Volume 17 Supplement 1
Taurine in health and diseases: consistent evidence from experimental and epidemiological studies
© Yamori et al; licensee BioMed Central Ltd. 2010
Published: 24 August 2010
Taurine (T) was first noted as beneficial for stroke and cardiovascular diseases (CVD) prevention in genetic rat models, stroke-prone spontaneously hypertensive rats (SHRSP). The preventive mechanisms of T were ascribed to sympathetic modulation for reducing blood pressure (BP) and anti-inflammatory action. Recent epidemiological surveys revealed the involvement of inflammatory mediators in the pathogenesis of stroke and also atherosclerosis for which T was proven to be effective experimentally. Arterio-lipidosis prone rats, a substrain of SHRSP selectively bred for higher reactive hypercholesterolemia, quickly develop not only arterial fat deposition but also fatty liver which could be attenuated by dietary T supplementation. CARDIAC (CVD and Alimentary Comparison) Study was a WHO-coordinated multi-center epidemiological survey on diets and CVD risks and mortalities in 61 populations. Twenty-four-hour urinary (24U) T was inversely related significantly with coronary heart disease mortality. Higher 24U-T excreters had significantly lower body mass index, systolic and diastolic BP, total cholesterol (T-Cho), and atherogenic index (AI: T-Cho/high density lipoprotein-cholesterol) than lower T excreters. T effects on CVD risks were intensified in individuals whose 24U-T and -magnesium (M) excretions were higher. Furthermore, higher Na excreters with higher heart rate whose BP were significantly higher than those with lower heart rate were divided into two groups by the mean of 24U-T, high and low T excreters. Since the former showed significantly lower BP than the latter, T may beneficially affect salt-sensitive BP rise. Included among the typical 61 populations, were Guiyang, China or St. John’s, Newfoundland, Canada where in which the means of both 24U-T and -M were high or low, respectively. The former and the latter had low and high CVD risks, respectively. Australian Aboriginals living at the coastal area in Victoria were supposed to eat T- and M-rich bush and sea foods and be free from CVD 200 years ago, but they presently have nearly the highest CVD risks indicating that T- and/or M-containing seafood, vegetables, fruits, nuts, milk, etc, similar to prehistoric hunters’ and gatherers’ food should be good for CVD prevention. The preventive effects of T, good for health and longevity, first noted experimentally, were also proven epidemiologically in humans.
The health effects of taurine (T), “a wonder molecule”, was first noted in our genetic rat models for hypertension (Spontaneously Hypertensive Rats: SHR) [1, 2] and stroke (Stroke-prone SHR: SHRSP) [3, 4] and are now being confirmed epidemiologically by our WHO-coordinated Cardiovascular Diseases and Alimentary Comparison (CARDIAC) Study covering 61 populations in the world [5–8]. Advances in extensive studies on experimental models indicate that T is preventive against hypertension , stroke and atherosclerotic arterial diseases [10–12]. T is also expected to be effective for the prevention of nonalcoholic steato-hepatitis (NASH) increasing now in developed countries . Accumulating evidence from CARDIAC Study indicates that common T intakes reduce cardiovascular disease (CVD) risks and contribute to the longevity of the Japanese  which have the lowest coronary heart disease (CHD) mortality in developed countries. Furthermore, the recent health study has revealed that CHD risks are definitely lower in the individuals and populations with higher 24-hour urinary (24U)-T and -magnesium (M) excretions .
1) Taurine (T) and prevention of cardiovascular diseases (CVD)
Since SHRSP was established as a genetic model developing stroke, extensive nutritional and pharmacological studies have been conducted experimentally [7, 9, 10, 15]. Our experiments to feed SHRSP on high or low fish protein diets with or without 1 % salt in drinking water first demonstrated that fish protein rich in T attenuated salt-induced severe hypertension and decreased stroke incidence from 80% down to 10% [4, 15]. High fish protein diet with low salt in drinking water was proven to be most effective to reduce stroke down to 0%. We further investigated the effects of several amino acids contained in fish protein in SHRSP and confirmed that T is effective for reducing blood pressure (BP) in SHRSP . Among our experiments to prove the effect of various nutrient and amino acid supplementations on BP and stroke incidence in SHRSP, sulfur amino acids, such as T and methionine, were effective on the reduction of BP and stroke incidence . Other than sulfur amino acids reducing BP, lysine had no effect on BP but was also effective for the prevention of stroke. We speculate therefore that enough amino acid supply to the vascular wall also might be protective against stroke [6, 15].
Therefore, we further analyzed the nutritional mechanisms of stroke in SHRSP and also in humans. The common predilection site of stroke is the basal ganglia which are fed through perforating arteries branching recurrently from the cerebro-basal arteries. Blood flow through such recurrent arteries is reduced hemorheologically in hypertension, and thus vascular damage develops due to the reduced blood supply to these arterial walls [15, 16]. Anatomically the vascular wall of these recurrent arterial branches should receive nutritional supply only from the blood stream inside the vessel through the blood-brain barrier, whereas the cerebro-basal arteries receive nutritional supply through capillaries around the vascular wall, (“vasa vasorum”). Our morphological electron microscopic studies in 1980’s for the first time demonstrated that vascular damages start at the outer layer of the vascular smooth muscle cells located at the furthest site from the vascular lumen [15, 16]. Moreover, we proved that macrophages were activated in response to the vascular damages that occurred initially at the outer layer of perforating arteries in the brain. Such nutritional vascular damages are followed by inflammatory reactions. At the advanced stage vascular damages occur at the inner layer of cerebral vessels which leads to vascular wall rupture that causes cerebral hemorrhage or to thrombosis inside the damaged blood vessels that causes cerebral infarction [15, 16]. These pathological processes were further confirmed in human autopsy materials by an immuno-histochemical technique  in which macrophages were recruited to cause and heal cerebro-vascular damages. Vascular smooth muscle cells initially remained intact near the intima close to the vascular lumen as in SHRSP. Therefore, we can speculate that the activation of macrophages and other inflammatory cells are supposed to further damage cerebral arteries, causing severe vascular lesions such as angio-necrosis. However, when these inflammatory cells contain much T from nutrients, T-chloramine neutralizes the adverse action of radicals produced from chlor  and may help vascular cells survive or regenerate to repair the wall .
After our demonstration of the importance of inflammation in stroke in rat models, the pathogenic concept of stroke as well as atherosclerosis in humans has also changed greatly . High sensitive C-reactive protein (CRP), a marker and product induced by inflammatory reaction, was confirmed to be the reliable predictor of ischemic stroke and atherosclerotic CHD by extensive cohort studies [21, 22]. Therefore, the control of local inflammation by T appears to be important for the prevention of stroke. The effect of fish protein on the incidence of stroke was experimentally first demounted in SHRSP in the 1970’s [4, 15], and the cod protein feeding was reported to be clinically effective for reducing CRP in humans . T or sulfur amino acids rich in fish protein may protect cerebral vessels through its anti-inflammatory action by the local formation of T-chloramines. Consistent with these studies, our world-wide epidemiological study showed that among 5 diet-related factors T/creatinine (Cr) ratio was proven to be a potent preventive factor against stroke as well as CHD as mentioned later .
2) Taurine (T) and lipotoxicity in the vascular wall and liver
By our further effort for establishing a better model of atherosclerosis from SHRSP, the selective sib-mating of the substrain of SHRSP, developing greater reactive hypercholesterolemia in response to high fat cholesterol (HFC) diet feeding, was started in 1972 . The strain developed not only reactive hypercholesterolemia but also ring-like fat deposits in small mesenteric arteries within 2 or 3 weeks on HFC diet. This appeared to be a good model for studying the initial process of fat deposition on arterial walls in the development of atherosclerosis  because similar ring-like fat deposits were noted at autopsy in the atherosclerotic lesions of cerebro-basal arteries in the human brain.
Dietary T supplementation was proven to be effective for attenuating the development of hypercholesterolemia and for decreasing fat deposits in the mesenteric arteries of the selected SHRSP fed on HFC diets [26, 27]. Such cholesterol-lowering effect was also confirmed in volunteer medical students who took 6g of T per day for 3 weeks . These beneficial effects of T on hypercholesterolemia and arterial fat deposits were experimentally confirmed to be due to the increased bile acid production and the activation of 7α-hydroxylase , the rate limiting enzyme in the process of the conversion of cholesterol into bile acids. This has been proven to be due to the enhanced gene expression of cholesterol 7α-hydroxylase . When T feeding lowered cholesterol levels, the gene expression was proportionally accelerated in relation to the reduced cholesterol level. Moreover, T supplementation was proven to effectively increase low density lipoprotein (LDL) receptors in the liver by an experiment of T supplementation accelerating the decay curve of radio-labeled (125I) LDL . Therefore, cholesterol-lowering mechanisms of T are summarized to be due to an increase in LDL receptors and accelerated conversion into bile acids by T, and other mechanisms such as T’s effect to reduce intestinal acyl-CoA:cholesterol acyltransferase activity [26, 31].
We are presently interested in the activation of LOX-1, a receptor for oxidized LDL that was up-regulated in SHRSP fed on HFC diet . T actually decreased arterial fat deposition . Therefore, T is speculated to attenuate the increase of LOX-1 receptors though a possible local antioxidant action by T-chloramine formation [19, 31]. The suppressive effect of T on LOX-1 was noted actually in experimental diabetic or hypertensive models treated by T [33, 34].
In conclusion, our experimental studies consistently indicate greater prospective for T to contribute to the nutritional prevention of CHD, as well as stroke and probably NASH, the increasing health problem of mankind exposed to urbanization and westernization of dietary habit and life styles.
3) Taurine (T) and coronary heart diseases (CHD)
3-1) T’s role in CVD prevention
These experimental findings to support the beneficial effect of T and other nutrients on CVD prevention led Y. Yamori to propose an international cooperative study on the association of dietary factors with CVD risks and CVD mortality in 1982. The protocol of this study obtained an international consensus of two meetings organized by WHO-Collaborating Center for Primary Prevention of CVD in 1983 and 1985 [5–7]. The CARDIAC Study is a multi-center cross sectional epidemiological survey for which about 100 males and 100 females aged 48 to 56 were randomly selected from each population and invited to participate in a health examination. This consisted of weight, height, BP measurement by an automated BP measurement system, blood tests for serum total cholesterol (T-Cho) and high density lipoprotein-cholesterol (HDL), as well as an analysis of biomarkers (the daily excretions and their ratios to Cr) of Na, potassium (K) M, T, isoflavones and urea nitrogen for estimating dietary intakes of salt, vegetables, milk products, seafood, soybean products and protein by sampling 24U [5–8, 37, 38]. The associations of nutrition with BP and with CVD mortalities were analyzed in “Core” Study and in “Complete” Study, respectively. “Core” Study demonstrated that the population averages of BP, both systolic and diastolic BP (SBP and DBP), were positively associated with the average population intake of daily Na estimated by 24U-Na excretion [7, 37, 38], and the population average of M/Cr in 24U were inversely associated with SBP and DBP indicating a significant association with DBP . “Complete” Study showed significant positive association of the age-adjusted mortality rates of stroke with the population averages of 24U-Na excretion or 24U-Na/K ratio, and with the arachidonic acid ratio in the plasma phospholipids , but the rates were significantly inversely related with T-Cho. Moreover, CHD mortality rates were significantly positively related with the population averages of serum T-Cho and inversely related with polyunsaturated/saturated fatty acid ratios, n-3 fatty acid ratios of plasma phospholipids or 24U-T, indicating a protective effect of seafood intake on CHD [8, 37].
3-2) Influence of T, M and combined T and M on CVD risks
4) Taurine and salt-related hypertension
5) Taurine (T) and magnesium (M) in high and low risk populations
6) Bush food rich in T and M, needed for health
Moreover, they had no salt at all before Captain Cock reached Australia at the beginning of 18th century. Our CARDIAC data help us to speculate how Aboriginals should have been free from CVD risks, based on our comparison of CARDIAC Study individuals consuming a high amount of T and M but less Na with those consuming less T and M but a great amount of Na. CVD risks were clearly and highly significantly lower in the CARDIAC Study participants taking a high amount of T and M but less Na, corresponding to the nutritional balance of Aboriginal ancestors eating traditional bush food. High T and M but less Na-containing foods were supposed to be taken commonly by the ancestors of humans living on hunter-gatherers’ foods like Aboriginal ancestors for nearly 10 times longer than the period after the start of agriculture and farming. Therefore, these dietary conditions seem to be more suitable for the human genome to live a healthy life without CVD.
7) T and M in cardiovascular pathophysiology and longevity
Both T and M are basically important for the maintenance of life. T is involved in cellular physiology by its effect on osmoregulation, anti-oxidant, membrane stabilization and calcium regulation [47–49], and also on lipid metabolism related to dyslipidemia and atherosclerosis through its role in bile acid conjugation [47, 48]. Recently, T-conjugated endogenous bile acid derivative, ursodeoxycholic acid was focused on as a chemical chaperone which was proven to reduce endoplasmic reticulum (ER) stress and restore glucose homeostasis in a mouse model of type 2 diabetes . The alleviation of ER-stress may restore insulin sensitivity in the liver, muscle and adipose tissue, thus contributing to the resolution of fatty liver diseases, diabetes and obesity. High dietary T administration was proven to reduce apoptosis and atherosclerosis possibly via normalization of ER stress .
Moreover, in relation to the ageing of vascular tissue and the accelerated senescence of endothelial progenitor cell (EPC) noted in SHRSP , T was reported to attenuate EPC senescence in SHRSP and to modulate clinically the deterioration of endothelial function in smokers [53–55]. These classical and new concepts of the pathophysiological roles of T suggest that a high T intake may contribute to longevity through CVD health and lifestyle-related diseases.
On the other hand, M is the 8th abundant element in the weight, the number of atoms and the volume percentage of all atoms on the earth. It is also the most abundant intracellular divalent cation and is involved in the various biological functions of about 300 enzymes as their coenzyme. They include all enzymatic reactions requiring ATP, such as Na-K ATPase, important for intracellular ionic balance. Therefore, M is supposed to be causatively and clinically related to cardiovascular health, hypertension and diabetes [56–58]. Lowering of intracellular free M was observed in SHRSP in the process of aging and development of hypertension . Dietary M supplementation increased intralymphocytic free M and attenuated the grade of hypertension . These experimental findings were recently confirmed clinically in patients with mild hypertension whose ambulatory BP was significantly decreased concomitantly with the increased intracellular free M and K, and decreased intracellular free Ca and Na, by the dietary supplementation of 600 mg of pidolate M . In this clinical experiment, M supplementation increased serum M and 24U excretion of M. Therefore, the aforementioned epidemiologically observed 24U-M excretion was regarded to correspond to dietary M intake. M was also reported to decrease BP by inhibiting sympathetic nerve by blocking N-type Ca channels .
Since the evolutional origin of life of human beings was inside the sea containing abundant M and food gatherers lived on seafood rich in T, both M and T are assumed to be essential for the homeostasis maintaining cardiovascular health.
In addition to the pathophysiological and various physiological functions of T, the preventive effect of T was first experimentally demonstrated in hypertensive rat models, SHR and SHRSP developing hypertension and stroke genetically. World-wide epidemiological studies conducted for the last 25 years revealed that 24U-T was inversely associated with the age-adjusted mortality rates of stroke and CHD. High 24U-T, particularly combined with high M excretion, was associated highly significantly with lower CVD risks, obesity, hypertension, hypercholesterolemia and AI. These findings indicate the consistency of the beneficial T effects on animal models and humans proven either experimentally or epidemiologically. Such consistency of the extensive basic and epidemiological findings of T effects and the effects combined with M indicates greater prospective for T to contribute to the nutritional prevention of CVD and lifestyle-related diseases.
List of abbreviations used
body mass index
arterio-lipidosis prone rats
- CARDIAC Study:
Cardiovascular Diseases and Alimentary Comparison study
coronary heart diseases
diastolic blood pressure
high density lipoprotein
low density lipoprotein
systolic blood pressure
spontaneously hypertension rats
stroke-prone spontaneously hypertension rats
Epidemiological and experimental studies by the authors’ group was supported partly by Grants-in–Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, the Japanese government, and by the donations to WHO from many companies and over 300,000 individuals in total. Our appreciation should be extended to all participants in WHO-CARDIAC Study and to collaborating workers in world-widely distributed study centers.
This article has been published as part as part of Journal of Biomedical Science Volume 17 Supplement 1, 2010: Proceedings of the 17th International Meeting of Taurine. The full contents of the supplement are available online at http://www.jbiomedsci.com/supplements/17/S1.
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