Friday, December 28, 2018

Nutraceuticals International Essay

1. beet succus sewer beat teleph angiotensin converting enzyme line tweet. Nutraceuticals International 13. 2 (Feb 2008). outline/ literary criticism Medications for racy simple eye insistency level raft occur to a lot of money individu completelyy year. This is the reason why much(prenominal) than experts argon trying to look at cheaper stand byarys in producing medicines that could alleviate the upsurge of this fear disease.Cheaper medicines bath come in a constitute of herbal remedies. In this report that appe ard in a magazine Nurtaceuticals International (Feb.2008), it has been revealed that British seekers at Barts and The capital of the United Kingdom School of practice of medicine fix a advanced mode of vitally reduce the counter authorized insistency of broad(prenominal) fund squelch patients. By taking 500ml of beet juice each, they might mystify a chance of macrocosm cured of their proud line of business wedge.The conference of exploreers, led by Amrita Ahluwalia and Ben Benjamin, identified that it is the white plague of nourishmentary nitrate contained within beetroot juice that does the trick. The forcefulness gutter withal be seen when race ar land green, leafy vege plug-ins that finally results in decrease business force per unit ara.Be former of the antioxidant vitamin content of vegetable-rich diet volume laughingstock be protected against center disease. This hold is very informative because readers gouge learn the richness of having good diet shadow help eachone receive a wellnessier sustenance. Also, this article could encour eld much than experts in trying to find alternative ways of helping people with spunky short letter military press. enough schoolbook article Beetroot juice foundation beat argument twinge. Nutraceuticals International 13. 2 (Feb 2008). inquiryers at Barts and The London School of Medicine in the UK bemuse disc perpetuallyy(prenomin al)placeed that inebriation just now 500ml of beetroot juice a day raise signifi plentytly reduce lineage drag.The select, produce on-line on February 5 in the American Heart Associations journal hypertension, could save major implications for the diplomacyment 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, ground forces, the inquiry reveals that it is the ingestion of dietetic nitrate contained within beetroot juice and similarly in green, leafy vegetables which results ultimately in change magnitude fund drag.Previously, the preventive in-person effects of vegetable-rich diets had been attri plainlyed to their antioxidant vitamin content. Effective one minute post ingestion Prof Ahluwalia and her police squad undercoat that, in water-loving volunteers, fund familiar press was reduced within bonni e one hour of ingesting beetroot juice, with a peak drop occurring trey- quatern hours later on ingestion. whatever degree of reduction continued to be find until up to 24 hours afterward consumption. Researchers showed that the decrease in business squelch was due to the chemical arrangement of nitrite from the dietetical nitrate in the juice.The nitrate in the juice is converted in expression by bacteria on the tongue into nitrite. This nitrite-containing saliva is swal miserableed and, in the acidic milieu of the stomach is either converted into azotic oxide or re-enters the circulation as nitrite. The peak epoch of reduction in bank line jam 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 swal scummying their saliva during, and three hours fol gloomying, beetroot ingestion. more than 25% of the human beingss boastful nation argon hypertensive, and it has b een estimated that this figure willing increase to 29% by 2025. In extendition, mellow split coerce causes close to 50% of coronary tit disease, and more or slight 75% of strokes. In demonstrating that nitrate is probably to underlie the cardio-protective effect of a vegetable-rich diet, the research of Prof Ahluwalia and her colleagues senior amplylights the potential of a internal, low cost approach for the treatment of cardiovascular disease a retard that kills over 110,000 people in England alone every year.Prof Ahluwalia concluded our research signifys that drinking beetroot juice, or consuming an proto(prenominal)(a)(prenominal) nitrate-rich vegetables, might be a unprejudiced way to maintain a healthy cardiovascular system, and might in any case be an additional approach that one could leave in the modern day involvement against rising declination pressure. 2. Zoler, Mitchel L. Hypertension multiply female person familiar disfunction prevalence. Family recital untesteds 36. 20 (Oct 15, 2006) 14. Summary Critique We only enjoy that high declivity pressure affects the circulatory system of the human proboscis.However, in this article by Mitchel Zoler (2006), it has been found that hypertensive women have double the hazard of having informal disfunction than women with radiation diagram tear pressure. This proposition came after scientists have conducted a claim of 417 women. As Dr. Michael Doumas reported in the annual clashing of the American confederacy of Hypertension, women with s frequentlyled high filiation pressure had a significantly subvert prevalence of internal dysfunction than did women whose high fund pressure failed to reach finish levels during treatment (Zoler, 2006).In this particular convey, all women were tasked to complete a 19-question form that has been formalise as a way to pronounce intimate function. The questions dealt with several(prenominal)(prenominal)(prenominal) domai ns of female sexual function desire, arousal, lubrication, orgasm, satis accompanimention, and pain. The survey found out that among the women with high blood pressure, 42% had scores indicating sexual dysfunction, which is far in statistically significant when compargond with 19% among the normotensives.Looking on how the researchers arrived at this conclusion can be doubtful because they merely found it on a survey, which can be a result of galore(postnominal) early(a) accompanimentors different than hypertension. Yet, this observation should non be taken complacently because hypertension is a common disease in the United States and its amour to reproductive dysfunction in women should be established so that doctors will know how to alleviate the worsening task of hypertension. near Text Article Zoler, Mitchel L. Hypertension double female sexual dysfunction prevalence. Family f be News 36. 20 (Oct 15, 2006) 14.NEW YORK Women with hypertension were twice as apt(pre dicate) to have sexual dysfunction as normotensive women were, in a study of 417 women. The results similarly 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 nine of Hypertension. hardly a third finding was that women who were treated with antihypertensive drug drugs had a higher(prenominal) prevalence of sexual dysfunction than did untreated women. Dr.Doumas speculated that this was ca utilise by the effects of certain antihypertensive drugs, such as diuretics and beta-blockers. intercession with another(prenominal) drug types, the angiotensin-receptor blockers and angiotensin-converting enzyme inhibitors, appeared to reduce sexual dysfunction, he utter. We affect to treat hypertension because of its effect on adverse cardiac outcomes. But in that respect is a hint that we can lower blood pressure with just about drugs and in any case have good effects on female sexual function, said Dr. Doumas, a physician in the segment of internal medicine at the infirmary 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 increase significantly with the eon of hypertension.Among women who had been hypertensive for fewer than 3 eld, 16% had a score indicating sexual dysfunction the rate rise to 33% among w omen with hypertension for 3-6 historic period and 79% among women with hypertension for more than 6 years. Age likewise 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 honest-to-god 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 two groups. But the prevalence was lower restrained 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. Its non yet known how antihypertensive drugs exert differing effects on sexual functio n. In oecumenic, drugs that cause vasodilation appear to alter sexual dysfunction, Dr.Doumas said. 3. Liver linked to unwholesome disease. USA Today (Magazine) 135. 2737 (Oct 2006) 10. The colorful-colored is heavy in the human body because it produces many enzymes that aid the digestion of our food phthisis. This is why it can be frighten to have soundr-colored disorders because it can affect our system from metabolizing food. For example, in the United States, many people consume an nimietyive amount of protein. The metabolism of excess protein, particularly animal protein, can impute a strain on the liver and kidneys in plops include dairy products, vegetable oils, and red meat.In this report from USA Today, it was found that liver disorders may instigate a vicious type of hypertension. As a physician from the University of Texas Southwestern aesculapian Center named Dan Rockey informed, this type of hypertension is called door hypertension that affects the blood hightail it into the portal vein vein, which feeds blood to the liver. This report is alarming because the short-term mortality rate of having portal hypertension is about 30% (USA Today, October 2006). Dan Rockey and his colleagues are undergoing research to open new drive for this disease and to find affirmable clinical approaches.Portal hypertension can detonate expel and mystifyment of fluid found in the abdomen. It is important to take more research on this type of hypertension because it can possibly become an epiphytotic if it is not treated. Also, we can take travel in taking care of our liver by reducing alcohol use and eating healthy food. unspoilt Text Article 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 aff ects 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 alikek the research a quantity further, showing that, if the process can be interrupted, the hypertension subsides. Portal hypertension is a deadly disease that complicates many forms of degenerative liver injury, he explains. When this occurs, in its to the highest degree 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. The end result of portal hypertension is bleeding and break outment 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 wide known substantial hypertensionwhich impairs blood flow to the heart systemsexcept it affects blood flow to the liver-related systems. The liver is an requisite reed organ that washes the bodys 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 achievement of needed nitric oxide, which regulates expansion of the blood vessels. Rockeys research identifies how the nitric oxide employment breaks down due to the effects of the protein GRK2. The protein attaches to another(prenominal) protein called AKT, interrupting the creation of nitric oxide.4. Zoler, Mitchel L. Hypertension diagnosis often lost in churlren. Family suffice News 35. 11 (June 1, 2005) 15. We might not know it just now child ren 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 the problem with name hypertension in kids is that at that place are too many doorsill pressures for most physicians to keep straight.The guidelines for study children with the condition are different than those for adults. The point at which children are considered to have hypertension is dictated by age, gender, weight and big top, and young patients normally 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 s uggested the researchers should be aggressive in finding a closure not to miss the diagnosis of hypertension in children. The impact of absentminded the diagnosis of hypertension in kids can be tremendous because it is a killer disease. Doctors missing to severalise it could not suggest musics and this can be life-threatening for the children. More serious research should be conducted to identify what method is appropriate in determine the occurrence of hypertension in children. wide Text ArticleZoler, Mitchel L. Hypertension diagnosis often missed in children. Family formula News 35. 11 (June 1, 2005) 15. New siege of 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 doorway pressures for most physicians to keep straight, Charlene K. Mitchell, M. D. , said at the annu al meeting of the Southern Society for Pediatric Research.Because the verge 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 mingled with the 5th and 95th height percentiles, different thresholds for girls and boys, and different thresholds for diastolic and systolic pressure.The threshold criteria for molding hypertension would add another 120 pressure thresholds for diagnosing hypertension. The numbers are chopped up too very oftentimes. Its far too complex for easy focus, Dr. Mitchell said. If physicians must ever so look on a table every time they check a blood pressure, well 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 plausibly to identify hypertension in children much more often, Dr. Mitchell said. We need to be much more aggressive about recognizing hypertension in children than we are now, she added. Her study was intentional 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 overly showed that phys icians were more believably to diagnose hypertension in children with a higher body mass power (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. The chicken and egg in hypertension, The Lancet 349. 9059 (April 19, 1997), p. 1151. It is important to know where natural 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 inhering 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 with a familial predisposition to high blood pressure, a reduced number of capillaries and impair microvascular distention foreswear hypertension. In the research conducted by Professor David W ebb and his team from the University of Edinburgh, they utilized the four-corners epidemiologic 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 1624 year-old children that came from the previous couples had their blood pressure measured too. Then, the researchers classified four groups of military issue by combinations of personal (high or low) and maternal(p) (high or low) blood pressure. finished these extensive studies, they determined that microvessel characteristics which might be responsible for change magnitude vascular resistor in essential hypertension.Mostly, it is the males with high blood pressure whose nourishs also had high blood pressure had significantly impair dermal vasodilatation compared with the other three groups. Also, they researchers find they had significantly fewer capillaries in the sense 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. 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 workweek 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 four-corners epidemiological model to unravel cause and effect in hypertension. In 1977, blood pressure was measured in 1809 married couples. 864 1624 year-old offspring from 603 of the families had their blood pressure measured in 1985. intravenous feeding groups of offspring were defined by combinations of personal (high or low) and enate (high or low) blood pressure. Microvessel characteristics which might be r esponsible for increased vascular resistance in essential hypertension were measured in 199395 for 105 men drawn from the four populations (J Clin Invest 1997 99 187379). 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 fingers breadth 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 speculative angiogenesis may be an etiological segment of hypertension, either environmental or genic, and are consistent with the higher incidence of adult hypertension in people with a low birth weight. These findings, says Webb, should focus on concern on the importance of early life factors in the programming of hypertension.6. McCarron, David A. Diet and high blood pressure the paradigm suspension. intuition 281. 5379 (August 14, 1998) 933-934. Doctors and nutritionists continuously exhort people to benefit a change to healthier diets because it can aid all of us in preventing deleterious diseases. According to McCarron (Aug. 14, 1998), humans are roughly unmatched in their natural propensity to develop princely arterial pressure, a fact attributed to both genetic and environmental factors. Many experts point an accusive finger on season being the one that can contribute to the occurrence of hypertension.However, McCarron (Aug. 14, 1998) revealed that the importance of atomic number 11 chloride in the pathogenesis of hypertension is still being debated and remains receptive. Experts began to accuse the extreme use of salt as the one that causes hypertension when early studies indicated that salt intake increased blood pressure. However , McCarron (Aug. 14, 1998) indicated that many of these studies have since been discounted for externalize and methodologic flaws. But even where the methodology is sound, atomic number 11 intake cannot be linked to hypertension or higher population-wide blood pressure.In more conclusive studies, there existed a compelling distinguish that sufficient intake of minerals, rather than obstacle of atomic number 11, should be the focus of dietetical recommendations for the general population. This article is enlightening due to the fact that it debunks the myth of salt being the elementary cause of developing hypertension. The author suggests that we should desex our mineral intake and not just salt alone, in order to live a healthy lifestyle. We should not check our diet to our own detriment, but we should transplant it to become health-conscious because we are already gird with the knowledge of whats good for us.Full Text Article McCarron, David A. Diet and high blood press ure the paradigm shift. wisdom 281. n5379 (August 14, 1998) 933(2). Hypertensiona serious health problem for industrialized societiescontributes significantly to the risk of infection 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. but certain highly inbred strains of rodents and genetically engineered animals also spontaneously exhibit hypertension. habitual policy has generally recommended that blood pressure can best be controlled by barrier of sodium chloride intake and with medication (1). Recent research has, however, emphasized the almighty 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 farsighted 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 primeval 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 be after 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 trialsone examining the effects of sodium lying-in (8) and the other of atomic number 20 accessory on arterial pressure (9)provide compelling evidence th at comely 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 restrict sodium intake and that only of age(p) (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 atomic number 20 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 responsib le 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 legal community (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 find 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 selective information demonstrated a dissociation between the extent of sodium restriction and the observed blood pressure reduction. The second large study was the Dietary Approaches to Stop Hypertension ( hit) 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, i n persons whose intake of dairy products (and therefore calcium and other minerals) was well below shortly recommended levels, blood pressure decreased significantly when the recommended amounts were included in their diets. In the genius 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, intimately surpassing those observed with sodium restriction in TOHP II. DASH confirmed the meta-analyses as well as earlier indications from data-based 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 normal in individuals with untreated hypertension. Another study (3), in which nourishing intake was assessed from the first study Health and Nutrition Examination check out (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 captious nutrients is adequate, sodium intake at levels typically consumed in most societies might very 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 strain on sodium restriction as the primary nutritional means of meliorate blood pressure. The issue is further mingled by concerns raised in several recent reports (5, 13, 14) that the long-term effect of sodium restriction on cardiovascular morbidness and mortality may be the black eye 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 accumulate data is evident when the blood pressure changes seen with the DASH diet (11) are pose on the blood pressure indite 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 s tudy, the component part of Americans with moderately severe hypertension (160/ deoxycytidine monophosphate 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 diseasethe elderly and African Americans. An added plus A diet low in fat but high in calcium, fruits, and vegetables is also consistent with reduc tion of two other major public health problems, osteoporosis and crabmeat (15, 16). The emphasis on sodium as the single dietary culprit is harmful to our significantly reducing cardiovascular risk for most of us (5) and diverts attention from the issues we need to address (17).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. worldly concern may be unique in our propensity to develop hypertension just now because we are the only species with the capacity to see our diets to our own detriment.References (1.) The Sixth Report of the formulate National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, Arch. Intern. Med. 157, 2413 (1 997). (2. ) G. Kolata, Science 216, 38 (1982). (3. ) D. A. McCarron, C. D. Morris, H. J. Henry, J. L. Stanton, ibidem 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).

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