Abstract-Improving diet and lifestyle is a critical component of the American Heart Association's strategy for cardiovascular disease risk reduction in the general population. This document presents recommendations designed to meet this objective. Specific goals are to consume an overall healthy diet; aim for a healthy body weight; aim for recommended levels of low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides; aim for normal blood pressure; aim for a normal blood glucose level; be physically active; and avoid use of and exposure to tobacco products. The recommendations are to balance caloric intake and physical activity to achieve and maintain a healthy body weight; consume a diet rich in vegetables and fruits; choose whole-grain, high-fiber foods; consume fish, especially oily fish, at least twice a week; limit intake of saturated fat to Ͻ7% of energy, trans fat to Ͻ1% of energy, and cholesterol to Ͻ300 mg/day by choosing lean meats and vegetable alternatives, fat-free (skim) or low-fat (1% fat) dairy products and minimize intake of partially hydrogenated fats; minimize intake of beverages and foods with added sugars; choose and prepare foods with little or no salt; if you consume alcohol, do so in moderation; and when you eat food prepared outside of the home, follow these Diet and Lifestyle Recommendations. By adhering to these diet and lifestyle recommendations, Americans can substantially reduce their risk of developing cardiovascular disease, which remains the leading cause of morbidity and mortality in the United States.

Abstract-A substantial body of evidence strongly supports the concept that multiple dietary factors affect blood pressure (BP). Well-established dietary modifications that lower BP are reduced salt intake, weight loss, and moderation of alcohol consumption (among those who drink). Over the past decade, increased potassium intake and consumption of dietary patterns based on the "DASH diet" have emerged as effective strategies that also lower BP. Of substantial public health relevance are findings related to blacks and older individuals. Specifically, blacks are especially sensitive to the BP-lowering effects of reduced salt intake, increased potassium intake, and the DASH diet. Furthermore, it is well documented that older individuals, a group at high risk for BP-related cardiovascular and renal diseases, can make and sustain dietary changes. Key Words: AHA Scientific Statements Ⅲ blood pressure Ⅲ diet Ⅲ hypertension E levated blood pressure (BP) remains an extraordinarily common and important risk factor for cardiovascular and renal diseases, including stroke, coronary heart disease, heart failure, and kidney failure. According to the most recent NHANES survey (1999 to 2000), 27% of adult Americans have hypertension (systolic BP Ն140 mm Hg, diastolic BP Ն90 mm Hg, or use of antihypertensive medication), and another 31% have prehypertension (systolic BP of 120 to 139 mm Hg or diastolic BP of 80 to 89 mm Hg, not on medication). 1 Prehypertensive individuals have a high probability of developing hypertension and carry an excess risk of cardiovascular disease as compared with those with a normal BP (systolic BP Ͻ120 mm Hg and diastolic BP Ͻ80 mm Hg). 2 It has been estimated that among adults Ͼ50 years of age, the lifetime risk of developing hypertension approaches 90%. 3 Recent data indicate that the prevalence of hypertension is increasing 4 and that control rates among those with hypertension remain low. 5 On average, blacks have higher BP than nonblacks, 4 as well as an increased risk of BP-related complications, particularly stroke 6,7 and kidney failure. 8 BP is a strong, consistent, continuous, independent, and etiologically relevant risk factor for cardiovascular and renal disease. 9 Notably, no evidence of a BP threshold exists; ie, the risk of cardiovascular disease increases progressively throughout the range of BP, including the prehypertensive range. 10 It has been estimated that almost a third of BP-related deaths from coronary heart disease occur in individuals with BP in the nonhypertensive range. 11 Elevated BP results from environmental factors, genetic factors, and interactions among these factors. Of the environmental factors that affect BP (diet, physical inactivity, toxins, The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a...

Abstract-High intakes of dietary sugars in the setting of a worldwide pandemic of obesity and cardiovascular disease have heightened concerns about the adverse effects of excessive consumption of sugars. In 2001 to 2004, the usual intake of added sugars for Americans was 22.2 teaspoons per day (355 calories per day). Between 1970 and 2005, average annual availability of sugars/added sugars increased by 19%, which added 76 calories to Americans' average daily energy intake. Soft drinks and other sugar-sweetened beverages are the primary source of added sugars in Americans' diets. Excessive consumption of sugars has been linked with several metabolic abnormalities and adverse health conditions, as well as shortfalls of essential nutrients. Although trial data are limited, evidence from observational studies indicates that a higher intake of soft drinks is associated with greater energy intake, higher body weight, and lower intake of essential nutrients. National survey data also indicate that excessive consumption of added sugars is contributing to overconsumption of discretionary calories by Americans. On the basis of the 2005 US Dietary Guidelines, intake of added sugars greatly exceeds discretionary calorie allowances, regardless of energy needs. In view of these considerations, the American Heart Association recommends reductions in the intake of added sugars. A prudent upper limit of intake is half of the discretionary calorie allowance, which for most American women is no more than 100 calories per day and for most American men is no more than 150 calories per day from added sugars. (Circulation. 2009; 120:1011-1020.)Key Words: AHA Scientific Statements Ⅲ cardiovascular diseases Ⅲ carbohydrates, dietary Ⅲ diet Ⅲ beverages Ⅲ carbonated beverages Ⅲ lipids N ew evidence on the relationship between intake of sugars and cardiovascular health has emerged since the last American Heart Association (AHA) scientific statement was published in 2002. 1 In 2006, the AHA published revised diet and lifestyle recommendations that recommend minimizing the intake of beverages and foods with added sugars. 2 The present statement expands on that recommendation by reviewing the evidence for recommending a specific upper limit of intake for added sugars. Because the focus of the present statement is on added sugars, recommendations for intake of naturally occurring sugars and complex carbohydrates are beyond its scope. Consumption of Sugars in the United StatesSugars are a ubiquitous component of our food supply and are consumed as a naturally occurring component of many foods and as additions to foods during processing, preparation, or at the table. 3 There are various definitions for sugar. Table 1 The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclos...

Abstract-Plasma leptm concentration IS increased m hypertensive obese humans, but whether leptm contributes to the increased arterial pressure m obesity 1s not knownIn this study, we tested whether chronic increases m leptm, to levels comparable to those m obesity, could cause a sustained increase m arterial pressure and also the importance of central nervous system (CNS) versus systemic mechanisms Five male Sprague-Dawley rats were implanted with chronic nonoccludmg catheters m the abdominal aorta and both carotid arteries for CNS mfunon, and five other rats were implanted with an abdominal aorta catheter and femoral vem catheter for intravenous (IV) mfuslon After 7 days of control, leptm was infused mto the carotid arteries or femoral vem at 0 1 pg/kg/mm for 5 days and 1 0 pg/kg/mm for 7 days, followed by a 7-day recovery period. The carotid artery and IV mfuslons of leptm at 1 pg/kg/mm slgmficantly increased plasma leptm levels, from 1.2?0 4 ng/mL to 91f5 ng/mL and from 0 9+-O 1 ng/mL to 9429 ng/mL, respectively, but there was no slgmficant increase m either group at the low dose Food intake also did not change at the low dose but decreased by approximately 65% m the carotid group and 69% m the IV group after 7 days of the 1 pg/kg/mm mfuslon Mean arterial pressure (MAP) Increased slightly at the low dose only m the carotid group, but this was not statlstlcally slgmficant At the higher dose, however, MAP increased significantly from 862 1 mm Hg to 942 1 mm Hg m the carotid group and from 87?1 mm Hg to 9321 mm Hg m the IV group. Heart rate also increased algmficantly m both groups at 1 pg/kg/mm leptm mfuslon Fasting blood glucose and msuhn levels decreased significantly at 1 pg/kg/mm m both the carotid artery group (-10 5% and -82 5%, respectively) and the IV group (-13 6% and -80 4%, respectively) All variables returned to control levels after leptm mfuslon was stopped. These results Indicate that chronic increases m clrculatmg leptm cause sustained increases m arterial pressure and heart rate and are consistent with a possible role for leptm m obesity hypertension.(Hypertension. 1998;31[part 2]:409-414.)Key Words: leptm n hypertension H sympathetic nervous system n blood pressure n heart rate n food intake

To create a drug, nature's blueprints often have to be improved through semisynthesis or total synthesis (chemical postevolution). Selected contributions from industrial and academic groups highlight the arduous but rewarding path from natural products to drugs. Principle modification types for natural products are discussed herein, such as decoration, substitution, and degradation. The biological, chemical, and socioeconomic environments of antibacterial research are dealt with in context. Natural products, many from soil organisms, have provided the majority of lead structures for marketed anti-infectives. Surprisingly, numerous "old" classes of antibacterial natural products have never been intensively explored by medicinal chemists. Nevertheless, research on antibacterial natural products is flagging. Apparently, the "old fashioned" natural products no longer fit into modern drug discovery. The handling of natural products is cumbersome, requiring nonstandardized workflows and extended timelines. Revisiting natural products with modern chemistry and target-finding tools from biology (reversed genomics) is one option for their revival.

This study examined the control of renal hemodynamics and tubular function, as well as systemic hemodynamics, during obesity-induced hypertension in chronically instrumented conscious dogs. Mean arterial pressure, cardiac output, and heart rate were monitored 24 hours a day using computerized methods, water and electrolyte balances were measured daily, and renal hemodynamics were measured each week during the control period and 5 weeks of a high-fat diet. After 7 to 10 days of control measurements, 0.5 to 0.9 kg of cooked beef fat was added to the regular diet, and sodium intake was maintained constant at 76 mmol/d throughout the study. After 5 weeks of the high-fat diet, body weight increased from 24.0±1.0 to 35.9±4.9 kg, mean arterial pressure increased from 83±5 to 100±4 mm Hg, cardiac output increased from 2.86 ±0.27 to 4.45 ±0.55 L/min, and heart rate rose from 68 ±5 to 107 ±9 beats per minute. Associated with the hypertension was an increase in cumulative sodium balance to 507 ±107 mmol after 35 days and a rise in sodium iothalamate space, an index of extracellular fluid volume, to 131 ±4% of control. Sodium retention was due to increased tubular reabsorption, because glomerular filtration rate and effective renal plasma flow increased throughout the 5 weeks of the high-fat diet, averaging 135 ±4% and 149±19% of control, respectively, during the fifth week of the high-fat diet. Plasma renin activity and plasma insulin concentration increased from 0.46±0.12 ng angiotensin I/mL per hour and 11.1±2.6 (iXS/mL, respectively, to 1.10±0.23 ng angiotensin I/mL per hour and 30.1 ±7.0 fiU/mL after 5 weeks. Because decreased sodium excretion occurred despite elevated mean arterial pressure, obesity-induced hypertension in dogs is associated with a shift of renal pressure natriuresis that is caused by increased tubular reabsorption, although the exact mechanism by which this occurs is still unclear. W eight gain appears to be an important factor in elevating blood pressure in many essential hypertensive individuals. 14 Epidemiological studies have shown that hypertension is more prevalent in obese than in nonobese individuals and that blood pressure is correlated to body weight, even in normotensive subjects. "5 Experimental studies have demonstrated that weight gain, even over a period of a few weeks, consistently elevates blood pressure and weight loss decreases blood pressure independent of changes in sodium intake. "10 Although this association between obesity and hypertension is widely recognized, the mechanisms responsible for weight-related changes in blood pressure have not been elucidated.Much of the evidence for various mechanisms postulated to cause obesity-induced hypertension derives from studies that have attempted to correlate various abnormalities in obesity with hypertension. Establishing cause-and-effect relations has been hampered by the lack of suitable animal models that mimic obesityinduced hypertension in humans and that allow sequen-

Plasma levels of IL-6 correlate with high blood pressure under many circumstances, and ANG II has been shown to stimulate IL-6 production from various cell types. This study tested the role of IL-6 in mediating the hypertension caused by high-dose ANG II and a high-salt diet. Male C57BL6 and IL-6 knockout (IL-6 KO) mice were implanted with biotelemetry devices and placed in metabolic cages to measure mean arterial pressure (MAP), heart rate (HR), sodium balance, and urinary albumin excretion. Baseline MAP during the control period averaged 114 +/- 1 and 109 +/- 1 mmHg for wild-type (WT) and IL-6 KO mice, respectively, and did not change significantly when the mice were placed on a high-salt diet (HS; 4% NaCl). ANG II (90 ng/min sc) caused a rapid increase in MAP in both groups, to 141 +/- 9 and 141 +/- 4 in WT and KO mice, respectively, on day 2. MAP plateaued at this level in KO mice (134 +/- 2 mmHg on day 14 of ANG II) but began to increase further in WT mice by day 4, reaching an average of 160 +/- 4 mmHg from days 10 to 14 of ANG II. Urinary albumin excretion on day 4 of ANG II was not different between groups (9.18 +/- 4.34 and 8.53 +/- 2.85 microg/2 days for WT and KO mice). By day 14, albumin excretion was nearly fourfold greater in WT mice, but MAP dropped rapidly back to control levels in both groups when the ANG II was stopped after 14 days. Thus the approximately 30 mmHg greater ANG II hypertension in the WT mice suggests that IL-6 contributes significantly to ANG II-salt hypertension. In addition, the early separation in MAP, the albumin excretion data, and the rapid, post-ANG II recovery of MAP suggest an IL-6-dependent mechanism that is independent of renal injury.

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