Just me but I’d replace the steelcut oatmeal with eggs. Gundry says they will poke holes in your gut and should be replaced with sorghum. Elsewhere it says soaking and cooking will greatly reduce lectins. Also people with the CGMs say it drives up the glucose.
I know the fiber is good.
I do eat eggs with my breakfast
Do Metformin, Berberine, and Farxiga do anything to prevent diabetes? Or just treat it? I think Metformin can be preventative, but not approved for that.
Supposedly they keep blood sugar down, to save my pancreas among other benefits. I don’t want to use a keto diet; I want to build metabolic flexibility. I need to get my sleep working and stay on the IM and short- term fasting program. Fasting has always been a good reset for my insulin sensitivity.
great thought process, however, since rapamycin is known to have an undesired impact on both in some populations regardless, perhaps a better marker or two would be something related to inflammation CRP and immunity Neutrophil?
Those seem like reasonable things to track and are usually tracked as part of phenotypic age calcs, so cheap and easy to do.
What I’d really like to track (as doses get higher) are TREGs. Dudley lamming has suggested this as something we should track… but I can’t find anyone who provides these blood tests at any reasonable costs. Dudley seems to think these are the best way to track immune system function.
None of the regular blood test resellers offer it (from what I can find). Perhaps I’m looking for the wrong thing (I just search on “tregs” in the search bars for these companies.
Neutrophils, CRP and WBCs could be a good way to test except for me, none of these 3 factors have changed from before taking Rapamycin. Also, Rapa is purported to reduce CRP due to it’s Senolytics effects. LDL and HBA1C seem to be the best at this point as they are dysregulated.
“Use it or lose it” - maybe once a month you should give your pancreas a bit of “exercise “.
(I do).
You mean high carb/sugar meal?
For very low carb diet people, some sort of protocol to avoid losing metabolic flexibility seems prudent. I eat a lot of fruit and veg; my efforts focus on avoiding glucose spikes and extended elevations of glucose and insulin. Food order, movement after eating, not eating at night, etc.
New video by Dr. Carvalho brings up this hypothesis, ‘thrifty genes’.
The title of that video is a bit goofy. “Cholesterol is natural, how can it be bad for us?” First of all, we all know of natural substances that are toxic, natural is not such a useful word anymore. Additionally, cholesterol per se is not “bad” for anybody, since without cholesterol, we’d all be dead. It’s necessary for life, period. That being said, the devil is in the details and the poison is in the dose. Maybe I’m just being pedantic.
Since I started taking Rapa, my blood lipids increased significantly, and my BG took a minor but noticeable tick up. So I’m taking a Rapa break and testing my blood levels after my pause to see if they go back down to my baseline. If I’m back to my baseline at my next check, I’ll go back on Rapa but this time with lower dosing. If on the lower dose they are still noticeably affected, I’ll be looking into possibly a statin or how I could convince a doctor to give me a prescription for a pcsk9 inhibitor.
Using my LDL and BG as a guide, I’m OK with looking for a minimum effective Rapa dose, rather than “the largest dose my body will possibly tolerate without exploding!” I have a feeling it will take a bunch of tweaking for me to find that. I wish I was one of the people that can take Rapa without significant disregulation of LDL or BG, but I’ll be happy if I can eke out something good from this.
“Among individuals with increased 10-year risk for ASCVD, rosuvastatin 5 mg daily lowered LDL-C significantly more than placebo, fish oil, cinnamon, garlic, turmeric, plant sterols, and red yeast rice.”
Recent study on rosu vs supplements on LDL-C
I’m waiting for my first shipment of rapa to arrive. Still reading and learning. I’m just “thinking out loud” here…
I was taking nexium for GERD and frequently Imitrex for migraines. I was obese. My blood pressure was on the rise. My physician wanted to start me on antihypertensives. At 52 years old with a wife and two teenagers I’d like to stick around as long as possible. Something triggered. I’ve lost over 70lbs. Calorie restriction and exercise. I’m 6’ and 188lbs. I no longer take any medication. 99% of GERD is gone. I took a TUMS a few weeks ago after an unusually big meal. I haven’t had a migraine in the past 9 months. Blood pressure was 120/73 yesterday.
I try to avoid drugs/medications as much as possible. Seems like most medications fix one thing but cause another. For example, Nexium (or PPIs in general) reduce the absorption of magnesium in a population that’s already magnesium deficient so imagine what that does to your body over years. PPIs come with many other risks. That’s just one. So that’s why I would prefer to avoid medications. But, taking rapamycin weekly or biweekly for the possibility of life extension seems worth it to me. However, the more I read about it. I’m like… it seems like taking this drug often causes elevated LDL and A1c. So then you find yourself taking at least 2 more drugs to counter that. Then you run the risk of, “what are the side effects of those 2+ drugs.” And, “what am I going to need to take to counter that?” The next thing you know you might find yourself taking 5-6 drugs when you were taking none before. Which gets be back to where I started. This is why I try to avoid drugs as much as possible.
I can share my anecdotal N=1 results and while I have done nothing other than introduced rapamycin (6mg/week) and acarbose 6 months ago both biomarkers for serum lipids and blood sugar decreased from baseline. I don’t know what effect would acarbose have on fasting glucose, which decreased too and so did my HBA1C. It might be my personal biology or what MB stated in several papers that both lipids and sugar dysregulation is therapeutic effect and/or temporary as both sugar and lipids were dysregulated at 3 months into rapamycin.
My lifestyle is quite sedentary but I try to get 30 minutes of exercise every morning and take bike to work which is another 30 minutes plus some 7000 steps I make walking the dogs. My diet is far from perfect but I have been practicing 10% CR and started this rapamycin journey with a low bodyfat to begin with.
I had many of the same thoughts and ended up concluding that the simple solution is probably best: just eat less food (i.e. fast/CR). Rapamycin promotes metabolic pathways that are predominantly active when fasting, and these pathways (such as gluconeogenesis) are maladaptive in the fed state.
I agree with this (not using drugs). Most people that have a lot of trouble are pushing their luck on dosage. I found when I reduced my dosage to a lower level and used dosing every two weeks things smoothed right out. You may have no trouble at all and if you do you can quit.
Not medical advice.
These are my thoughts. My initial interest in rapamycin was obviously healthspan/lifespan. I was taking my time starting it until I recently read about the possibility it might rest the “set point” after weight loss. I’ve struggled with my weight most of my life. Recently lost over 70lbs and don’t want to gain it back. Maintenance has always been a struggle for me in the past so this set point theory with rapamycin is extremely appealing to me. I’ll definitely be giving rapa a try. Hopefully, I’ll get lucky and fall into the group of people that don’t require medication for ldl and a1c. We shall see
Very good point. If you eat a normal diet and do not fast, that could be the reason why LDL and HBA1C could increase. I have not been fasting at all.
My father fasts OMAD and has just started Rapa. However he already has high LDL but it will be interesting to see if it gets worse and what will happen to his blood glucose.
Yes… rapamycin induces “benevolent” diabetes similar to starvation, during which skeletal muscle develops insulin resistance so that blood glucose can be reserved for the brain. This may be fine during genuine fasting, but when induced by rapamycin can render the body unable to handle the surge in blood glucose after meals.
When I took my first dose of 1mg rapamycin (with 600mg berberine), I tried to avoid any spikes in blood for the day by eating a vegan keto diet, where many calories come from fat (lots of high fiber nuts, oats, veggies for SCFA). Ideally I want to do a full fast, but find it really hard to go an entire day without food, so this was the next best thing in my mind. I normally eat a high carb, fruit based diet with good amounts of meat.
When I tried the OMAD diet, I found that I had a habit of eating extremely high glycemic index foods as I try to pack in a days worth of calories into the 1hr feeding window, leading to massive spikes in blood sugar that could be potentially detrimental when combined with rapamycin. Hopefully your father has a better OMAD protocol than the one I practiced.