Hypertension is a major cause of cardiovascular disease and deaths worldwide especially in low- and middle-income countries. Despite the availability of safe, well-tolerated, and cost-effective blood pressure (BP)-lowering therapies, <14% of adults with hypertension have BP controlled to a systolic/diastolic BP <140/90 mm Hg. We report new hypertension treatment guidelines, developed in accordance with the World Health Organization Handbook for Guideline Development. Overviews of reviews of the evidence were conducted and summary tables were developed according to the Grading of Recommendations, Assessment, Development, and Evaluations approach. In these guidelines, the World Health Organization provides the most current and relevant evidence-based guidance for the pharmacological treatment of nonpregnant adults with hypertension. The recommendations pertain to adults with an accurate diagnosis of hypertension who have already received lifestyle modification counseling. The guidelines recommend BP threshold to initiate pharmacological therapy, BP treatment targets, intervals for follow-up visits, and best use of health care workers in the management of hypertension. The guidelines provide guidance for choice of monotherapy or dual therapy, treatment with single pill combination medications, and use of treatment algorithms for hypertension management. Strength of the recommendations was guided by the quality of the underlying evidence; the tradeoffs between desirable and undesirable effects; patient’s values, resource considerations and cost-effectiveness; health equity; acceptability, and feasibility consideration of different treatment options. The goal of the guideline is to facilitate standard approaches to pharmacological treatment and management of hypertension which, if widely implemented, will increase the hypertension control rate world-wide.

: There is abundant evidence that the risk of atherosclerotic vascular disease is directly related to plasma cholesterol levels. Accordingly, all of the national and transnational screening and therapeutic guidelines are based on total or LDL cholesterol. This presumes that cholesterol is the most important lipoprotein‐related proatherogenic risk variable. On the contrary, risk appears to be more directly related to the number of circulating atherogenic particles that contact and enter the arterial wall than to the measured concentration of cholesterol in these lipoprotein fractions. Each of the atherogenic lipoprotein particles contains a single molecule of apolipoprotein (apo) B and therefore the concentration of apo B provides a direct measure of the number of circulating atherogenic lipoproteins. Evidence from fundamental, epidemiological and clinical trial studies indicates that apo B is superior to any of the cholesterol indices to recognize those at increased risk of vascular disease and to judge the adequacy of lipid‐lowering therapy. On the basis of this evidence, we believe that apo B should be included in all guidelines as an indicator of cardiovascular risk. In addition, the present target adopted by the Canadian guideline groups of an apo B <90 mg dL⁻¹ in high‐risk patients should be reassessed in the light of the new clinical trial results and a new ultra‐low target of <80 mg dL⁻¹ be considered. The evidence also indicates that the apo B/apo A‐I ratio is superior to any of the conventional cholesterol ratios in patients without symptomatic vascular disease or diabetes to evaluate the lipoprotein‐related risk of vascular disease.

The rates of coronary disease have accelerated dramatically amongst South Asians, driven to an important extent by the atherogenic dyslipidemia and type 2 diabetes that have become so common amongst them. These precursors of vascular disease appear at lower absolute amounts of adipose tissue in South Asians than in whites. In this paper, we set out a new hypothesis—the adipose tissue overflow hypothesis—to account for these findings. The adipose tissue mass within our bodies can be divided into three different compartments: superficial subcutaneous adipose tissue, deep subcutaneous adipose tissue and visceral adipose tissue. The superficial subcutaneous adipose tissue compartment is the primary compartment, is present throughout the body, and constitutes the vast majority of the adipose tissue in the lower limb. With energy excess, the secondary adipose tissue compartments—the deep subcutaneous (mainly upper body) and the visceral adipose tissue compartments—become more prominent. Superficial subcutaneous adipose tissue is relatively inert metabolically, whereas the other two compartments are characterized by higher transmembrane fatty acid flux rates and thus are more closely linked to dyslipidemia and dysglycemia. We hypothesize that the superficial subcutaneous adipose tissue compartment is larger in whites than in South Asians. If so, as obesity develops, South Asians exhaust the storage capacity of their superficial subcutaneous adipose tissue compartment before whites do and that is why they develop the metabolic complications of upper body obesity at lower absolute masses of adipose tissue than white people.

Summary: Evidence shows a strong relationship between obesity, cancer and cardiovascular disease (CVD) risk. However, there is not enough evidence of the role of visceral obesity on both CVD and cancer. Visceral obesity may be more pro‐oncogenic than total body fat. Therefore, it is important to know whether abdominal obesity can lead to both CVD and cancer. The present integrative review aimed at evaluating epidemiological evidence on the potential connection of visceral obesity in the occurrence of cancer and CVD. The following databases were searched: SCOPUS, PubMed, Science Direct, Lilacs, SciELO, Google Scholar, Web of Science, Scopus and ProQuest. The presence of visceral obesity can increase the risk of some specific cancer types, but there is controversial evidence about CVD risk based on sex‐specific and ageing analyses. There is enough evidence that visceral obesity increases the risk of colorectal, pancreatic and gastro‐oesophageal cancer. However, for some types of cancer such as breast, endometrial and renal, visceral obesity is a risk only in post‐menopausal women. Regarding prostate cancer, the evidence is controversial. Despite the risk of visceral obesity being consistently associated with CVD in adults, this association disappears in sex‐specific and older adults analyses. Moreover, in older adults, the results are controversial due to the use of different measures such as waist circumference and visceral adipose tissue. However, the evidence showing visceral obesity as a risk factor to CVD remains controversial. Sex differences, ageing and body mass index (BMI) category can potentially modify this association. Therefore, further epidemiological studies with analyses stratified by sex and samples including older adults aged 65 and older are needed.