Just got the results back from my recent LifeExtension “Male Panel” that I also did in June last year before I started semaglutide. I’ve had many of these component tests at various points throughout the year but it’s nice to be able to compare the exact same battery of tests using the same lab.
Several high points -
fasting glucose from 104 mg/dL to 83 mg/dL
A1C from 5.3% to 4.9%,
hsCRP from 1.36 mg/L to .45 mg/L
uric acid from 7.6 mg/dL to 5.4 mg/dL
insulin from 20.5 uIU/mL to 15.9 uIU/mL.
Homocysteine is up a bit, from 9.6 umol/L to 11.4 umol/L.
Given the amount of abdominal fat that I lost, I was surprised that my estradiol has increased somewhat, from 20.4 pg/mL to 27.6 pg/mL.
Another interesting note - Being overweight/obese is a well-known risk factor for Vitamin D deficiency. For as long as I’ve been testing my Vitamin D (about 4 years), it’s been a struggle to keep it above 30 ng/mL, even with relatively high dose supplementation (50,000 IU once weekly). Last summer’s test showed 31.5 ng/mL. Without any supplementation, I’m now at 34.7 ng/mL.
The aim of the present study was to determine whether treatment with liraglutide, a glucagon-like peptide 1 (GLP-1) receptor agonist, would alter mammalian target of rapamycin complex 1 (mTORC1) signaling and/or…"
What about this study SHC posted in a previous post. Is no one concerned about potential mTOR-activation/interactions with Rapamycin?
It seems like it would be relatively easy to manage the dosing schedule of rapamycin and liraglutide… at least if taking both on a weekly schedule.
In pharmacokinetic studies, liraglutide exhibits its maximum concentration after 8 to 12 hours, and its half-life is 13 hours after a single injection. Source: Liraglutide (Victoza) - PMC
So - perhaps, assuming a weekly dose, take liraglutide on day 4 or 5 after taking rapammycin - when the rapamycin / mTOR inhibition has largely receeded, and then have 2+ days after dosing liraglutide before the next rapamycin dose?
Thanks Rapadmin, that sounds like a reasonable approach. Admittedly this is the first time I’m looking into this topic at all, so I’m quite uninformed. I also don’t know at all how the side-effects/safety profile/accessibility of Liraglutide compares to that of other GLP-1 receptor agonists.
However with regard to Semaglutide, SHC commented that the half-life “seems to be as long as a week”. I have not looked into any studies concerning the potential effects of other GLP-1 receptor agonists than Liraglutide on mTOR signaling. But if they may also activate mTOR, using Semglutide in combination with Rapa as was suggested in this thread, may potentially result in some undesired interactions? At least it may be something to look into a bit more before jumping on that bandwagon?
Me either - definitely something we should look into prior to taking the drug if we are thinking of using it. And your other points also are good. I haven’t researched this drug (or class of drugs) but have heard all the amazing results that the medical press is reporting, and the studies of great results for lowering weight relatively easily and substantially.
How much does semaglutide decrease their pace of aging via methylation tests? If what you say is true, this is HUGE… Does concurrent metformin use help?
do the different peptides affect their pace of aging? One of them is a GH/IGF1 agonist…
I got my first package yesterday. 7mg first dose. I still feel some hunger/desire to eat but it’s not as craving as it usually is? need to wait for the rest of the day to see how things go…
@AlexKChen Do you keep an eye on biomarkers and use the Phenotypic Age Calculator - and will you do so again after adding Semaglutide? Are you not worried about potential drug interactions (thought you are taking Empagliflozin/Canagliflozin, Acarbose, Metformin and Rapa, is that correct? Do you take all three anti-diabetic drugs daily or intermittently, if I could ask?) Thanks.
I don’t do blood tests very often ($$). In general I have super-youthful values and not much changes them (it’s the more expensive markers, like epigenetic age, that are more informative).
There are no bad interactions between the standard ITP-approved classes of longevity drugs. More synergistic than bad.
Ok with 7mg oral semaglutide I still definitely have an appetite. Maybe it isn’t as strong as it used to be (enough to drink 3 entire liters of nut milk/day) - I’ll evaluate the rest of the night
Just curious, why do you drink nut milk instead of eating whole nuts? Seems like a waste to throw away the fibers. I would think that whole nuts are more filling than nut milk. Also, are you trying to lose weight?
@AlexKChen Thanks for your feedback. The risk to develop an infection when combining Rapa with an SGLT2-inhibitor seemed to increase for me - so I had to stop taking the SGLT2-inhibitor for several days after taking Rapa. I’d like to add back in Metformin, and potentially even acarbose. But I’m not sure how to combine the three, as I’m wondering if it may make one more prone to develop uti’s for example.
Plus, already being low in weight: would it not increase the risk to develop hypoglycaemia and/or metabolic acidosis (albeit people with T2D seem at more risk of that, but still I’m concerned about combined antihyperglycemic therapy)?
Weight is a proxy for reducing calorie consumption - I do have habit of overeating even if it’s entirely healthy food. I’m genetically thin like many Asians but this still doesn’t prevent me from needing to reduce cals
I finally fell below 100lbs for the first time since July
You are right. This is an issue I’ve long ran into. Prior to starting CR I used to have a BMI of just below 18, and received quite some backlash for that until my fat percentage was measured and it turned out to be in the higher range. (Which I had long thought, as I was pretty ‘plump’. And on the Asian side of my family no person has a BMI of 18). While doing mild CR my BMI is much below 18.
Several other studies have found that at the same BMI, Asians have higher risks of hypertension and cardiovascular disease than their white European counterparts, and a higher risk of dying early from cardiovascular disease or any cause. (2–4)
[…]
Should BMI or Waist Circumference Cut Points Be Ethnicity Specific?
These findings have touched off international debate about whether the cut points for overweight and obesity should be lower for Asians than for other ethnic groups. (11) In 2004, the World Health Organization weighed the evidence on Asians higher risk of weight-related diseases at lower BMIs. It declined to set different cutoff points for Asians, citing a lack of agreement among researchers as to what those lowered cutoffs should be. (12) With the emergence of more research, however, several groups have begun to set lower cutoff points for BMI and abdominal obesity metrics among Asians. (13,14) China and Japan define overweight as a BMI of 24 or higher and obesity a BMI of 28 or higher; in India, overweight is defined as a BMI of 23 or higher, and obesity, a BMI of 27 or higher. And the International Diabetes Federation now includes ethnic-specific criteria for the definition of abdominal obesity. (14) Ethnic Differences in BMI and Disease Risk | Obesity Prevention Source | Harvard T.H. Chan School of Public Health
took another 7mg dose earlier today. It does not completely eliminate/suppress hunger. I just bought and ate two boxes of blueberries. But maybe it’ll allow me to be content with those 2 boxes.
I did get ubereats food earlier today.
I have lost some weight the past few weeks w/o it, I’ll see if I can get down to 95lbs in two weeks.
What’s your reasoning for wanting to reduce your body fat % from 10% to 5-7%? Are you concerned about the negative effects of having a very low body fat %?