5. The most studied mechanism of metformin action is its ability to boost AMPK activity.

 

So it would seem you can use Metformin to activate AMPK and thereby regulate mTOR. Or you can go after mTOR directly with Rapamycin. Given the track record of Metformin that would seem the better route, and if you're already taking it then, in the absence of other information, adding Rapamycin would seem to be overdoing it. 

Addition: OK I found a reference

BF: Most people eat too much and this causes mTOR to be chronically elevated, which may preclude optimal results using the other interventions. Rapamycin directly suppresses mTOR. So we believe that inducing autophagy (removal of accumulated cellular waste), which happens when mTOR is suppressed, is a logical first step. What we are finding, however, is that most of our supporters already take metformin, practice intermittent fasting, and/or ingest nutrients that boost a cellular enzyme called AMPK, which indirectly suppresses mTOR. So we feel they may be able to skip rapamycin at first and proceed to boosting their NAD+ as I next describe. We will know more about the additive benefits of rapamycin when a clinical trial we are helping fund wraps up in a few months.

There you go, if you are taking Metformin, practice fasting, supplements and diet, then the expense and trouble of Rapamycin is probably not necessary. 

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  • I'm actually wondering if the blocking of gluconeogenesis may be a downside to using Metformin in combination with prolonged fasting. I would be curious to learn if combining it with Rapamycin would give the body flexibility to rely on gluconeogenesis when it is needed.

    This is interesting:

    Anti-aging combinations

    Rapamycin (or another rapalog) should be a cornerstone of anti-aging combinations (Figure (Figure1),1), given its universal anti-aging effect and the ability to delay almost all diseases of aging.

    Rapamycin and metformin: Both drugs extend lifespan in animals and have non- overlapping effects. In addition, they may, in theory, cancel possible metabolic side-effects of each other. As we discussed here (see rapamycin section) as well as in [31, 130], rapamycin in different settings may either increase or decrease insulin sensitivity. Similarly, calorie restriction increases insulin sensitivity, whereas severe calorie restriction (starvation) decreases it [129, 245]. In any case, rapamycin prolongs life span, indicating that insulin resistance is benevolent [130]. Unfortunately, the fear of this benevolent ‘side effect’ is delaying applications of rapamycin for prevention of age-related diseases. The simplest approach is to monitor glucose levels in individuals taking rapamycin. In addition, metformin, an anti-diabetic drug that reverses insulin resistance, could be combined with rapamycin.

    And vice verse, metformin may potentially increase blood lactate levels. Rapamycin decreases lactate production [164]. Each drug prolongs lifespan in mice, prevents cancer, atherosclerosis, and other diseases of aging.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5482593/

    I have a prescription for Metformin but can maintain a FBG in the low 80's without it. I want to build up the ability to fast to 72 hours. My understanding is that the body relies on gluconeogenesis to maintain glucose when fasting over multiple days. I could really use more information.

    Reply Like 2
      • Christine
      • Christine
      • 1 mth ago
      • Reported - view

      Christine My update, I have not noticed any change in glucose with the small dose of rapa. (My glucometers do each have a bias, so now I don´t really know my baseline, however, the difference is consistent. So if one shows 75, the other shows 93 and the next day one shows 79 and the other 97 and so on.)  I have managed to do several longer fasts. Several 48 hours, two 60 our fasts and a 72hour fast. My mother also joined me on a 60 hour fast 🙂

      Cyclical keto works great for me, IR is in my family, and I feel much better when I limit high carb foods to a few weekends when my priority is building muscle, building hormones, social life or feeding my microbiome. That said, as I progress, I notice I am more metabolically flexible. I have my cheat days after a HIT, and I feel the same meal is more easily tolerated in a body with near depleted glycogen stores than in one with fully stuffed glycogen stores. (What may have been my body at my highest weight, when following an average diet.) Even a year ago, I´d have highish fbg the morning after eating carbs, while now, glucose clears after an hour mostly.  This tells me that glucose can more easily find its way to glycogen stores which seems more likely when there is capacity to store.

      I do believe a lot of diets really mainly work because of cutting sugar, starch and fried food.  If you take a pound of vegetables, the protein suited for your weight, a few berries and herbs, there is room left for either some fats or some carbs for burning. Some people feel equally good with both, some don´t.

      Reply Like
  • Updated information. I'm working with a really good aging MD who recommends that since I'm already taking Metformin, exercise and fast, that doing Rapamycin on top of that is probably overkill. And it's expensive. 

    Again with managing your state you want to achieve homeostasis. This is to find the balance between two extremes, whether it be in exercise, caloric consumption or what have you. Note this is not the same as "moderation", as in "everything in moderation". That is the rallying cry of people who want an excuse to keep eating their meat, cheese, alcohol or whatever vice the have. Some things are definitively bad for you in any quantity so you don't want it in moderation.

    But for the things that are good for you - such as exercise - you don't want too little, and you don't want too much. Taking this example, people tend to think that if a little exercise is good then a lot must be better - not true! just one example is that elite athletes have impaired immune systems due to the constant exercise. 

    Another example is the Ketogenic diet fad. Yes, ketosis is good, in small quantities. Doing a monthly or bi-yearly multi day water only fast does amazing things, but you don't want to try and achieve that 24/7! Your body is designed to work on glucose - carbohydrates! But there again, people consume too many simple carbohydrates, and instead of being sensible and finding balance they go to the other extreme and try to eliminate them. It's madness. 

    Reply Like
      • Larry
      • Larry.1
      • 2 mths ago
      • 1
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      Dan I've been on 1000 mg Metformin, 3mg/week Rapamycin and do 16 hour fast 6 days a week. Is it overkill? We just don't know. I acknowledge Rapamycin is expensive but I think for me it's worth it. Dr Peter Attia who is on Metformin, Rapamycin also does extensive fasting (7 day water only fasts every 3 months) and IF.  He thinks it's worth it with our current knowledge. He also is very skeptical about efforts to boost NAD+. 

      https://podcastnotes.org/2019/09/09/attia-9/

      Reply Like 1
      • Danmoderator
      • skipping my funeral
      • dantheman
      • 2 mths ago
      • Reported - view

      Thanks for the information, yes we don’t really know yet.

      Reply Like
      • Kerry
      • Kerry
      • 2 mths ago
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      Larry Good post. I also follow Attia. He recently listed his bearishness on NAD+ oral precursors as being his biggest change from a year ago. He is getting ready to start NAD+ oral precursors.

      Reply Like 1
  • 54 yr old male, APOE 3/4. Mom has AD, dad had PD. Made radical lifestyle changes 3 yrs ago (after finding out I was APOE 3/4) to prevent AD. I went strict ketogenic  70/20/5 LCHF (fats come from plant fats, avocado, nuts, EVOO), minimal wild animal protein (salmon/sardines/bison), and whatever carbs in above ground green veggies (very low carb vegetables). No alcohol. I started 18/IF for 2 years (promptly lost 50 lbs), and then went OMAD (one meal a day) 13 months ago. My blood BHB ketones are typically 2.0 mmol/L daily, my fasting insulin and glucose are very low. My hs CRP is almost zero. I also run 5k intense cardio + 30 minutes resistance exercise DAILY. I have a Functional Medicine Doctor, we practice the Bredesen AD prevention protocol, as well as hormonal supplements, and regular supplements (resveratrol, curcumin, DHA/EPA, etc). I've had a Neuroquant volumetric MRI, awaiting SPECT scan (cerebral blood flow), and CCAC, as well as baseline in depth cognitive testing protocol...all to baseline and follow longitudinally. 

    I want do counter that the "body needs glucose from carbs" is a complete myth. The liver produces ALL the glucose it needs from proteins/fats. The US food guide states the minimum RDV for carbohydrates is...ZERO. There are no "essential carbs"

    https://www.dietdoctor.com/have-to-eat-minimum-amount-carbs

    I have become super lean and fit, cardio and muscular, lost 50 lbs, and my biomarkers are stellar (all without carbs for 3 yrs).

    Ketones and ghrelin hormone are HIGHLY neurobioenergetic for hippocampal neurons: ancestrally conserved pathways in our evolution. 

    I am seriously looking at Rapamycin now as additional intervention. I've read almost 3,000 papers on AD, and have come to the conclusion that its a vascular mediated disease. It explains all the risk factors (age, APOE, hypertension, diabetes, ischemic stroke, smoking), the science is so powerful showing the causality. Rapamycin can help prevent vascular (including BBB) dysfunction. Rapaymcin is so intriguing, it acts systemically on so many pro longevity pathways. I don't think I need metformin, would go directly to Rapamycin. 

    Reply Like 3
      • BobM
      • BobM
      • 2 mths ago
      • Reported - view

      MAC 

      Excellent post Mac. And congratulations on all of your progress. Excellent discipline!

      I’m really interested in what/ how you will do your Rapamycin. And then how you will measure any change.

      Thanks!

      Reply Like
      • Danmoderator
      • skipping my funeral
      • dantheman
      • 2 mths ago
      • Reported - view

      MAC apoe4 males don't have to be concerned about Althzeimers. Guess what, I have it too! A few years ago a Stanford researcher did a review of the data and found the gene is only indicative of AD for females. I did a full genome test and had an included session with a genetics advisor, she also knew of the male apoe4 connection and wasn't concerned at all. 

      Otherwise a correction on glucose is that yes it is produced from carbohydrates. In full ketosis your body switches to burn ketone bodies produced from fat, but this is a non preferential pathway. Have you ever done a water only fast of at least a week duration? I do it twice a year, it's quite enlightening to experience full ketosis versus normal glucose burning.

      Reply Like
      • MAC
      • MAC
      • 2 mths ago
      • Reported - view

      Dan  Hi Dan, and you actually believe that?? Anyone who tells you you don’t have to worry about AD, especially if you have APOE4, is blowing smoke.

      You know that E4 is the “frailty gene”...we are not meant to live a long life. E4 % representation in old age cohorts is extremely low!! AD and longevity is a polygenic risk dynamic. 

      Yes I’ve read all the literature on the low risk for E4 males. I know non E4 males and AD came out of NOWHERE! 40-50% of AD is NON E4. You can roll the dice, and I respect that. But hell no, I am doing on full prevention warfare. I am taking the reverse hypothesis: I am high risk, shortened lifespan n=1 and will prevent/extend. 

      Even if AD dosent get you, one of cancer or CVD or some other secondary complication will. This is a long term anti-aging war. My lifestyle interventions are all about lifespan/health span extension. We don’t (sorry I don’t) have the luxury of narrow genetic haplotypes like the Okinawans/Sardinians/Cretans with longevity. 

      What brain and blood biomarkers are you tracking?

      Reply Like
      • Danmoderator
      • skipping my funeral
      • dantheman
      • 2 mths ago
      • Reported - view

      Yes I stated it, apparently I do believe it, unless I've already got altheizimers and just think that I believe it, or not think as the case may be 🙂 

      You're quite passionate about your views on this and I want to ensure we continue to have civil discussion on the board. Briefly I'll note I've spent my adult life pursuing superior health and longevity, so there's no rolling dice, but being a scientist my approach naturally is derived from the existing scientific data with a 'holistic' or 'meta' approach to synthesizing it. Backing that up is that I've conducted personal experiments these many decades and have hard results supporting the approach. However it's quite different from yours. Regardless the conversation has wandered off topic so we should probably stop here.

      Reply Like
      • MAC
      • MAC
      • 2 mths ago
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      Dan my apologies if I offended you or anyone. I always try to stick the science as I see it, but always open to other interpretations. 

      Reply Like 1
      • Danmoderator
      • skipping my funeral
      • dantheman
      • 2 mths ago
      • Reported - view

      MAC No offense at all! We're having a healthy discussion here. Actually I'd like to have some debate, perhaps a dedicated forum, for diet and lifestyle, but am cautious because these topics can become contentious. 

      Reply Like
      • MAC
      • MAC
      • 2 mths ago
      • Reported - view

      Dan we are all self-hackers, otherwise we wouldn't be on these forums! We cannot wait for western medicine to save us from chronic illness. I personally believe we must take responsibility for our own n=1 self well being. I don't have the answers to longevity nor can I say with ANY proof that anything I am doing will delay any chronic disease. The best that I can hope for is somehow/someway I can baseline and track my inner health longitudinally, and show "positive" trends.

      My physical/cardio health is now excellent, and I believe this is a huge part of longevity enhancement. In all the human lifestyle intervention literature, cardio respiratory fitness is always associated with longevity (aside from extreme fitness athletes who push the limits of the heart muscle, and elevate risk of AFIB/ ischemic risk).

      Association of Cardiorespiratory Fitness With Long-term Mortality Among Adults Undergoing Exercise Treadmill Testing

      https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2707428

      This is an excellent study, using a standard controlled cardio test, tracking longitudinally, AND it's outcome is ACM (All Cause Mortality, ergo longevity)

      Have a look at Figure 2.

      Can someone show me a lifestyle intervention study, in HUMANS, showing a better ACM outcome? I don't think I've found one yet.

      There is no "pharma" hack here...pure and simple cardio fitness. There are many evolutionary theories abound that associate our bipedalism and running capability to brain size expansion.

      Have we lost our ways in a western sedentary society? 

      Reply Like
    • MAC Hi Again !

       

      Since you have serious interest in physical health I'd like to add this link. Muscular strength and cardiovascular. (it can be stretched to whole body health)

      I personally will incorporate tougher resistance training in my efforts.

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3496010/

       

      This link (even though I dont think the reading is great) bring focus on the muscular fitness and the related effects on whole body health. A couple of years ago I had a rewarding conversations with a well renowned heart surgeon. He said that according to his experience and the lab results he had seen his personal interpretation was that persons who, after different kinds of heart surgery, started to do heavy resistance exercise (like in a gym) showed up with a healthier and younger heart. This even though they did not focus their training on cardiovascular fitness. The guess work was that the anabolic/pysiological response in the muscleoskeletal system was transmitted to the cells in the heart (and other parts of the body) so cardiofitness was also improved. This is of course an anecdotal story based on one person’s experience. But I find this being a good idea to have in mind. Especially since we now see how completely different organ systems interact. (Like the environment in intestine and how it can effect the brain)

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      • MAC
      • MAC
      • 2 mths ago
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      Staffan Olsson I practice BOTH in my daily routine, although I do resistance training more for skeletal muscle build, overall physical health, and strength/resiliency to help reduce risk of frailty as I age. I lost 50 lbs, and have become very lean and muscular on my diet/exercise protocol. The muscularity is all from the daily intense resistance exercise.

      Investigation of frailty as a moderator of the relationship between neuropathology and dementia in Alzheimer’s disease: a cross-sectional analysis of data from the Rush Memory and Aging Project

      https://www.thelancet.com/pdfs/journals/laneur/PIIS1474-4422(18)30371-5.pdf

      "Frailty and Alzheimer's disease pathology were independently associated with Alzheimer's dementia. When frailty was added to the model for the relationship between Alzheimer's disease pathology and Alzheimer's dementia, model fit improved. There was a significant interaction between frailty and Alzheimer's disease pathology. People with an increased frailty score had a weakened direct link between Alzheimer's disease pathology and Alzheimer's dementia; that is, people with a low amount of frailty were better able to tolerate Alzheimer's disease pathology, whereas those with higher amounts of frailty were more likely both to have more Alzheimer's disease pathology and for it to be expressed as dementia.

      In my readings, cardiorespiratory fitness is FAR more neuroenergetic than resistance training. My main dementia prevention objective is protecting the hippocampus.

      Sustained aerobic exercise increases adult neurogenesis in brain

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4818598/pdf/TJP-594-1855.pdf

      " Our results confirm that sustained aerobic exercise is key in improving AHN. We report a very modest effect of HIT and no effect of resistance training on AHN in adult male rats"

      Reply Like 1
      • MAC
      • MAC
      • 2 mths ago
      • 1
      • Reported - view

      Dan Some new literature on Rapamycin, including some new rapalogs that are HIGHLY specific to mTORC1! Its' the mTORC2 inhibition and impact on some of the "basic" biological functions such as glucose and lipid metabolism and the immune system that has me still mulling. New compounds that only impact mTORC1 would be hugely beneficial to human uptake.

      (In jurisdictions for which access to Sci-Hub is legal, you can search for the papers there. Per the Digital Millennium Copyright Act)

      TORwards a victory over aging

      https://www.ncbi.nlm.nih.gov/pubmed/31544928

      "The continuous expansion of our knowledge regarding how age-related conditions are influenced by mTOR signaling in many species and disease models, and the continued pursuit of safe, efficacious ways to reduce mTORC1 signaling confirm the value that persists in exploring the regulation of aging by mTOR"

      A novel rapamycin analog is highly selective for mTORC1 in vivo

      https://www.nature.com/articles/s41467-019-11174-0.pdf

      "DL001 inhibits mTORC1 signalling without impairing glucose homeostasis and with substantially reduced or no side effects on lipid metabolism and the immune system"

      Discovery of Small-Molecule Selective mTORC1 Inhibitors via Direct Inhibition of Glucose Transporters

      https://www.sciencedirect.com/science/article/abs/pii/S2451945619301783

      "Here we describe the identification, optimization and characterization of a chemical scaffold that demonstrated a profile consistent with the selective inhibition of mTORC1. Surprisingly, target identification revealed that class I glucose transporters, primarily GLUT1, was the primary target for these compounds yielding potent inhibition of glucose uptake. Upon further characterization, we have demonstrated that cellular inhibition of glucose uptake by these compounds leads to selective and potent inhibition of mTORC1 activity even in the presence of growth factors and other nutrients. Therefore, modulating the glucose-sensing mechanism would be an alternative approach to developing therapeutic tools to selectively target mTORC1 in the future."

      ----

      We keep coming back to glucose nutrient sensing as a very strong anti-aging signal. We all know the huge association of elevated glucose with chronic disease, implicated in ALL the major diseases of modern society: cancer, CVD, Alzheimers. Thousands of research studies on lesser organisms have consistently shown longevity associated with reduced glucose/essential amino acid nutrition levels and CR. Excess protein intake (especially the BCAA's found in animal protein) causes gluconeogenesis. These nutrition inputs may ALL have a common root molecular pathway: glucose. Just one of the many reasons why I practice a strict ketogenic/OMAD/low animal protein dietary protocol. Eschewing animal protein for high quality plant protein would take me out of ketosis.

      Reply Like 1
  • BobM   Thank you. OMAD is most definitely the toughest mental challenge to overcome. The ghrelin signal is super strong between say 11am until I eat my OMAD dinner at normally 6pm. It requires great fortitude/self control to ignore it.

    Per my original post on ghrelin signalling and neuroenergenesis:

    Ghrelin-Mediated Hippocampal Neurogenesis: Implications for Health and Disease

    https://www.sciencedirect.com/science/article/abs/pii/S1043276019301249

    Great question on "how you will measure any change". As an engineer, the old mantra "you cannot manage what you cannot measure" is extremely relevant here. As you can see, I have a pretty detailed monitoring of lifestyle interventions, most recently adding layered brain imaging/cognitive testing. The challenge will be teasing out the Rapamycin effect given I am simultaneously layering so many interventions that boost brain function/cardiovasculature.

    And given that I believe AD is a vascular mediated disease, I am currently studying what biomarkers I can track that signal the effect of the rapamycin intervention. Given my metabolic profile, current thinking is perhaps starting with a lower dosage, say 4 mg every 7 days (not settled).

    Practically, these Rapamycin tracking markers need to be reasonably accessible vs exotic academic lab tests.

    If you review this paper for example (albeit mice):

    Rapamycin rescues vascular, metabolic and learning deficits in apolipoprotein E4 transgenic mice with pre-symptomatic Alzheimer’s disease

    https://journals.sagepub.com/doi/pdf/10.1177/0271678X15621575

    They used conventional tests of ASL and CMRglc to assess the impact of Rapamycin. The SPECT scan I am scheduled for is really a cerebral blood flow scan. The CMRglc is not readily done and $$, but it's a gold standard for brain functionality and is readily available. Enhanced NO production and NF-κB signalling is also a direct result of Rapamycin intervention. There are a few other markers.

    Of course, will also be testing for some of the potential negative effects such as lipids/glucose/insulin/immune system functionality.

    Still researching...

    Reply Like 1
    • MAC Hi Mac! Since you have researched neuroprotection well, I wonder if you have any personal view on the usefulness of Taurine. I have used it intermittently at 1500 mg at bedtime for improved sleep and for its potential for promoting neurogenesis. But lower dosing has a negative effect on my sleep. 

       

      I find this recent review covering the neurological  effects of Taurine well. "Taurine and its analogs in neurological disorders: Focus on therapeutic potential and molecular mechanisms"

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6536745/

       

      Any focus on aptosis in cells other than braincells would be out of line.  A link more focusing on taurine as pro apoptosis in some cancers.

       

      https://academic.oup.com/abbs/article/46/4/261/1578

       

      Since preserving brainfunction is one of my main goals, I wonder about your view on this particular substance.  

      Reply Like
  • @ staffan_olsson I have not read much on Taurine, it's not on the mainstream "AD" radar for pharma interventions. From a brief read on the article, it appears that Taurine itself has very low bioavailability, and engineered analogs need are required for enhanced pharmokinetic activity (ie. crossing the BBB). There are some beneficial outcomes in some neurological mouse models reported, but at huge doses, mostly ip injected. Mouse models, unfortunately, have translated extremely poorly to humans when it comes to Alzheimers research (think Amyloid). Btw, IMHO, amyloid and tau are downstream pathological markers of the brain trying to deal with some other underlying upstream chronic dysfunction (e.g. vascular, BBB).

    To think that a single pharma molecule could "prevent" neurological disease, when the disease has so many apparent pathways leading to synaptic loss is perhaps wishful thinking. I am not sure your age or neurological state, but prevention with lifestyle interventions that act beneficially on EVERY cell in the body, is still the best protocol. 

    My sleep is still a work in progress, but a very important component of overall health and well being. Sleep disruption has 2 way associations with AD.  

    https://www.ncbi.nlm.nih.gov/pubmed/31536750

    For a good reference on the importance of sleep, read Matthew Walker (Why we Sleep). Petter Attia has several podcasts with Matthew as abbreviated option. https://peterattiamd.com/?s=walker 

    It appears that my keto diet, OMAD, supplements, hormone treatments "may" have disrupted my serotonin and/or circadian rhythm, and my sleep is somewhat fragmented (no issue falling asleep, but will awaken during). I just ordered a DREEM2 sleep tracker https://dreem.com/en?p=dreem2 so I can begin to understand my sleep patterns, and then implement lifestyle interventions to monitor improvement.

    What are your sleep symptom characteristics, attributable to any lifestyle changes, and does Taurine help?

    Reply Like
    • MAC hi! My pattern of sleep has been that I can easily fall asleep but might wake up after a few hours Usually 3-5 hours. I need more sleep than that. Melatonin accentuated this issue and I became wide awake after 3-4 hours. Melatonin did not work for me. I am surprised but 200 - 400 mg folic acid  makes me sleep better. (I have not had the same sucess with 5-MTHF). Taurine att 1500 mg improves my sleep but lesser dose Taurine disturbs my sleep. Magnesium citrate/bisglycinate improves my sleep. 

      Reply Like
  • Duy noted. My sleep hacking is still a work in progress. The melatonin (various doses) does not seem to impact my waking, although it definitely helps with falling asleep. I tried magnesium L-theronate at night (I normally take it in the day for simple Mg plasma level elevation), but found no improvement. I am not so advanced in my experimentation with sleep interventions. I am hoping that once I start tracking my sleep with the DREEM2, I can baseline, and then start further interventions. If I learn anything, will be glad to share. Even though my sleep is fragmented and I find myself yawning during the day, I still have plenty of energy and there's impact on my daily routines.

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