Generally speaking, there are supplements that are water soluble and supplements that are fat soluble and there are few that are neither, but manage to have some bioavailability.
I take too many supplements to take them all at meal time so I try to spread them out during the day. Since I only eat two meals a day starting at about 1 p.m., I take most of the water-soluble ones, like B vitamins, and others in the morning.
Some supplements, especially amino acids like l-tryptophan and l-tyrosine should be taken on an empty stomach to be effective.
If you take a magnesium supplement like magnesium glycinate or magnesium l-threonate they are best taken at bedtime on an empty stomach.
I recently changed from losartan, which is a very good medication, to telmisartan
which may be even better because of its dual effect of also being good for insulin resistance which is a problem as we get older. Also, if you haven’t tried pantethine it might lower your lipids even more. I was surprised at how effective pantethine was a lowering my lipids
Telmisartan could be an alternative treatment option, with dual benefits for diabetes mellitus
As telmisartan is reported to have a partial PPARγ-agonistic effect, the drug can regulate glucose and lipid metabolism, and improve insulin resistance" https://www.tandfonline.com/doi/full/10.2147/DMSO.S265399
Pantethine is a non-rate limited form of Vitamin B5 which operates primarily as a coenxyme-A precursor. I can, however, lead to bleeding lasting longer.
I like it personally for its ability to accelerate the conversion of acetaldeyde to acetate.
I recently had a tooth extracted while taking pantethine. Had bad pain for the following week. Went back to the dentist to have the stitches removed, and he said ‘It hurt for a week? Not supposed to happen.’ I had a ‘dry socket’. Some problem with clotting. Anyway, he did something to remedy the situation that required being sewed up again, and now hopefully no additional problems.
Only by ‘luck’ had I stopped pantethine a few days prior to my return visit. (And hopefully soon enough to prevent a second failure.) The luck was that I had banged myself in a couple place while hiking and the bruising was all out of proportion to the damage.
I had an another extraction back in February before starting pantethine that went fine.
I did a blood test yesterday for lithium. I have been varying my supplementation with a view for hitting about 50 micro molar. If others could do this and report back that would be useful. I will report the results when I get them.
@Jonas, be careful with lithium, it’s a psoriasis trigger. Mainly at therapeutic doses for bipolar disorder, but other evidence that inflammatory reaction is not always dose-dependent. Inositol seems to reverse it.
Lithium I noted recently is in fact an inhibitor of some of the SLC13 family of transporters. In particular it can at high enough levels block citrate (and other tricarboyxlates and dicarboxylates) from entering the cell. However, at the longevity levels it does not have this effect to any substantial amount).
Millimolar concentrations of Li+ resulted in decreases in apparent succinate affinity and in the I maxsuccinate. Furthermore, lithium inhibition under saturating sodium concentrations showed hyperbolic kinetics, suggesting that one of the three cation binding sites in NaDC-1 has a higher affinity for Li+ than Na+. We conclude that NaDC-1 is an electrogenic anion transporter that accepts either Na+ or Li+ as coupling cations. However, NaDC-1 contains a single high affinity binding site for Li+ that, when occupied, results in transport inhibition, which may account for its potent inhibitory effects on renal dicarboxylate transport.
You do get about 0.6-1 millimolar concentrations of lithium when medicating for mental health reasons.
This would explain why higher concentrations would cause kidney disease as it would prevent citrate from getting into the cell via the SLC13a series of transporters some of which are expressed in kidney tissue.
What I find particularly interesting is SLC13A5 (which is the main citrate transporter from plasma) is mainly expressed in the brain and liver.
What I wonder about in the other cells is whether citrate enters them through one of the other transporters, an unidentified transporter or whether citrate concentration is maintained via a transport out of the cell being blocked as a result of higher citrate concentration outside the cell.
I know it has an effect because of the experimental results, but I am not quite sure of the mechanism.
Having looked at this I am, however, thinking of dropping back from 15mg a week to 7mg a week. (Lithium). I will see what the results say.
I’m interested in trying low dose lithium for the mental/longevity benefits. Especially the first. I tend to get angry/annoyed etc, it might be because some terrible Eastern European genetics. My trigger is mostly “people being wrong” on the internet. I’m glad the cardiovascular thread has died down. But better mood is always better.
It helped Peter not ‘be an asshole’ as much, according to his wife
He managed to drop the F-bomb in the same video.