Nutraceuticals International Essay

1. â€Å"Beetroot juice ‘can beat blood pressure’. † Nutraceuticals International 13. 2 (Feb 2008). Summary/Critique Medications for hypertension can amount to a lot of money each year. This is the reason why many experts are trying to look at cheaper alternatives in producing medicines that could alleviate the upsurge of this dreaded disease. Cheaper medicines can come in a form of herbal remedies. In this report that appeared in a magazine Nurtaceuticals International (Feb.2008), it has been revealed that British researchers at Barts and The London School of Medicine found a new way of vitally reducing the blood pressure of hypertension patients. By taking 500ml of beetroot juice each, they might have a chance of being cured of their hypertension. The group of researchers, led by Amrita Ahluwalia and Ben Benjamin, identified that it is the â€Å"ingestion of dietary nitrate contained within beetroot juice† that does the trick. The effect can also be seen when people are eating green, leafy vegetables that ultimately results in decreased blood pressure. Because of the antioxidant vitamin content of vegetable-rich diet people can be protected against heart disease. This article is very informative because readers can learn the importance of having good diet can help everyone have a healthier life. Also, this article could encourage more experts in trying to find alternative ways of helping people with hypertension. Full Text Article: â€Å"Beetroot juice ‘can beat blood pressure’. † Nutraceuticals International 13. 2 (Feb 2008). Researchers at Barts and The London School of Medicine in the UK have discovered that drinking just 500ml of beetroot juice a day can significantly reduce blood pressure. The study, published on-line on February 5 in the American Heart Association’s journal Hypertension, could have major implications for the treatment of cardiovascular disease. Lead by Amrita Ahluwalia, professor at the William Harvey Research Institute at Barts and The London School of Medicine, and Ben Benjamin, professor at Peninsula Medical School, USA, the research reveals that it is the ingestion of dietary nitrate contained within beetroot juice – and similarly in green, leafy vegetables – which results ultimately in decreased blood pressure. Previously, the protective effects of vegetable-rich diets had been attributed to their antioxidant vitamin content. Effective one hour post ingestion Prof Ahluwalia and her team found that, in healthy volunteers, blood pressure was reduced within just one hour of ingesting beetroot juice, with a peak drop occurring three-four hours after ingestion. Some degree of reduction continued to be observed until up to 24 hours after consumption. Researchers showed that the decrease in blood pressure was due to the chemical formation of nitrite from the dietary nitrate in the juice. The nitrate in the juice is converted in saliva by bacteria on the tongue into nitrite. This nitrite-containing saliva is swallowed and, in the acidic environment of the stomach is either converted into nitric oxide or re-enters the circulation as nitrite. The peak time of reduction in blood pressure correlated with the appearance and peak levels of nitrite in the circulation, an effect that was absent in a second group of volunteers who refrained from swallowing their saliva during, and three hours following, beetroot ingestion. More than 25% of the world’s adult population are hypertensive, and it has been estimated that this figure will increase to 29% by 2025. In addition, hypertension causes around 50% of coronary heart disease, and approximately 75% of strokes. In demonstrating that nitrate is likely to underlie the cardio-protective effect of a vegetable-rich diet, the research of Prof Ahluwalia and her colleagues highlights the potential of a natural, low cost approach for the treatment of cardiovascular disease – a condition that kills over 110,000 people in England alone every year. Prof Ahluwalia concluded: â€Å"our research suggests that drinking beetroot juice, or consuming other nitrate-rich vegetables, might be a simple way to maintain a healthy cardiovascular system, and might also be an additional approach that one could take in the modern day battle against rising blood pressure. † 2. Zoler, Mitchel L. â€Å"Hypertension doubles female sexual dysfunction prevalence. † Family Practice News 36. 20 (Oct 15, 2006): 14. Summary Critique: We only know that hypertension affects the circulatory system of the human body. However, in this article by Mitchel Zoler (2006), it has been found that hypertensive women have double the risk of having sexual dysfunction than women with normal blood pressure. This proposition came after scientists have conducted a study of 417 women. As Dr. Michael Doumas reported in the annual meeting of the American Society of Hypertension, â€Å"women with controlled hypertension had a significantly lower prevalence of sexual dysfunction than did women whose hypertension failed to reach goal levels during treatment† (Zoler, 2006). In this particular study, all women were tasked to complete a â€Å"19-question form that has been validated as a way to evaluate sexual function†. The questions dealt with several domains of female sexual function: desire, arousal, lubrication, orgasm, satisfaction, and pain. The survey found out that among the women with hypertension, â€Å"42% had scores indicating sexual dysfunction†, which is far in statistically significant when compared with â€Å"19% among the normotensives†. Looking on how the researchers arrived at this conclusion can be doubtful because they merely based it on a survey, which can be a result of many other factors other than hypertension. Yet, this observation should not be taken complacently because hypertension is a common disease in the United States and its link to reproductive dysfunction in women should be established so that doctors will know how to alleviate the worsening problem of hypertension. Full Text Article: Zoler, Mitchel L. â€Å"Hypertension doubles female sexual dysfunction prevalence. † Family Practice News 36. 20 (Oct 15, 2006): 14. NEW YORK — Women with hypertension were twice as likely to have sexual dysfunction as normotensive women were, in a study of 417 women. The results also showed that women with controlled hypertension had a significantly lower prevalence of sexual dysfunction than did women whose hypertension failed to reach goal levels during treatment, Dr. Michael Doumas reported at the annual meeting of the American Society of Hypertension. But a third finding was that women who were treated with antihypertensive drugs had a higher prevalence of sexual dysfunction than did untreated women. Dr.Doumas speculated that this was caused by the effects of certain antihypertensive drugs, such as diuretics and [beta]-blockers. Treatment with other drug types, the angiotensin-receptor blockers and angiotensin-converting enzyme inhibitors, appeared to reduce sexual dysfunction, he said. â€Å"We need to treat hypertension because of its effect on adverse cardiac outcomes. But there is a hint that we can lower blood pressure with some drugs and also have good effects on female sexual function,† said Dr. Doumas, a physician in the department of internal medicine at the Hospital of Alexandroupolis in Athens. The study enrolled 216 women with hypertension and 201 normotensive women. Their average age overall was about 48, and all were sexually active. The women completed a 19-question form that has been validated as a way to evaluate sexual function. The questions dealt with several domains of female sexual function: desire, arousal, lubrication, orgasm, satisfaction, and pain. Among the women with hypertension, 42% had scores indicating sexual dysfunction, compared with 19% among the normotensives, which was a statistically significant difference. The prevalence of sexual dysfunction increased significantly with the duration of hypertension. Among women who had been hypertensive for fewer than 3 years, 16% had a score indicating sexual dysfunction; the rate rose to 33% among women with hypertension for 3-6 years and 79% among women with hypertension for more than 6 years. Age also showed a significant interaction with prevalence. Among women aged 31-40 years, the prevalence of dysfunction was 21%; the rate rose to 38% among women aged 41-50 and to 57% among women who were older than 50 years. The prevalence of sexual dysfunction was 48% among women treated for hypertension, compared with 33% among the untreated hypertensives, a significant difference. The average age was 48 years in both groups. But the prevalence was lower still among the hypertensive women who had their pressure controlled by treatment. With control defined as a pressure of less than 140/90 mm Hg, the prevalence of sexual dysfunction in women with controlled hypertension was 27%, significantly less than the 51% of women with uncontrolled hypertension who had dysfunction. It’s not yet known how antihypertensive drugs exert differing effects on sexual function. In general, drugs that cause vasodilation appear to improve sexual dysfunction, Dr. Doumas said. 3. â€Å"Liver linked to deadly disease. † USA Today (Magazine) 135. 2737 (Oct 2006): 10. The liver is important in the human body because it produces many enzymes that aid the digestion of our food intake. This is why it can be alarming to have liver disorders because it can affect our system from metabolizing food. For example, in the United States, many people consume an excessive amount of protein. The metabolism of excess protein, especially animal protein, can put a strain on the liver and kidneys in fats include dairy products, vegetable oils, and red meat. In this report from USA Today, it was found that liver disorders may trigger a deadly type of hypertension. As a physician from the University of Texas Southwestern Medical Center named Dan Rockey informed, this type of hypertension is called portal hypertension that â€Å"affects the blood flow into the portal vein, which feeds blood to the liver†. This report is alarming because the short-term mortality rate of having â€Å"portal hypertension is about 30%† (USA Today, October 2006). Dan Rockey and his colleagues are undergoing research to open new grounds for this disease and to find â€Å"possible clinical approaches†. Portal hypertension can trigger bleeding and development of fluid found in the abdomen. It is important to take more research on this type of hypertension because it can possibly become an epidemic if it is not treated. Also, we can take steps in taking care of our liver by reducing alcohol intake and eating healthy food. Full Text Article: â€Å"Liver linked to deadly disease. † USA Today (Magazine) 135. 2737 (Oct 2006): 10. Mechanisms causing a potentially deadly type of hypertension that result from liver damage have been identified by Don Rockey, a physician at the University of Texas Southwestern Medical Center, Dallas. Portal hypertension affects the blood flow into the portal vein, which feeds blood to the liver. Rockey identified the cellular activity that results in portal hypertension. He and his colleagues then took the research a step further, showing that, if the process can be interrupted, the hypertension subsides. â€Å"Portal hypertension is a deadly disease that complicates many forms of chronic liver injury,† he explains. â€Å"When this occurs, in its most severe form, the prognosis definitely becomes guarded,† often leading to the need for a liver transplant. The short-term mortality for patients with portal hypertension is about 30%. The latest research opens new ground and has implications for possible clinical approaches. â€Å"The end result of portal hypertension is bleeding and development of ascites [fluid in the abdomen]; so, if you could treat it early, you could prevent bleeding or the formation of ascites,† Rockey observes. Portal hypertension is similar to the widely known essential hypertension–which impairs blood flow to the heart systems–except it affects blood flow to the liver-related systems. The liver is an essential organ that washes the body’s blood of wastes and poisons. Cirrhosis of the liver occurs when the cells are damaged. Scarring often results, reducing blood flow and raising pressure on veins. The high pressure can cause veins to burst, resulting in internal bleeding and, potentially, death. Previous studies have shown that, at the cellular level, portal hypertension results from reduced production of needed nitric oxide, which regulates expansion of the blood vessels. Rockey’s research identifies how the nitric oxide production breaks down due to the effects of the protein GRK2. The protein attaches to another protein called AKT, interrupting the creation of nitric oxide. 4. Zoler, Mitchel L. â€Å"Hypertension diagnosis often missed in children. † Family Practice News 35. 11 (June 1, 2005): 15. We might not know it but children can develop hypertension too. Since the late 1980s, the rate of pre-hypertension and hypertension among U. S. children and teenagers has continued to increase. However, according to Zoler (June 1, 2005), experts miss 85% of these cases. In this article, Dr. Charlene K. Mitchell informed that â€Å"the problem with diagnosing hypertension in kids is that there are too many threshold pressures for most physicians to keep straight†. The guidelines for diagnosing children with the condition are different than those for adults. The point at which children are considered to have hypertension is determined by age, gender, weight and height, and young patients usually are not diagnosed until they have higher-than-normal readings for at least three visits. American Academy of Pediatrics guidelines require that blood pressure be taken at every doctors visit, but some physicians do not then calculate whether it is too high, especially if the child is healthy otherwise. This is why Dr. Mitchell suggested the researchers should be â€Å"aggressive† in finding a solution not to miss the diagnosis of hypertension in children. The impact of missing the diagnosis of hypertension in kids can be tremendous because it is a â€Å"killer† disease. Doctors missing to identify it could not suggest medications and this can be life-threatening for the children. More serious research should be conducted to identify what method is appropriate in determining the occurrence of hypertension in children. Full Text Article: Zoler, Mitchel L. â€Å"Hypertension diagnosis often missed in children. † Family Practice News 35. 11 (June 1, 2005): 15. New Orleans — A diagnosis of hypertension was missed in 85% of children with high blood pressure in a study of 287 youngsters who were examined at two university-based, pediatric clinics. The problem with diagnosing hypertension in kids is that there are too many threshold pressures for most physicians to keep straight, Charlene K. Mitchell, M. D. , said at the annual meeting of the Southern Society for Pediatric Research. Because the threshold for diagnosing hypertension varies by age, height, and gender, there are a total of 420 different diastolic and systolic pressures that determine whether a particular child has high blood pressure, said Dr. Mitchell, a pediatrician and internist at the University of Louisville (Ky. ). The total is 420 because there are 15 different age-specific threshold pressures for children aged 3-17 years, 7 different height-specific threshold pressures between the 5th and 95th height percentiles, different thresholds for girls and boys, and different thresholds for diastolic and systolic pressure. The threshold criteria for borderline hypertension would add another 120 pressure thresholds for diagnosing hypertension. â€Å"The numbers are chopped up too much. It’s far too complex for easy management,† Dr. Mitchell said. â€Å"If physicians must always look on a table every time they check a blood pressure, we’ll continue to see underdiagnosis. † Her solution to the number surfeit is to cluster several ages with a single diagnostic pressure threshold. However, eventually she would like to have study results establish pressure thresholds for diagnosing hypertension that are empirically derived, rather than based on statistics. If the diagnostic criteria are simplified, physicians will be much more likely to identify hypertension in children much more often, Dr. Mitchell said. â€Å"We need to be much more aggressive about recognizing hypertension in children than we are now,† she added. Her study was designed to assess physician accuracy at identifying hypertension in children aged 3-17 years being seen for routine, well-child visits from July 31 to Aug. 15, 2003. Of the 287 children examined, 90 (31%) had hypertension by current standards, and 35 (12%) had borderline hypertension. But only 15% of those with hypertension were diagnosed by their examining physicians. The results also showed that physicians were more likely to diagnose hypertension in children with a higher body mass index (BMI). The children who were correctly diagnosed as hypertensive were, on average, in the 92nd percentile for BMI. Those who had unrecognized blood pressure elevations were, on average, in the 76th percentile for BMI. 5. Bradbury, Jane. â€Å"The chicken and egg in hypertension†, The Lancet 349. 9059 (April 19, 1997), p. 1151. It is important to know where essential hypertension will trigger from because it can aid doctors to foresee the development of this dreaded disease. To wit, there is an ongoing debate of whether essential hypertension occurs when there is a perceived micro vascular abnormality or is when doctors see higher levels of blood pressure. In this article, UK clinicians found that males â€Å"with a familial predisposition to high blood pressure, a reduced number of capillaries and impaired microvascular dilatation precede hypertension†. In the research conducted by Professor David Webb and his team from the University of Edinburgh, they utilized the â€Å"four-corners epidemiological model† in predicting the triggering point of hypertension. Their study in 1977 determined the measure of blood pressure from 1809 married couples. In 1985, 864 of the 16–24 year-old children that came from the previous couples â€Å"had their blood pressure measured† too. Then, the researchers classified â€Å"four groups of offspring† by â€Å"combinations of personal (high or low) and parental (high or low) blood pressure†. Through these extensive studies, they determined that â€Å"microvessel characteristics which might be responsible for increased vascular resistance in essential hypertension†. Mostly, it is the males â€Å"with high blood pressure whose parents also had high blood pressure had significantly impaired dermal vasodilatation compared with the other three groups†. Also, they researchers observed they had â€Å"significantly fewer capillaries in the finger during venous occlusion†. This article can be helpful in the research of determining hypertension before it develops into a full-blown disease. Full Text Article: Bradbury, Jane. â€Å"The chicken and egg in hypertension†, The Lancet 349. 9059 (April 19, 1997), 1151. What comes first in essential hypertension-microvascular abnormalities or a rise in blood pressure? UK clinicians report this week that in men with a familial predisposition to high blood pressure, a reduced number of capillaries and impaired microvascular dilatation precede hypertension. Prof David Webb (University of Edinburgh, UK) and his team used the â€Å"four-corners† epidemiological model to unravel cause and effect in hypertension. In 1977, blood pressure was measured in 1809 married couples. 864 16–24 year-old offspring from 603 of the families had their blood pressure measured in 1985. Four groups of offspring were defined by combinations of personal (high or low) and parental (high or low) blood pressure. Microvessel characteristics which might be responsible for increased vascular resistance in essential hypertension were measured in 1993–95 for 105 men drawn from the four populations (J Clin Invest 1997; 99: 1873–79). Men with high blood pressure whose parents also had high blood pressure had significantly impaired dermal vasodilatation compared with the other three groups. They also had significantly fewer capillaries in the finger during venous occlusion. Factors which are associated with high blood pressure in offspring whose parent had high blood pressure are more likely to be causal than those that are associated with high blood pressure in the offspring irrespective of parental blood pressure, write the authors. The results suggest that defective angiogenesis may be an etiological component of hypertension, either environmental or genetic, and are consistent with the higher incidence of adult hypertension in people with a low birth weight. These findings, says Webb, should focus attention on the importance of early life factors in the programming of hypertension. 6. McCarron, David A. â€Å"Diet and high blood pressure – the paradigm shift. † Science 281. 5379 (August 14, 1998): 933-934. Doctors and nutritionists always exhort people to make a change to healthier diets because it can aid all of us in preventing deleterious diseases. According to McCarron (Aug. 14, 1998), â€Å"humans are nearly unique in their natural propensity to develop elevated arterial pressure, a fact attributed to both genetic and environmental factors†. Many experts point an accusing finger on salt being the one that can contribute to the occurrence of hypertension. However, McCarron (Aug. 14, 1998) revealed that the â€Å"importance of salt in the pathogenesis of hypertension† is still being debated and â€Å"remains undetermined†. Experts began to accuse the extreme use of salt as the one that causes hypertension â€Å"when early studies indicated that salt intake increased blood pressure†. However, McCarron (Aug. 14, 1998) indicated that â€Å"many of these studies have since been discounted for design and methodologic flaws. But even where the methodology is sound, sodium intake cannot be linked to hypertension or higher population-wide blood pressure†. In more conclusive studies, there existed a â€Å"compelling evidence that adequate intake of minerals, rather than restriction of sodium, should be the focus of dietary recommendations for the general population†. This article is enlightening due to the fact that it debunks the myth of salt being the primary cause of developing hypertension. The author suggests that we should limit our mineral intake and not just salt alone, in order to live a healthy lifestyle. We should not manipulate our diet to our own detriment, but we should shift it to become health-conscious because we are already armed with the knowledge of what’s good for us. Full Text Article: McCarron, David A. â€Å"Diet and high blood pressure – the paradigm shift. † Science 281. n5379 (August 14, 1998): 933(2). Hypertension–a serious health problem for industrialized societies–contributes significantly to the risk of coronary heart disease, congestive heart failure, stroke, and kidney failure. Among vertebrates, humans are nearly unique in their natural propensity to develop elevated arterial pressure, a fact attributed to both genetic and environmental factors. Only certain highly inbred strains of rodents and genetically engineered animals also spontaneously exhibit hypertension. Public policy has generally recommended that blood pressure can best be controlled by restriction of sodium chloride intake and with medication (1). Recent research has, however, emphasized the powerful role of total diet in the etiology and treatment of hypertension, suggesting that the focus of current public policy regarding nutrition and blood pressure is too narrow. Limitation of sodium chloride in food has historically been the dietary mantra of those who set nutritional policy for hypertension. Nevertheless, the importance of salt in the pathogenesis of hypertension has long been debated (2-4) and remains undetermined (5). The intense focus on sodium began when early studies indicated that salt intake increased blood pressure. These studies, many conducted decades ago, included epidemiologic surveys in primitive societies, clinical trials in patients with kidney disease, and animal investigations in which sodium intake levels cannot be realistically extrapolated to humans (6). Many of these studies have since been discounted for design and methodologic flaws. But even where the methodology is sound, sodium intake cannot be linked to hypertension or higher population-wide blood pressure (7). Two recent meta-analyses of randomized controlled trials–one examining the effects of sodium restriction (8) and the other of calcium supplementation on arterial pressure (9)–provide compelling evidence that adequate intake of minerals, rather than restriction of sodium, should be the focus of dietary recommendations for the general population. Assessing 56 trials of sodium restriction, Midgley et al. (8) concluded that individuals with normal blood pressure gained nothing from limiting sodium intake and that only older ([is greater than] 45 years) hypertensive people might benefit, a conclusion recently confirmed by other investigators (5). Midgley et al. also reported that the magnitudes of the blood pressure reductions were not consistently related to the amount of sodium intake, indicating that confounding factors were contributing to the changes in blood pressure. Indeed, in a meta-analysis of calcium supplementation trials, Bucher et al. (9) identified a small but consistent drop in blood pressure when normotensive and hypertensive persons consumed more calcium. They speculated that baseline calcium intake or increased biological need for minerals might be responsible for the blood pressure variability not otherwise accounted for in their analysis. These two reports presaged the outcomes of two large clinical trials from the NIH, published in 1997 (10, 11). The Trials of Hypertension Prevention (TOHP) II is the largest and longest study ever executed to test whether sodium restriction lowers arterial pressure and prevents the emergence of new hypertension cases (I0). No benefit was detected for the primary endpoint diastolic blood pressure. Systolic blood pressure decreased minimally (0. 7 mmHg), almost precisely the value that the Midgley (8) analysis projected. Furthermore, the TOHP II data demonstrated a dissociation between the extent of sodium restriction and the observed blood pressure reduction. The second large-scale study was the Dietary Approaches to Stop Hypertension (DASH) trial published in the New England Journal of Medicine (11). As would be predicted by Bucher et al. (9) in their meta-analysis of calcium studies, in persons whose intake of dairy products (and therefore calcium and other minerals) was well below currently recommended levels, blood pressure decreased significantly when the recommended amounts were included in their diets. In the DASH diet that was rich in dairy products, fruits, and vegetables and lower in fat (with sodium held constant), blood pressure decreased 5 to 6 mmHg in subjects with normal blood pressure; in those with mild hypertension, this blood pressure reduction was doubled, to 11 to 12 mmHg. Reductions of this magnitude have been observed previously only with antihypertensive medications. A second DASH diet, which included increased amounts of fruits and vegetables but did not include dairy products, produced more modest but still significant systolic blood pressure reductions, easily surpassing those observed with sodium restriction in TOHP II. DASH confirmed the meta-analyses as well as earlier indications from observational studies that dietary factors other than sodium markedly affected blood pressure (3, 12). For example, one of the earlier studies (12) identified inadequate calcium intake from dairy products as the dietary pattern most prevalent in individuals with untreated hypertension. Another study (3), in which nutrient intake was assessed from the first National Health and Nutrition Examination Survey (NHANES I), confirmed this dietary pattern in hypertensive individuals and identified the relative absence of fruits and vegetables in the American diet as the second best predictor of elevated blood pressure. These studies suggested that where intake of other critical nutrients is adequate, sodium intake at levels typically consumed in most societies might actually be associated with lower blood pressure. They also concluded that the absence of specific nutrients (calcium, potassium, and magnesium), resulting from low consumption of dairy products, fruits, and vegetables, is associated with hypertension in Americans (3, 12). The TOHP II study adds to the substantial body of literature that challenges the public health emphasis on sodium restriction as the primary nutritional means of improving blood pressure. The issue is further complicated by concerns raised in several recent reports (5, 13, 14) that the long-term effect of sodium restriction on cardiovascular morbidity and mortality may be the opposite of what has always been assumed. The DASH study provides a clear rationale for focusing our public health strategy on adequate intake of low-fat dairy products and fruits and vegetables. The consistency of the accumulated data is evident when the blood pressure changes seen with the DASH diet (11) are superimposed on the blood pressure profile of Americans as a function of calcium intake from (3) (see the figure). According to these data (3, 11), if the intakes of calcium and other nutrients obtained through low-fat dairy products, fruits, and vegetables were increased to the amounts readily achieved in the DASH study, the percentage of Americans with moderately severe hypertension (160/100 to 179/109 mmHg) would be decreased by nearly half, from approximately 9% to 5%. For the millions more with borderline elevations, the benefits are likely to be at least as great. Whether hypertension is genetic or environmental in origin, control of dietary mineral intake has a place in its management and prevention. As a society, we will not achieve the dramatic reversal in hypertensive heart disease that DASH and other studies clearly show is possible until we direct our efforts to the nutritional factors and dietary patterns that are actually relevant to this condition. In addition, diets low in fat but high in calcium, fruits, and vegetables are not prevalent in the subgroups of society at greatest risk for hypertensive cardiac disease–the elderly and African Americans. An added plus: A diet low in fat but high in calcium, fruits, and vegetables is also consistent with reduction of two other major public health problems, osteoporosis and cancer (15, 16). The emphasis on sodium as the single dietary culprit is counterproductive to our significantly reducing cardiovascular risk for most of us (5) and diverts attention from the issues we need to address (17). â€Å"Food products† such as snacks and soft drinks added to our diets in recent years have supplanted nutrient-rich foods such as fruits, vegetables, and milk. This shift in dietary patterns, and simultaneous suboptimal nutrient intake, is also far more likely to contribute to the prevalence of hypertension than salt, which has always been a component of the human diet. Humans may be unique in our propensity to develop hypertension simply because we are the only species with the capacity to manipulate our diets to our own detriment. References (1.) â€Å"The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure,† Arch. Intern. Med. 157, 2413 (1997). (2. ) G. Kolata, Science 216, 38 (1982). (3. ) D. A. McCarron, C. D. Morris, H. J. Henry, J. L. Stanton, ibid. 224, 139Z (1984). (4. ) J. D. Swales, Br. Med. J. 297, 307 (1988). (5. ) N. A. Graudal, A. M. Gallee, P. Gaffed, JAMA 279, 1383 (1998). (6. ) M. Muntzel and T. Drueke, Am. J. Hypertens. 5, 1S (1992). (7. ) Intersalt Cooperative Research Group, Br. Med. J. 297, 319 (1988). (8. ) J. P. Midgley, A. G. Matthew, C. I. T. Greenwood, A. G. Logan, JAMA 275, 1590 (1996). (9. ) H. C. Bucher et al. , ibid. , p. 1016. (10. ) Trials of Hypertension Prevention Collaborative Research Group, Arch. Intern. Med. 157, 657 (1997). (11. ) L. J. Appel et al. , N. Engl. J. Med. 336, 1117 (1997). (12. ) D. A. McCarron, C. Morris, C. Cole, Science 217, 267 (198Z). (13. ) M. H. Alderman, S. Madhavan, H. Cohen, J. E. Seatey, J. H. Laragh, Hypertension 25, 1144 (1995). (14. ) H. H. Alderman, H. Cohen, S. Madhavan, Lancet 351, 781 (1998).