Introducing DURK & SANDY’S “ESSENTIALS,” including their …

New Taurine & Bromine

Designing Your Life Extension Program:
Why NO LE Program Should Be
Without Very-Low-Cost High-Benefit TAURINE

By Durk Pearson & Sandy Shaw

Our New TAURINE Formulation Also Contains the Essential Trace Mineral BROMINE (as Bromide)

Natural TAURINE-BROMINE Compound Made in Your Body Is Potent Antimicrobial AND Antiinflammatory

T here are a very large number of dietary supplements on the market. The choice is certainly there, but since nobody can (or should) try to take everything, it leaves the difficult problem of picking and choosing the supplements that fit within your budget AND represent the most important elements to include in your personal program to increase health and lifespan. We hope to make this a little bit easier by identifying specific supplements—that we call ESSENTIALS—for their exceptional importance in a program (including ours) for health and long life. These are basic supplements for any well-designed health program and, as you will see, you don’t have to spend a lot for the ESSENTIALS.

The amino acid TAURINE is one of our ESSENTIALS, and represents a great value: for a low price, you get a nutrient that provides a dazzling array of health benefits throughout your body and brain.1 Plus, we include BROMINE (in the form of bromide), long suspected of being an essential trace element3 and now definitely shown to be essential,4 as it is required for proper assembly of collagen IV scaffolds crucial for organogenesis (development of organs). One paper notes that BROMINE deficiency “may be relevant to BM [basement membrane] alterations observed in nutritional and smoking-related diseases.”5 Another paper names diseases in which collagen IV scaffold is reported to be dysfunctional.6 More on BROMINE later in this article. Here we describe some of what researchers have uncovered about TAURINE.

To your health!

Taurine has been the focus of a considerable body of research. From 1927 to date, there have been 16,221 papers published on taurine. In 2013, 560 papers on taurine were published, 493 papers in 2012, 414 papers in 2011, 471 in 2010, and to date (July 14, 2014), 264 papers have been published with about another 5 1⁄2 months left in 2014.

TAURINE and Glutamate Neurotoxicity

A recent review paper1 provides a 13-page description of many of taurine’s effects, with 171 references. The authors start by describing a puzzling observation, that the administration of glutamate given at neurotoxic doses caused damage to every part of the central nervous system but that in the mouse neonatal retina bathed in glutamate, only the inner layers were seriously affected. The authors suggest that it is taurine (found in high concentrations in the retina) that is a likely source for at least some of the protection against high dose glutamate toxicity. As they point out, quantitative analysis has shown that in extracts of whole ocular tissue of the rat eye, taurine was the most abundant amino acid in the retina, vitreous, lens, cornea, iris, and ciliary body.

Remarkably, in the normal (control) retina, taurine exceeds the concentration of each of the other amino acids by tenfold or more. Experimental studies of primary ­neuronal cultures from the fetal rat brain have shown that taurine inhibits glutamate toxicity by a number of different mechanisms.1

The reviewers assert: “[b]ecause it is one of the few amino acids not used in protein synthesis, taurine is often referred to as a ‘nonessential’ amino acid, or more generously as a ‘conditionally essential’ amino acid. Considering its broad distribution, its many cytoprotective attributes, and its functional significance in cell development, nutrition, and survival, these are clearly misnomers. Taurine is undoubtedly one of the most essential substances in the body.”1 [Emphasis added.]

TAURINE Promotes Neurogenesis

One of the most important effects of taurine is its crucial role in neurogenesis, the production of new neurons that takes place only in specific brain areas of adult mammals throughout life.1 The review describes the function of taurine in this process: “[o]f particular interest is the fact that within the subventricular zone of the cultured adult mouse brain, taurine activates stem cells and neural precursor cells to differentiate into neurons rather than astrocytes [another type of brain cell]. The subventricular zone is one of the few regions in the brain in which neurogenesis continues throughout adulthood, and the cells from this region can proliferate and migrate via the rostral migratory stream to the olfactory bulb where they differentiate into neurons. Considering the high taurine content in the adult [mammalian] olfactory bulb, it is likely that taurine is an important factor for neurogenesis.” Further substantiation for this view is provided by in vitro studies showing that taurine promotes putative rod and cone photoreceptor development.1

TAURINE May Be Cytoprotective Against Amyloid Beta to Ameliorate Development and Progression of Alzheimer’s

Mounting evidence points to a causative role of amyloid beta accumulation in Alzheimer’s disease; it has also been linked to other neurodegenerative disorders such as Huntington’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, AIDS dementia complex, and brain cell death as a result of excitotoxicity, hypoglycemia, neurologic trauma, stroke, and epilepsy.6 “We show that taurine, a beta-amino acid found at high concentrations in the brain, protects chick retinal neurons in culture against the neuro­toxicity of amyloid beta and glutamate receptor agonists.”6 The authors propose that selective pharmacological modifications such as those observed for taurine might offer an “interesting therapeutic approach” in many neurological disorders, including Alzheimer’s.

The source of the neurotoxicity associated with amyloid beta is, at least in part, due to excitotoxicity caused by overactivation of glutamate receptors.7 Experiments in rat neuronal cultures showed that taurine could block the neurotoxicity of amyloid beta (which caused about 45% neuronal cell death in control cultures) even at the lowest concentration tested (0.5 µM).7 Taurine is an agonist of (activates) GABA receptors. The researchers added a GABA receptor antagonist to the cultured neurons treated with amyloid beta and taurine. They found that the GABA antagonist abolished the protective effects of taurine, confirming that the taurine protection was due to its activation of GABA receptors. These results show that overactivation of glutamate receptors are likely to play an important role in the neurotoxic effects of amyloid beta. The researchers also showed, using the same cell culture model, that taurine could block the neurotoxicity of glutamate added to cortical neurons and, again, addition of the GABA receptor antagonist abolished the protective effects of taurine against glutamate excitotoxicity.

The researchers7 concluded that GABA receptors play an important role in preventing amyloid beta neurodegeneration and “[m]ore importantly, they [the experimental results] indicate that the possible efficacy of taurine in the clinical treatment of AD [Alzheimer’s disease] should be further investigated.”

TAURINE Protects Against Age-Associated Decline in Kidney Function, a Major Source of Morbidity and Mortality

Decline of kidney function is a major accompaniment of aging and is an important risk factor for mortality. Failure of the kidneys can be corrected only by dialysis or by kidney transplants, both of which are life shortening and cause considerable loss of quality of life. Dialysis, for example, is not only unpleasant but it does not provide results that duplicate what functioning kidneys do. Acute kidney injury frequently accompanies sepsis, toxic injury, and shock.8 Chronic kidney damage is the major reason for requiring dialysis in end-stage renal (kidney) disease (renal nephropathy) that often occurs as a life-threatening complication in diabetes mellitus.

In an analysis of 942 community-dwelling elderly adults (mean age: 75 years) participating in the InCHIANTI study, researchers examined the predictability of survival based on different equations for estimating kidney function.9 The results showed that kidney function was a strong independent predictor of death over a six-year followup in this group, thought to be representative of the Italian population. Other studies also show that mild to moderate kidney dysfunction is associated with risks of all-cause mortality and cardiovascular disease, both morbidity and mortality.9 “… there appears to be little question that the prevalence of CKD [chronic kidney disease] is high in elderly people and is strongly associated with risk of death.”9

Mechanisms of TAURINE in the Kidneys

• Antioxidant Protection The major mechanism of taurine’s antioxidant protection against kidney damage was proposed to be taurine’s reactions to scavenge hypochlorous acid (BLEACH!), a potent oxidant metabolite of myeloperoxidase.8 The product of taurine’s chemical interaction with hypochlorous acid is, interestingly, taurine chloramine, which is both an antibacterial and an inflammatory.12,24 (Similarly, taurine chemically interacts with hypobromous acid (another oxidant metabolite of myeloperoxidase) to form taurine bromamine, also with antibacterial and antiinflammatory properties).

• Protection Against Ischemia-Reperfusion Injury As with other tissues subject to ischemia (reduction of blood flow and, hence, reduced oxygen supply) and then reperfusion (restoration of blood flow), the kidneys can be severely injured by ischemia followed by reperfusion. Experimental studies in cell cultures and animal models of ischemia-reperfusion have demonstrated protective effects by taurine. For example, a study of diabetic nephropathy in a type 2 diabetic rat model8C examined rats divided into three groups: a control group, a group treated with high glucose levels (30 mM) to induce a diabetic state (diabetic controls), and a diabetic group treated with taurine (200 mg/kg/day for 20 weeks). (This dose is very roughly equivalent to 1 gram of taurine per day for an adult human.) Markers of diabetic nephropathy include increased expression of growth factors such as vascular endothelial growth factor and changes in the kidney glomerular basement membrane, which thickens in diabetic nephropathy. There is also increased oxidative stress and fibrosis.

Results included significantly decreased fasting blood glucose levels in the taurine-treated diabetic group as compared to the diabetic controls; blood glucose levels were significantly increased in the diabetic controls as compared to the normal controls. Interestingly, adiponectin (which increases insulin sensitivity) was significantly decreased in the diabetic control group compared to the normal control group and increased in the taurine-treated diabetic animals (though not to a statistically significant level). “The thickness of the GBM [glomerular basement membrane] was increased in the diabetic control group compared to the normal control group, and significantly decreased in the taurine-treated diabetic group, approaching that of the normal control group.” Urinary malondialdehyde (a lipid peroxidation product of oxidative stress) was lower in the taurine-treated diabetic group than the diabetic control group.

• Protection Against Fibrosis The protection by taurine against increasing glomerular basement membrane thickness (as seen in the taurine-treated diabetic rats described above) is an antifibrotic effect of taurine. Fibrosis is seen in a great many diseases of aging, such as in the heart following heart attack. Taurine reduced the production of lung fibrosis by radiation in C57/BL6 fibrosis-prone mice.20

The authors8C concluded that taurine is “another candidate for the treatment of diabetic nephrop­athy.” [Emphasis added.] Keep in mind here that taurine is a safe nutrient, widely available and very inexpensive compared to other “candidate” treatments for diabetic nephropathy, which can be a major advantage in hard economic times. You don’t even need a doctor’s prescription—though we suggest that you consult regularly with a doctor knowledgeable about nutritional therapy to help you in keeping track of your results, arranging for lab tests and interpreting them, and to advise you concerning unexpected events (which can happen without warning if you have a serious medical condition such as type 2 diabetes).

• Protects Kidneys from Osmotic Stress, Such as ­Hyperglycemia Taurine is a major regulator of cellular response to osmotic stress (termed “cell volume regulation”) in the kidneys. As such, taurine is importantly involved in protection in the kidneys under conditions of hypo- or hypernatremia (low or high levels of sodium) or when exposed to conditions of hypoglycemia or hyperglycemia. (Interestingly, taurine is involved in the adaptation of fish when they go from fresh water to sea water or vice versa.)8 As shown in Figure 4,8 taurine moves out of cells exposed to hypotonic solutions, while entering cells exposed to hypertonic solutions.

TAURINE Protects the Liver From Acetaminophen-induced Liver Failure

TAURINE Protects the Liver Against Fatty Liver and Against Injury-Induced Development of Fibrosis

Liver Disease Is One of the Leading Causes of Death Worldwide21

Your liver provides an important first level of defense against the damaging effects of drugs, pollutants, toxins, and substances consumed with food or water. As a result, the liver is exposed to a wide variety of carcinogens, mutagens, and other damaging agents that it has to metabolize to a form that can be quickly excreted. That can involve, for example, converting a chemical into a water soluble form for excretion via the urine. Taurine is an important protective substance that helps prevent liver damage from occurring during the performance of the liver’s detoxification function.8D It also helps prevent the development of liver fibrosis and/or fatty liver that can occur as a common response to chronic liver injury.8D,8F The ­researchers8D identified the protective mechanism as being the inhibition of proliferation of hepatic stellate cells which generate the extracellular matrix that makes up the fibrotic tissue in the damaged liver.

Another paper,8E noting the acetaminophen (an anti-pain drug)-induced liver failure that can result from overdose, studied Swiss albino male rats that were treated with acetaminophen (APAP) to cause liver failure following 1, 2, 3, 4, or 5 days of pretreatment with taurine (150 mg/kg body weight) or no taurine. (This taurine dose is roughly equivalent to a little less than one gram per day for an adult human.) In animals receiving APAP but not receiving taurine, liver enzymes (as detected by measurement of serum ALT, ALP, LDH, and NO) were dramatically elevated. These measures were significantly reduced by pretreatment with taurine. APAP was also shown to increase lipid peroxidation in the liver, but this was significantly inhibited by taurine pretreatment. Importantly, liver glutathione levels were rapidly depleted in the APAP treated rats, but taurine treatment before and after APAP administration significantly protected against this effect—apparently by directing cysteine into the glutathione synthesis pathway. The researchers note that CYP2E1 is the form of CYP450 that catalyzes the metabolism of APAP to the liver-toxic NAPQ1, and that taurocholic acid, formed in the body by the reaction of taurine and cholic acid, is a potent inhibitor CYP2E1.8E

Increased levels of TNF-alpha (tumor necrosis factor alpha) play an important role in liver injury, such as that resulting from ischemia-reperfusion and fulminant liver failure. APAP treatment caused increases in TNF-alpha in the experimental rats, but treatment with taurine either before or after APAP administration significantly decreased TNF-alpha as compared to the APAP rats not receiving taurine.

The researchers emphasize that acetaminophen can be used safely for reduction of mild to moderate pain at the normal dose (as specified on the label) but it doesn’t have a large therapeutic index (the ratio of the toxic dose to the therapeutic dose), meaning that it is important not to exceed the recommended dose or to use it chronically. MOREOVER, IT IS IMPORTANT TO KNOW THAT EVEN A SINGLE DAILY ALCOHOLIC DRINK TAKEN IN CONJUNCTION WITH THE REGULAR USE OF ACETAMINOPHEN INCREASES THE RISK OF LIVER INJURY. We suggest avoiding acetaminophen entirely. It is unfortunate that the drug is often combined with hydrocodone in pain killers prescribed by dentists for toothaches!

The researchers8E conclude that: “… taurine deserves further consideration as a potential alternative for preventing liver injury caused by acetaminophen-overdose.” Importantly, acetaminophen-induced liver injury is the most common cause of poisoning requiring hospitalization in the U.S.

TAURINE Protects Against Fatty Liver

A common complication of type 2 diabetes is fatty liver. Taurine treatment protects against the development of fatty liver in hamsters on a high fat/cholesterol dietary regime.8F Interestingly, the LDL receptor gene expression was increased in the hamsters. The LDL receptor is important in transporting serum cholesterol to the liver for its clearance from the bloodstream.

If you are taking a variety of dietary supplements, herbs, and medicinal drugs, we recommend that you have regular lab tests for kidney and liver function to make sure these organs are functioning normally. They are involved in the metabolism and excretion of everything that enters your body in order to maintain blood concentrations of a wide variety of constituents at closely regulated levels. You only get one liver. Unlike the kidneys, where if worst comes to worst you can survive on dialysis (though it really cannot closely mimic what a normal kidney does), you can’t survive without a liver—and getting a liver transplant and the immunosuppressive regime that goes with it is life shortening.

TAURINE and Cardiovascular Disease

Human clinical studies review taurine’s beneficial effects in the treatment of alcoholism, hypertension, ischemic heart disease, atherosclerosis, and diabetic cardiomyopathy.2,2A However, the purported “gold standard”—a long-term randomized double blind trial of taurine and the treatment of one or more of these diseases—has not yet been carried out. The authors of one of the reviews2 note that in the absence of such a trial, taurine cannot be “unequivocally” recommended as a nutritional intervention for the prevention or treatment of cardiovascular disease. As such studies are costly, take several years or more, and have been performed with other important nutrients in a limited number of large human interventional trials without coming to an “unequivocal” conclusion, one doubts very much that such a trial would deliver the desired conclusive proof that everyone seems to be looking for.

Even the much-touted FDA-approved drugs, having undergone large randomized double blind clinical trials in order to receive FDA approval, are rarely conclusive, as treatment benefits compared to risks will vary as a result of individual differences (which is why subgroup analysis is so important). Also, it is not uncommon for unforeseen adverse effects to show up only after drugs reach the market. For a nutrient such as taurine that cannot be patented, it is unlikely that large, expensive clinical trials would ever be funded. However, there is a fairly large and growing literature available on taurine’s mechanisms, on taurine’s effects in animal models of human disease, as well as taurine treatment in short-term human clinical trials, and, importantly, extensive evidence of nontoxicity of taurine at low doses to doses of several grams a day.

Subgroup Analysis Tells the Story:

Significant Inverse Association between Serum TAURINE and Coronary Heart Disease Risk in Women with High Serum Cholesterol

In a nested case control study8B of 223 coronary heart disease patients and 223 matched controls (participants in the New York University Women’s Health Study) where serum taurine had been measured BEFORE the appearance of coronary heart disease, the researchers evaluated the association of serum taurine levels and the risk of developing coronary heart disease.

Overall, there was no statistically significant association between the risk of coronary heart disease (CHD) and serum taurine levels. But, in considering just the subgroup of women with high total serum cholesterol (>250 mg/dl), there was a significant inverse association between serum taurine levels and CHD. Keeping in mind that taurine would be just one of the factors involved in CHD risk, the study supports the hypothesis that taurine may be protective against cardiovascular disease.

TAURINE May Protect Against Arrhythmias


Sudden cardiac death is associated with a number of cardiovascular conditions, such as arrhythmias following heart attack and, in the case of heart failure, 50% of patients are estimated to die of fatal cardiac arrhythmias.10 Mechanisms of taurine that could contribute to protection against cardiac arrhythmias include membrane stabilization and prevention of intracellular calcium (Ca2+) overload.2 Taurine has also been reported to suppress the sympathetic nervous system,2 excessive activation of which can cause arrhythmias.

Taurine depletion has been linked to electrical and contractual abnormalities (such as increased excitability) in skeletal muscle (different from cardiac muscle) of aged rats; taurine supplementation (1 g taurine/kg/day) improved these measures, moving them toward more normal adult values.10 (This dose in rats is roughly equivalent to 4 to 5 grams per day for an adult human.)

TAURINE Regulates Sensitivity of Platelets to Aggregation

Reference #2 discussed the sensitivity of platelets to aggregation-inducing stimuli under conditions of taurine depletion, normal amounts of taurine, or taurine supplementation. Taurine-depleted cats, for example, were reported to be twice as sensitive to platelet aggregation (clotting) as cats receiving adequate amounts of taurine. In humans with normal taurine status, supplementation with extra taurine (400 mg/day or 1600 mg/day) resulted in platelets having increased resistance to aggregation by 30% or 70%, respectively. Thus, the tendency of platelets to aggregate is depressed by taurine. Fatal dilated cardiomyopathy can be prevented in both cats and dogs by taurine supplementation.2 Commercial cat and dog food generally contains adequate amounts of taurine to prevent the development of this condition—something that has been known for quite a long time, so your pet doesn’t end up at the veterinarian emergency room with a possibly fatal case of heart failure.

Inflammation Linked to Coagulation

As the authors of another paper10K explained, “… increased inflammation may derive from increasing activation of the coagulation system with age. Coagulation may be considered part of the inflammation system with many shared components and strong interactions. The increased hypercoagulable state observed with aging may account for the higher incidence of arterial and venous thromboses in elderly persons.”

TAURINE’s Mechanisms for Protection against Ischemic Stroke

In a rat model of ischemic stroke (middle cerebral artery occlusion),10B researchers administered 50 mg/kg of taurine (intravenously) one hour following the induction of ischemia. Taurine treatment markedly reduced the observable effects of stroke, including neurological deficits, brain swelling, and cell death, and resulted in decreased infarct volume (cells killed by ischemia) 72 hours after the induction of ischemia. Inducers of stroke damage importantly included upregulation of PARP (poly(ADP-ribose)polymerase), a major enzyme that responds to DNA damage, and upregulation of NFkappaB-induced inflammation. These changes were reversed by taurine.

The study10B also reported that taurine reduces the expression of a number of inflammatory cytokines (such as tumor necrosis factor alpha), as well as reduces the activity of myeloperoxidase, a major source of stroke injury.10C

Researchers used the middle cerebral artery occlusion model of stroke in rats to investigate a drug that is a specific PARP inhibitor for its possible protective effects against stroke.10D Results were consistent with those for taurine in the study described above;10B PARP inhibition protected neurons and white matter from stroke injury and death, and prevented the translocation of apoptosis-inducing factor (AIF) to the nucleus where it unleashes its program of cell death. PARP is the subject of a rapidly growing body of research as it is importantly involved not only in response to DNA damage, but mild inhibition of the enzyme may be a potential anti-aging treatment.10E,10F PARP overactivation during DNA damaging events such as strokes can deplete cellular supplies of NAD+, resulting in cellular energy deprivation and thus stressing damaged cells even further. [See “It’s a NAD+, NAD+, NAD+, NAD+ World” in our Life Extension News, September 2013 and “It’s a NAD+, NAD+, NAD+, NAD+ World Part II” in our Life Extension News, November 2013.]

TAURINE Protects Against Cognitive Decline by Preventing Excitotoxic Cholinergic Dysfunction

Cholinergic dysfunction as a contributory factor to cognitive decline with age and to the development of Alzheimer’s disease are areas of extensive research. Choline acetyltransferase, the enzyme required to convert choline to acetylcholine, has been reported to be inhibited as a result of the action of excitatory amino acids.10G Since taurine is well known to provide protection against excitotoxicity (such as that caused by excessive levels of glutamic or aspartic acids), it is a plausible hypothesis that it may help protect choline acetyltransferase from the negative effects of excitatory amino acids. In paper #10G, researchers studied the effects of excitotoxic amino acids on retinas from 8 – 9 day old chick embryos. Exposure to 15 hours of treatment with kainate or glutamate resulted in maximal inhibition (80 – 90%) of choline acetyltransferase, reducing the activity of the enzyme rather than reducing its cellular content.

As noted above, taurine6 has been shown to protect against neurotoxicity induced by amyloid beta and glutamate receptor agonists. This supports the proposed protection by taurine against the cholinergic dysfunction (inhibition of choline acetyltransferase) caused by glutamate and kainate.

Along that line, another paper10H reported that inhibition of choline acetyltransferase was a mechanism for the cholinergic dysfunction induced by amyloid beta peptide oligomers.


TAURINE and Fish Oil Decrease Fat Accumulation, Improve Glucose and Insulin Levels in Type 2 Diabetic Mice

Researchers tested the effects of EPA- and DHA-rich fish oil and taurine in a diabetic/obese KK-A(Y) mouse model of type 2 diabetes.10J Because both taurine and fish oil have exhibited protective effects against type 2 diabetes, and because the combination had been reported in very few studies, the researchers decided to examine the effects of the agents singly and in combination. The animals were put on an experimental diet for 4 weeks. The diets contained the basal ingredients plus soybean oil or fish oil supplemented with 0%, 2%, or 4% taurine.

The results showed the fish oil plus 4% taurine diet suppressed WAT (white adipose tissue) weight gain and reduced blood glucose and insulin levels. The WAT weight gain in the mice receiving the fish oil plus 4% taurine diet was significantly lower than that in the mice fed fish oil alone. Moreover, blood glucose and insulin levels in the mice fed the fish oil + 4% taurine diet were the lowest among the six groups.

The researchers identified inhibition of fatty acid synthesis and promotion of beta oxidation (metabolism of fat) in the liver as one of the reasons for the decreased WAT weight gain in the animals fed fish oil and taurine.

TAURINE Improves Condition of Patients with Chronic Periodontitis

We add here an example of taurine’s amazing versatility as a broadly protective nutrient: a study showing improvements in 10 nonsmoking male patients with chronic periodontitis.17 Periodontitis is a disease that involves infection and inflammation, among other problems.

The researchers cited prior related work: one study described a topical application of 1% taurine on two basement membrane proteins (laminin 5 and type IV collagen expressions) of regenerating oral gingival epithelium provided histologic evidence of rapid reepithelization of human gingival wounds. Another in vitro study suggested taurolidine, a taurine derivative, be used as an antimicrobial in both surgical and non-surgical management of periodontitis. Two animal studies proved taurine to be beneficial in tissue repair in periodontitis. The researchers also noted that in studies of epilepsy patients, the dosage of taurine used ranged from 375 to 8,000 mg/day.

One group of patients received taurine 500 mg a day for 15 days followed by placebo once a day for 15 days. The other group of patients received the same regimen but in reverse: they got placebo once a day for 15 days followed by taurine at 500 mg/day for the following 15 days. This study was double blinded.

Results: There was a significant reduction in TBARS, a measure of lipid peroxidation, in patients following administration of taurine, consistent with findings in animal studies (cited in the text). Glutathione levels rose while glutathione peroxidase levels declined in gingival tissue and in plasma following taurine administration. The researchers also reported a reduction in probing pocket depth and improved clinical attachment level following taurine administration.

To be sure, this is a very small study for a short time period. It would have been nice to have had more data, such as (for example) levels of inflammatory cytokines in the circulation. Nevertheless, it helps point out the potentially broad protective capability of taurine. This is protection that we want and we suspect you want, circulating in your bloodstream!


TAURINE Even Improved Tinnitus in Rats that Developed Tinnitus As a Result of Exposure to Loud Noise

Tinnitus, the very common condition of hearing noises (buzzing, hissing, snapping, crackling, popping) in the absence of any actual background sound is very difficult to treat and, depending on the individual, can range from merely annoying to very unpleasant to actually disabling. For those plagued by it, there can never be any actual silence.

You might wonder how scientists developed an animal model of tinnitus with which to study the effects of potential treatments. After all, the animals can hardly tell you when they are hearing noises (buzzing, hissing, etc.). A 2010 paper18 explains: in humans, loud noise is a tinnitus-inducing stimulus, which can be observed as decreased inhibition (overexcitation) in the auditory pathway. This decreased inhibition in the auditory pathway is also seen in an animal model of tinnitus caused by exposure to loud noise. Taurine is reported to act as an inhibitory neuromodulator by acting at glycine, GABA(A), and GABA(B) receptors, which convey inhibitory neuronal signaling.18 In this way, taurine reduces cellular excitability. Taurine can pass the blood-brain border via a Na+/Cl- dependent taurine transporter.18

One group of animals was exposed to loud noise to induce tinnitus, while another group was unexposed. The animals were tested for hearing threshholds. In the rats exposed to loud noise, the hearing threshhold of the exposed ear was slightly (though not significantly) elevated relative to their unexposed ear. The higher dose of taurine (4 mg/ml in their drinking water) with which tinnitus rats were treated produced a significant therapeutic effect by the ability of these rats to respond to pure tone discrimination functions at levels converging on those of the rats that were not exposed to loud noise. No therapeutic effect was seen at the low dose of taurine (1 mg/ml). After the experiments, when no more taurine was being administered, the rats’ hearing returned to that indicative of tinnitus. Improvements were greater at higher doses of taurine and at higher sound frequencies. The authors note that earlier work of theirs showed that tinnitus did not correlate well with loss of cochlear hair cells.

In this study,18 control rats with normal hearing (they were not exposed to loud noise) on a moderately high level of supplemental taurine had improved auditory discrimination performance across a broad frequency range. In fact, taurine improved auditory discrimination in unexposed rats at both the low and high concentrations.

On the basis of the amount of water consumed by each rat, the average daily taurine dose was 66.6 ± 20.3 mg/kg/day at the low taurine concentration and 293.6 ± 75.8 mg/kg/day at the high taurine concentration. (The higher dose was roughly equivalent to 1.5 gram of taurine per day for an adult human.)

This was a very well done, very convincing study suggesting that taurine may benefit humans suffering from tinnitus. Since tinnitus can be caused by more than one mechanism, benefits may vary.


TAURINE Protection During and After Radiation Exposure—Such as Nuclear Power Accidents

Concern about damage to nuclear reactors in Japan following a large tsunami after a gigantic undersea earthquake was the apparent impetus for looking into protection against radiation exposure, as published in this large review paper.E The researcher considered not only protection against radiation damage but also protection against infections likely to become a problem following the immune suppression induced by radiation. Taurine can provide protection in both these areas. Considerable data are provided (983 references!).

The authors advocate the use of “cocktails” of protective substances as being more likely to provide the desired protection than single substances alone. As they explain it: “[f]or obtaining an optimal therapeutic response, it is probably best in all these cases to use a cocktail of protective substances rather than one substance alone, since there are good theoretical reasons to believe that many of the substances concerned may interact with another in a synergistic fashion—especially when they have completely different biochemical functions or different localization in the cells (e.g., water-soluble versus lipid-soluble antioxidants), or otherwise have completely different mechanisms of action (e.g. free radical scavengers versus redox-active metal ion chelators).”E

The authors also complain that available, safe and cheap agents are not more commonly used for the treatment of ubiquitous medical conditions. “It is very strange, when considering how abundant those research data are that show very significant protective effect for some of the substances mentioned here against permanent organ damage caused by ischemia-reperfusion, and how non-toxic and cheap some of them (like taurine, melatonin and glutathione) also are, that the use of these substances has not already become standard routine, e.g. for treatment of stroke patients or patients with myocardial infarction, but also for treatment of other diseases and injuries where permanent organ damage develops as a consequence of ischemia/reperfusion and post injury inflammatory response (e.g. severe head trauma and drowning).”

The author also notes that “[t]aurine can undoubtedly help to improve protection of the ‘civilian population’ (both in the case of hypervirulent influenza and radiation sickness), i.e. reduce the risk that the patient will die from a harmful inflammatory over-reaction, because of its anti­oxidant effect and capacity for scavenging some of these highly reactive antibacterial and antiviral weapons that have low specificity (are imprecisely targeted) and therefore may be especially dangerous to the ‘civilians,’ such as peroxynitrite and hypohalite [hypochlorous and hypobromous acid] ions.”


TAURINE’s Antinociceptive (Anti-pain) Effects May Be Mediated Via GABA(A) and GABA(B) Receptors and Peripheral Cholinergic Mechanisms

The study of pain is complex. As an example, what may relieve one type of pain may not relieve another type. Pinning down the mechanisms responsible for pain relief is also difficult because many different biochemical pathways can be involved. People in severe pain may not be particularly driven by the desire to understand the mechanisms of pain relievers as much as they are to get pain relief any way they can. It is really crucial, though; if you want to find a more effective way to relieve pain you need to understand chemical mechanisms. For one thing, it is often the case that combining different substances will give you a superior effect and/or reduce side effects, as compared to even the best, most powerful single pain killers such as opiates. On the basis of the available evidence, it appears that taurine has anti­nociceptive (anti-pain) effects, but it is likely to work best in combination with other substances having such effects but working by different mechanisms and, hence, potentially acting together synergistically.

In a recent paper,B determining whether a hot plate test is detecting pain relief or sedation was described this way: “A mouse was placed on a rubber cylinder (height 2.5 cm, diameter 6 cm) after drug or vehicle administration. We recorded the time that elapsed before the mouse jumped off the rubber cylinder. When time taken to step off the rubber was longer than that observed among controls, sedation had been achieved.” This was to determine whether the effect of the treatment on pain had been affected by a sedative effect of the treatment, an effect that had to be considered in evaluating the effect of pain relief on animal behavior. (Did the mouse delay flicking its tail because its pain was reduced or because it was sedated?)

“When given alone, intrathecal glycine, taurine, or muscimol had no effect on the pain threshhold index (p>0.05 vs. vehicle controls).” However, when administered with bicuculline, which induces hyperalgesia (high level of pain), glycine, taurine, or muscimol (a cholinergic drug) induced analgesia. The intrathecal administration of muscimol and taurine had more prolonged anti-hyperalgesic effects than did intracisternal administration, as determined by the hot plate test. No sedation was produced by mice injected with glycine, taurine, or muscimol.

In conclusion, the researchers found taurine as well as muscimol or glycine to have antinociceptive effects when administered with bicuculline, an agent that induces hyper­algesia in mice. They find that GABA(A) receptor antagonism may represent a possible strategy for treatment of allodynia or hyperalgesia. An earlier paperC had results that suggested that the antinociceptive effects of taurine may be partly mediated by spinal GABA(A) ­receptors.

In a 1992 paper,D researchers studied the effects of taurine administered by injection at about the L5-L6 intervertebral space (intrathecal) on pain in mice in the acetic acid injection-induced abdominal stretch assay, the hot plate and tail flick assays. (The names of these tests sound like something out of The Inquisition … but it’s a study of pain so you can’t avoid inflicting it. In the usual animal studies where painful procedures are involved, scientists are studying something that allows them to anesthetize the animals.) In this study, the researchers found that pretreatment with 12 nmol taurine injected 2 minutes prior to the administration of acetic acid abdominal stretch, expressions of pain were significantly inhibited. But they did not observe pain relief in the tail flick and hot plate assays. Pretreatment with naloxone did not prevent the antinociception (anti-pain effects) seen in the acetic acid abdominal stretch tests, indicating that the taurine anti-pain effect in this test did not involve endogenous opioids.

BROMINE, an Essential Trace Element Is INCLUDED (as bromide) in our new Taurine/Bromine Formulation AT NO EXTRA CHARGE


A Naturally Formed TAURINE-BROMINE Compound (Taurine bromamine) is Part of the Immune System

And is Both Antibacterial and Antiinflammatory

A little known compound, taurine bromamine, produced naturally by the reaction of taurine and hypobromous acid (the latter generated by the enzyme myeloperoxidase), reveals another pathway of taurine activity with important health benefits by enhancing your immune defenses while decreasing inflammation. This is unusual in that increasing immune defenses usually INCREASES inflammation by activating immune system inflammatory cells that attack pathogens. (Taurine chloramine is also produced by taurine reacting with hypochlorous acid resulting from the action of myeloperoxidase, and has similar effects to taurine bromamine.11,12)

Myeloperoxidase is recognized as a significant independent risk factor for coronary heart disease, and has been found circulating at elevated levels is patients with confirmed atherosclerosis.13 Hence, the reaction of taurine with oxidant products of myeloperoxidase, such as hypochlorous and hydrobromous acids, to less oxidizing metabolites (taurine chloramine and taurine bromamine) with antiinflammatory and antibacterial properties, is one mechanism of taurine’s protection against heart disease. As one paper19 explained, the reaction of hypochlorous acid and superoxide creates toxic hydroxyl radicals; taurine protects against the creation of these hydroxyl radicals by reacting with hypochlorous acid to convert it to taurine chloramine.

A new paper (just arrived in our mailbox)23 provides new information on the myeloperoxidase derived oxidants hypochlorous and hydrobromous acids. The authors explain “… there is strong evidence for MPO [myeloperoxidase] and its associated oxidants in the development of atherosclerosis, together with numerous other inflammatory conditions, neurodegenerative disease, kidney disease, lung disorders, and cancer.” They point to forms of damage that may be relevant to age-­associated diseases, such as the reaction of tryptophan residues (tryptophan as incorporated in a protein) with hypochlorous and hypobromous acids that has been shown to contribute to protein unfolding and enzyme inactivation in mechanistic studies, and thus may do the same in vivo. The potentially broad range of damage done by these oxidants is also suggested by evidence they cite of the reactivity of hypobromous acid with the unsaturated bonds of fatty acids and cholesterol. The livers of patients with fibrotic and nonalcoholic fatty liver disease have been found to contain readily detectable myeloperoxidase. Microglia, brain resident immune cells, contain both NADPH oxidase and myeloperoxidase and thus, when activated, can generate hypochlorous acid, potentially contributing to neurodegenerative conditions. The reaction of taurine with hypochlorous and hypobromous acids to form the reaction products taurine chloramine and taurine bromamine is therefore a very important protective mechanism against the collateral damage to tissue that would otherwise occur as a result of myeloperoxidase’s normal physiological activities.

Inflammatory Environment Surrounds Cancer Cells May Be Inhibited By Antiinflammatory TAURINE BROMAMINE

Taurine bromamine decreases the production of proinflammatory mediators such as tumor necrosis factor alpha, IL-6, IL-8, PGE2, and others. (A recent paper13B reported that inflammatory environments as found around tumors attract cells called multipotent stromal cells (MSC) that are involved in wound repair and regeneration and that are important in tumor development; the paper mentioned IL-6 and IL-8 as examples of inflammatory cytokines found around tumors, noting that they are highly expressed in breast cancer cells and make significant contributions to the recruitment of these multipotent stromal cells.)

Taurine bromamine also reacts with and inactivates hydrogen peroxide and has antiinflammatory properties, such as inducing the synthesis of heme oxygenase-1, a stress-inducible enzyme, and inhibits the activation of NFkappaB, a master regulator of inflammatory gene activation.11 Taurine chloramine, also a natural product derived from taurine reacting with hypochlorous acid generated by myeloperoxidase, increases the activity of heme oxygenase-1 and catalase and also increases intracellular levels of glutathione to protect macrophages in inflamed tissue from oxidative stress.11B

Eosinophils are importantly involved in asthma, producing a variety of proinflammatory cytokines that play a major part in the tissue-damaging effects seen in asthma.11C This cell culture study of the effects of taurine bromamine on Jurkat cells reported the inhibition of tumor necrosis factor alpha-induced activation of NFkappaB. As NFkappaB is a master regulator of proinflammatory genes, this evidence supports taurine bromamine’s antiinflammatory effects.

The author11 reports on prior research in which he was a contributor showing that topical taurine bromamine was very effective against acne vulgaris, the bane of pimply adolescents, teenagers, and young adults. Six weeks treatment with taurine bromanine in patients with acne resulted in improvement in 90% with a 65% reduction in acne lesions. The same author11 reports that taurine bromamine has a ­bactericidal activity approaching that of hypochlorous acid (BLEACH is the sodium salt of hypochlorous acid). He reports that taurine bromamine (TauBr) “killed all tested bacteria at non-cytotoxic [no tissue damage] antiinflammatory concentrations.”11

While we mention the use of a topical TauBr cream, remember that TauBr is formed naturally in the body when there is an adequate supply of the essential trace element bromine. But because it may be difficult to get bromine from an ordinary diet, and because bromine is not generally included in multinutrient supplements, you can assure yourself of an adequate daily dose of bromine by taking our taurine/bromamine formulation. Note that this bromine is present in the form of the bromide ion, not as highly toxic and chemically reactive elemental bromine!


An Early Link between Hypochlorous Acid and Heart Disease

An interesting historical aspect of hypochlorous acid (bleach) are early studies published in a book for public education on the possible unintended consequences of chlorination of water to kill bacteria and other pathogens.A The findings included description of and photos of atherosclerotic lesions produced in the linings of artery walls in chickens given chlorinated (tap) water to drink as compared to chickens given purified water containing no chlorinated compounds. Apparently, this truthful but unwanted revelation of possible adverse effects of chlorinating water upset FDA bureaucrats, who labeled the booklet fraudulent and the physician-author a quack, prohibiting the further distribution of the book via the U.S. mail.

The beneficial effects of chlorinating water, which has prevented many millions of cases of waterborne diseases, was without question, but the potential toxicity of chlorinated compounds formed in the process16 should have been treated seriously and, of course, the prohibition of the distribution of the book violated the First Amendment. There was probably concern about public opposition to chlorination of water as well as possible lawsuits alleging that one’s heart disease was caused by chlorination of public water supplies. But the FDA still did not have the authority to prohibit shipment or sale of the book. The U.S. Supreme Court has repeatedly ruled that the public’s reaction to truthful information cannot be used by government to prohibit the dissemination of such information. If the only information that could be disseminated was that which would be analyzed unemotionally by the public, much information would be suppressed.


Sandy was very pleased to experience a significant reduction in her painful knee osteoarthritis when she began taking an additional supplemental dose of taurine, 1⁄2 tsp twice a day. She estimated her pain was reduced by about 60%. But she was even more delighted by the pain relief—about 75%—that she got after a few days on our taurine plus bromide formulation. It isn’t surprising that the taurine bromamine that results from the chemical reaction of taurine and hypobromous acid (the latter created by the enzyme myeloperoxidase) would help relieve pain due to its powerful antiinflammatory effects. As myeloperoxidase oxidative products are highly inflammatory and released by inflammatory immune cells infiltrating osteoarthritic joints,22 the pain relief is, we think, very likely to be a result of taurine, taurine bromamine, and taurine chloramine.

BROMIDE Found in Seawater and in Human Blood

Bromine content (as bromide ion) of seawater (mol/kg) was reported to be 0.000844.14 Bromide has been determined in human blood;15 the overall mean was 5.3 ±1.4 mg/L and varied from 2.5 to 11.7 mg/L. People aged 45 – 65+ were more likely to have higher bromide levels than younger persons and average bromide levels were higher in females in most age groups. The paper15 also reported that the DAILY INTAKE of bromide from normal (the term “normal” was here undefined) diets is in the range of 0.1 to 0.3 mg Br/kg body weight or approximately (the authors calculate) 8 mg/day for adults. Bromide is reported15 to be mostly excreted via the kidneys.

BROMIDE in Drinking Water

According to the World Health Organization (WHO)(2009), “Bromide in Drinking Water. Background document for development of WHO Guidelines for Drinking-water Quality,” concentrations of bromide in fresh water range from trace amounts to about 0.5 mg/l.

Dietary Sources of BROMIDE

According to the WHO document mentioned in the paragraph above, the typical daily dietary intake of bromide in the U.S. is 2 – 8 mg from grains, nuts, and fish. In the Netherlands, the WHO document reports the average bromide intake of 8.4 to 9.4 mg/day.

Relationship between Sodium Chloride (Salt) and Bromide

Increased consumption of table salt (sodium chloride) increases the excretion of bromide. One possible downside of consuming high levels of salt could be the loss of bromide and, therefore, of taurine bromamine. This was explained by the author in reference #E:

The quoted selections below and the immediately following references are by Olav Albert Christophersen:

“Radiation protection following nuclear power accidents: a survey of putative mechanisms involved in the radioprotective actions of taurine during and after radiation exposure”

“Bromide is normally much more abundant than I- in the blood, but the Br- concentration of blood plasma is most likely strongly dependent on the average Br/Cl ratio of the diet. During precipitation of NaCl from evaporating seawater, there is a strong fractionation of Br- relative to Cl- because of the larger ionic radius of Br-622 compared to Cl-. This may explain why the Br/Cl ratio of table salt analysed in Finland623 was only 1⁄27 of the Br/Cl ratio found in seawater.”622

“In the most common form of allergic asthma,625,628 as well as in other allergic inflammation, eosinophils are major players. In asthma and other allergic diseases, it is therefore the products formed by reaction between taurine and such hypohalite ions that are formed by eosinophil peroxidase that might be most important as anti-inflammatory mediators. Since chloride is of very little importance here, and the production of hypobromite by the eosinophil peroxidase reaction must depend strongly on the bromide concentration in the blood, it may be expected that the reduction of plasma bromide concentrations happening as a consequence of the ingestion of much ordinary table salt may be an important cause of enhanced disease activity (because of reduced production of the inhibitor taurine bromamine) in asthma and other allergic diseases. It may be theoretically expected that a combination of taurine supplementation with normalization of the bromide concentration in blood plasma to the same level as is commonly found in mammals when living in their natural environments might have substantial therapeutic effect by helping to maximize the production of anti-inflammatory taurine bromamine in tissue areas affected by allergic inflammation with eosinophil accumulation and activation.”


622. Krauskopf KB. Introduction to Geochemistry, 2. Ed. Singapore: McGraw-Hill Book Company; 1982.

623. Koivistoinen P, ed. Mineral Element Composition of Finnish Foods: N, K, Ca, Mg, P, S, Fe, Cu, Mn, Zn, Mo, Co, Ni, Cr, F, Se, Si, Rb, Al, B, Br, Hg, As, Cd, Pb and Ash. Acta Agriculturae Scandi navica. Supplementum 22. Stockholm 1980.

625. Nagata M, Saito K. The roles of cysteinyl leukotrienes in eosinophilic inflammation of asthmatic airways. Int Arch Allergy Immunol. 2003; 131(Suppl 1): 7-10.

626. Mori M, Takaku Y, Kobayashi T, Hagiwara K, Kanazawa M, Nagata M. Eosinophil superoxide anion generation induced by adhesion molecules and leukotriene D4. Int Arch Allergy Immunol. 2009; 149 (Suppl 1): 31-8.

627. Nakagome K, Nagata M. Pathogenesis of airway inflammation in bronchial asthma. Auris Nasus Larynx. 2011 Feb 18. [Epub ahead of print]

628. Wang W, Hansbro PM, Foster PS, Yang M. An alternate STAT6-independent pathway promotes eosinophil influx into blood during allergic airway inflammation. PLoS One 2011; 6: e17766.

How to Use the New TAURINE/BROMINE Formulation

Each ½ tsp. Serving Contains 1.5 gram of taurine and 6 mg of bromide

We recommend taking one serving twice a day. (This is the amount we both take.) Our new formulation comes as crystals, which is the least expensive form as it avoids the cost of encapsulation. The product has ABSOLUTELY NO TASTE, so you can mix it in any liquid (dissolves fastest in a warm or hot drink) without worrying about an effect on flavor.

Interestingly, if the salt the average American consumes daily were in the form of sea salt, the amount of bromide ingested with that salt would be about 15 mg.

The amount of supplemental bromide that we have chosen for our Taurine/Bromine formulation is very small compared to the doses used medically. It is a bit more than the 8 – 9 mg of bromide contained in a healthy marine food rich diet consumed in the Netherlands. The World Health Organization considers 24 mg bromide to be an acceptable total daily intake for a 60 kg adult, with a safety factor of 10 below the NOEL, No Observable Effect Level.

For bromide content of ocean water, see the Handbook of Chemistry and Physics, CRC Press.

For further information on safe bromide intake levels, see section …

16. How to Use the New Taurine/Bromine formulation
Dietary Sources of BROMINE
BROMINE in Drinking Water
“Background document for development of WHO Guidelines for Drinking-water Quality” WHO/HSE/WSH/09.01/6

Available here without charge:


A. Joseph M. Price. Coronaries Cholesterol Chlorine. (1967) (We bought another copy, having lost our original copy, from on June 28, 2014 for $.01 + $3.99 shipping & handling. Unfortunately this wasn’t the first edition, and only the first edition includes the very impressive photographs of the hypochlorite induced atherosclerotic chicken arteries.
B. Lee and Lim. Intracisternal or intrathecal glycine, taurine, or muscimol inhibit bicuculline-induced allodynia and thermal hyperalgesia in mice. Acta Pharmacol Sin. 31:907-14 (2010).
C. Serrano, Serrano, Guerrero, Fernandez. Role of GABA(A) and GABA(B) receptors and peripheral cholinergic mechanisms in the antinociceptive action of taurine. Gen Pharmacol. 25(6):1123-29 (1994).
D. Hornfeldt, Smullin, Schamber, et al. Antinociceptive effects of intrathecal taurine and calcium in the mouse. Life Sci. 50:1925-34 (1992).
E. Christophersen. Radiation protection following nuclear power accidents: a survey of putative mechanisms involved in the radioprotective actions of taurine during and after radiation exposure. Microb Ecol Health Dis. 23:14787 (2012).
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5. Hudson et al. Alport’s syndrome, Goodpasture’s syndrome, and type IV collagen. N Engl J Med. 348:2543-56 (2003).
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8. Chesney, Han, Patters. Taurine and the renal system. J Biomed Sci. 17 Suppl 1:S4. doi: 10.1186/1423-0127-17-S1-S4 (2010).
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8E. Das, Ghosh, et al. Acetaminophen induced acute liver failure via oxidative stress and JNK activation: protective role of taurine by suppression of cytochrome P450 2E1. Free Radic Res. 44(3):340-55 (2010).
8F. Chang, Chou, Chiu, et al. Preventive effects of taurine on development of hepatic steatosis induced by a high-fat/cholesterol dietary habit. J Agric Food Chem. 59:450-7 (2011).
9. Pizzarelli, Lauretani, Bandinelli, et al. Predictivity of survival according to different equations for estimating renal function in community-dwelling elderly subjects. Nephrol Dial Transplant. 24:1197-205 (2009).
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10B. Sun et al. Anti-inflammatory mechanism of taurine against ischemic stroke is related to down-regulation of PARP and NF-kappaB. Amino Acids. 42:1735-47 (2012).
10C. Breckwoldt, Chen, Stangenberg, et al. Tracking the inflammatory response in stroke in vivo by sensing the enzyme myeloperoxidase. Proc Natl Acad Sci USA. 105(47):18584-9 (2008).
10D. Komjati, Mabley, Virag, et al. Poly(ADP-ribose)polymerase inhibition protects neurons and the white matter and regulates the translocation of apoptosis-inducing factor in stroke. Int J Molec Med. 13:373-82 (2004).
10E. Canto and Auwerx. Interference between PARPs and SIRT1: a novel approach to healthy ageing?” Aging. 3(5):543-7 (2011).
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10J. Mikami, et al. Dietary combination of fish oil and taurine decreases fat accumulation and ameliorates blood glucose levels in type 2 diabetic/obese KK-A(Y) Mice. J Food Sci. 77(6):H114-20 (2012).
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