Thanks for the great idea!
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From: https://www.pnas.org/content/115/43/10836 (Bruce Ames)
Taurine (2-Aminoethanesulfonic Acid).
Taurine is another example of a conditional vitamin because it is synthesized by animals (including humans), but not in sufficient amounts. It has been shown to be important in preventing numerous health problems, such as CVD, brain function, diabetes, and mitochondrial diseases, as summarized below. Because of taurine’s extensive involvement in health problems that lead to long-term damage, it is proposed here that it is also a longevity vitamin.
The synthesis of taurine involves cysteine decarboxylation and sulfhydryl oxidation. The rate of its biosynthesis is species-dependent, with a low level in humans, compared with rodents (which led to the suggestion that supplementation might be beneficial) (49). It is located in the cytosol and in mitochondria and it is present in virtually all human tissues at millimolar concentrations; it is especially high in electrically excitable and secretory tissues and in platelets. A 70-kg human contains about 70 g of taurine (50). An excellent review of all of the earlier work on taurine is available in Huxtable (50). Most of taurine is acquired from the diet, mainly from fish and other seafood, seaweed, eggs, and dark-meat poultry (51).
Taurine is particularly important in the mitochondria, where it is present as 5-taurinomethyl-uridine in tRNA-leu and tRNA-trp, and as 5-taurinomethyl-2-thiouridine in tRNA-glu, tRNA-gln, and tRNA-lys. In all five tRNAs, it is located in the wobble position, where it functions to read accurately alternate codons in the mitochondrial genome (52). A taurine modification defect in mitochondrial tRNA is associated with the mitochondrial diseases MELAS (mitochondrial encephalopathy, encephalopathy, lactic acidosis, and stroke-like episodes) and MERRF (myoclonus epilepsy with ragged-red fibers) (52), suggesting causality, and also that a taurine deficiency could result in the same diseases. Because of the involvement of mitochondria in energy production, there has been much interest in taurine in sports medicine in humans with reference to exercise-induced fatigue and recovery, as has been reviewed previously (53). In addition, a strong case has been made that taurine is the main buffer in mitochondria (54) and that it moderates mitochondrial oxidant production (55).
Another possibly important function of taurine is its detoxification of chloramine (a very toxic membrane-soluble oxidant) via its conversion to taurine-chloramine (56, 57).
Examples of several important insidious long-term pathologies that taurine would protect against are: CVD, brain dysfunction, and diabetes. Taurine effects on CVD have been examined by numerous RCTs and have been reviewed previously (51). Taurine supplementation lowers blood pressure, improves vascular function, and raises plasma hydrogen sulfide levels as shown in a recent RCT with prehypertension patients (58). Taurine consumption was the most significant factor associated with reduced risk of ischemic heart disease (IHD) in two international epidemiological studies of CVD in 61 populations (25 countries; n = 14,000): Japanese people in Okinawa had the highest taurine dietary intake and the lowest incidence of IHD and longest lifespan. In contrast, Japanese immigrants in Brazil who eat little seafood, but more meat and salt, had a 17-y shorter lifespan as a consequence of a very high IHD mortality (59). Other human clinical studies showed that taurine decreases platelet aggregation, serum cholesterol levels, LDL/triglyceride levels, and enhances cardiac function (60).
Taurine plays an important role in brain development, including neuronal proliferation, stem cell proliferation, and differentiation; it has no toxic effects in humans (61). It is a neuromodulator in the central nervous system: it activates the GABA- and glycine-insensitive chloride channel and it inhibits the N-methyl-d-aspartate receptor. It is also neuroprotective and has a role in neural development and neurogenesis; it was shown in an RCT that symptoms of psychopathology were improved by its administration in patients with first-episode psychosis (62).
Diabetic remediation by taurine has been reviewed previously (63, 64). Its supplementation remediates diabetic pathologies, including retinopathy, neuropathy, nephropathy, cardiopathy, atherosclerosis, altered platelet aggregation, and endothelial dysfunction (65). In patients with type 1 and type 2 diabetes the taurine transporter is up-regulated in mononuclear blood cells, indicating that increased levels of taurine are sought by the cell (66, 67). In rats, taurine reduces oxidative stress caused by diabetes (68, 69).
Taurine is important for fetal development, because the human fetus cannot synthesize taurine, which is provided by the mother via the taurine transporter, and it is necessary for organ development and protects against development of type 2 diabetes (70). Therefore, taurine is also a survival vitamin. Transport of taurine (53) is required for normal development of numerous fetal tissues in several experimental animals. Taurine functions as an osmolyte; it was shown to be important in that respect in a variety of species, including rodent investigations that are consistent with the above results on humans (70, 71) (SI Appendix, SI-4 Conditional Vitamins).
Taurine is well established as an important conditional vitamin for survival functions and for healthy longevity in both humans and experimental animals. I expect that a large class of new conditional vitamins will be discovered. Possible candidates are lipoic acid, ubiquinone, and carnitine.
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I didn’t see Nutricost tested on the Taurine page on consumerlab. Where did you see that?
I like Nutricost as well. I thought originally they short-changed the amount you get, but it turns out I was wrong. Nutricost should be fine.
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This one doesn’t get talked about enough, although I think it’s generally that taurine reacts with HOCl/hypochlorous acid to form taurine chloramine. HOCl is produced by our neutrophils via the enzyme myeloperoxidase (it’s also the active species in bleach), and is quite reactive and toxic, whereas taurine chloramine is less reactive and has anti-inflammatory activity.
HOCl also inhibits PARP activity, which plays a role in DNA repair, and appears to correlate with species longevity. Its ability to chlorinate bases might also be problematic.
The presence of increased levels of chlorinated nucleosides in the inflammatory exudate of humans (30) and rats (31), and elevated levels of 5ClU in atherosclerotic plaques compared to healthy arteries (32) suggest that the chlorination of nucleic acids may be relevant under pathological conditions.
Various cultured mammalian cells can incorporate 5CldC into genomic DNA (54). Similarly, 5ClU can be readily converted to 5CldU by thymidine phosphorylase, before incorporation into DNA via the action of DNA polymerase (55, 56). 5CldU is also formed from 5CldC via deamination mediated by cellular enzymes (54). This is significant because 5CldU is a well-established thymidine analogue mutagen that mispairs with guanosine, causing G·C → A·T and A·T → G·C transitions (57), and can induce sister chromatid exchanges (55, 56). 5CldC also perturbs epigenetic signals by mimicking 5-methyl-cytosine and enhancing the binding of methyl-CpG binding proteins (58). This is significant as methylation of cytosine occurs predominantly in CpG dinucleotides (where a cytosine nucleotide occurs next to a guanine nucleotide in a linear sequence) in islands of concentrated CpG sequences located in promoter regions. Methyl-CpG binding proteins facilitate the recruitment of histone modifying enzymes, which triggers a cascade of events resulting in gene silencing (e.g., of tumor suppressor genes) (59, 60). HOCl can preferentially chlorinate cytosine at CpG dinucleotides (61). In addition, treatment of cells with 8ClA results in the accumulation of 8-chloro-ATP and incorporation of this modified base into the cellular mRNA (62). This leads to the inhibition of mRNA synthesis and eventual cell death via apoptosis (62). [ref]
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I see some discussion of Nutricost re: reputation/quality of their product.
I’ll just mention that I had a bad experience with them.
I had been buying their 25-gram container of TUDCA (and others of their products) roughly every 3 weeks for a long time. A few months ago, the TUDCA was quite obviously different from before. The powder didn’t dissolve nearly as well in water and tasted different, as if someone tried to give it a grapefruit flavor. I saw similar complaints around that time in review on Amazon of that product. Their customer support at first was very friendly and quick to respond, but when I asked whether they could provide me with a third-party analysis that confirms the identity of the product and its purity, given that they advertise “third party-tested for purity and safety”, they stopped responding.
Disappointing. I stopped buying their products.
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Great video on Taurine by Physionic.
Key takeaway is taurine can cause mild dyslipidemia. It seems that maybe disabling MTOR will have that effect.
It seems like things that increase autophagy may increase lipids as a byproduct. But that’s just a WAG on my part.
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That makes sense as I believe that cholesterol is the medium of transport to remove the waste products as a result of autophagy.
Makes me wonder though if very low cholesterol indicates a low level of senescent cells requiring autophagy, or as a result of pharmaceuticals we are impeding the autophagy process by limiting the means of transport of waste.
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I think 7-8 g may be a little overkill unless in people that are very old or heavy. 3 g daily appears to be enough to double blood taurine levels in old women, which would put their levels at similar to those of young adults. Effects of Dietary Taurine Supplementation on Blood and Urine Taurine Concentrations in the Elderly Women with Dementia - PubMed
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Its still one of these things where you are trying to fix the symptoms rather than the cause. In itself useful, but ideally fix the cause.
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HOW? (to fix the cause)
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AIUI there are two main causes. One is the inefficiency of mitochondria, the other (which is affected also by the first) is the shortage of nuclear Acetyl-CoA.
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Good point, but I take taurine in my coffee. Coffee hinders the absorption of Taurine to a point so I am taking extra to compensate. However, taurines effects are also synergistic with caffeine according to some studies.
Highlights
Caffeine and taurine (C&T) synergistically relieve sleep-deprived (SD) fatigue.
C&T improve SD-induced cognition deficits and locomotor imbalance.
C&T act as multiple roles in the actions against both central and physical fatigue.
Anti-fatigue effect of C&T is closely related to oxidative stress, inflammatory factors.
https://www.sciencedirect.com/science/article/pii/S1756464622003681
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It turns out Energy drinks like Red Bulls and Monsters have been onto something for years.
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What is your evidence that mitochondrial inefficiency drives the age-related decline in taurine levels? I dug around and could find no evidence that mitochondria are involved in taurine biosynthesis. It’s certainly important in mitos: it’s needed for a posttranslational modification of mitochondrial tRNAs’ uridines at the anticodon wobble position for proper anticodon–codon interactions to allow ribosomes to synthesize mitochondrial-encoded proteins, and the Yadav paper shows that TAU supplementation restores levels of mitochondrial electron chain complexes. But all that shows mitochondria are impaired by low TAU, not that impaired mito drive low TAU in the first place.
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I don’t have any specific evidence on this. Obviously taurine metabolism will require some enzymes to be produced. My hypothesis essentially rests on the failure to produce proteins in either the right quantities or at all (I think it is probabilistic).
It remains, however, that taurine levels will be a secondary effect of some primary cause whether that is the failure to produce specific proteins or something else.
What’s his evidence for this? All the trials I could find reported that taurine supplementation either reduced or had no effect on LDL-C.
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The evidence was stated in the video with his references. There may be contradictory evidence from other sources.
Others here may find this interesting:
Reporting on a Nine Month Self-Experiment in Taurine Supplementation
Today’s post is a report from the community on the impact of taurine supplementation on a few biomarkers of interest. Taurine is a dietary amino acid, and circulating levels of taurine influence any number of biological processes. Taurine levels decrease with age in a variety of species; in humans circulating taurine is halved by age 50. You might recall that supplementation with taurine was demonstrated to modestly extend life in mice and improve health in old non-human primates. This may be largely due to enhanced performance of the antioxidant glutathione, and you might recall that other approaches to upregulation of glutathione activity have been shown to produce benefits in old humans, dampening oxidative stress and associated inflammation.
A few human clinical trials of taurine supplementation have been conducted, but the results are not all that conclusive, other than to demonstrate that this form of intervention is very safe. So why not give it a try, and see what results? If you look back in the Fight Aging! archives, you’ll find an outline for a self-experiment with taurine supplementation. Taurine is cheap and readily available as as a supplement, and inexpensive blood tests can be used to assess outcomes. Here, the self-experimenter chose to focus on phenotypic age and the biomarkers used to construct this assessment of phenotypic age. Only one marker of oxidative stress was used, an assessment of circulating oxidized LDL particles.
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The self-experimenter was a vegetarian in his 50s.
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3 grams per day of taurine was taken orally for 9 months.
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Diet and lifestyle was kept consistent, as much as possible in a busy life.
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Phenotypic age acceleration: -9.00 to -10.85 years
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Albumin: 4.1 to 4.3 g/dL (reference range is 3.6-5.1 g/dL)
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Creatine: 0.72 to 0.65 mg/dL (desired range is 0.70-1.30 mg/dL)
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Fasting Glucose: 93 to 90 mg/dL (desired range: 65-99 mg/dL)
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C-Reactive Protein: 0.30 to 0.34 mg/L (considered low risk under 1.00 mg/L)
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Alkaline Phosphatase (ALP) 53 to 50 U/L (reference range is 35-144 U/L)
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Lymphocyte Percentage 33.1% to 40.7% (normal range is 20% to 40%)
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Mean Cell Volume (MCV): 87.8 to 88.6 fL (desired range is 80.0-100.0 fL)
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Red Cell Dist Width (RDW): 13.3% to 13.5% (desired range is 11.0-15.0%)
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White Blood Cells (WBC): 4.8 to 3.9 Thousand/uL (reference range is 3.8-10.8 Thousand/uL)
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Taurine: 43.6 to 114.9 umol/L (reference range is 29.2-132.3 umol/L)
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Oxidized LDL: 105 to 82 ng/mL (reference range is 10-170 ng/mL)
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LDL and HDL cholesterol levels were largely unchanged.
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Absolute Lymphocytes: 1589 to 1587 cells/uL (desired range is 850-3900 cells/uL)
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Absolute Monocytes: 312 to 269 cells/uL (desired range is 200-950 cells/uL)
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Absolute Neutrophils: 2832 to 1981 cells/uL (desired range is 1500-7800 cells/uL)
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Lymphocyte: Monocyte Ratio: 5.1 to 5.9
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Other complete blood count statistics were largely unchanged.
Going from the data provided, the supplementation successfully increased a low circulating taurine level to a high circulating taurine level as intended, and modestly reduced phenotypic age. The most interesting change seen in the biomarkers making up the phenotypic age metric is the increased lymphocyte percentage. This change was entirely due to the absolute neutrophil count decreasing from 2832 to 1981 cells/uL, while other absolute counts for white blood cell types remained much the same. Neutrophil counts can be raised temporarily by transient infection or inflammation, but per the self-experimenter, ~2800 had been a fairly consistent level for absolute neutrophil count for some years prior to this self-experiment. The observed reduction is thus a novel change, and likely due to the taurine supplementation.
A second interesting point is the reduction in oxidized LDL, a marker of oxidative stress and also a contributing factor in the development of atherosclerosis. As a sidebar, also note the low creatine levels, characteristic of vegetarians since dietary creatine is mostly found in meat.
The modestly favorable results shown here form only a single data point and should be taken as an anecdote, of course. It would be interesting to see the results of a few hundred participant clinical trial of taurine supplementation that focused on the various modern approaches to measuring biological age, such as epigenetic clocks. One shouldn’t expect there to be a rush to do this, however. Trials are expensive, and there is little spare funding to be found in the business of selling well-established supplement compounds. At the end of the day modest effect sizes are modest effect sizes, and we’d like to focus on better approaches to the problem of aging - but if the intervention is both very cheap and very safe, then it may well be worth the effort to further establish the degree to which it can be useful.
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All the more reason to supplement Taurine. Based on this N=1 analysis, I’d say the experiment is a success for this individual. It also shows how effective 3 g daily is. I’ll still strive for 4-5 g daily intake.
I would like to note that the biggest reason I take Taurine is it’s abilities as a senomorphic. Unfortunately, this data point did not test senescent cell load.
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