PDF The Plateau-proof Diet for Persons with Hypertension

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A growing body of evidence shows that low-fat diets often don't work, in part because these diets often replace fat with easily digested carbohydrates.

PDF The Plateau-proof Diet for Persons with Hypertension

Hundreds of diets have been created, many promising fast and permanent weight loss. Remember the cabbage soup diet? The grapefruit diet? How about the Hollywood 48 Hour Miracle diet, the caveman diet, the Subway diet, the apple cider vinegar diet, and a host of forgettable celebrity diets? The truth is, almost any diet will work if it helps you take in fewer calories. Diets do this in two main ways:. The best diet for losing weight is one that is good for all parts of your body, from your brain to your toes, and not just for your waistline.


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It is also one you can live with for a long time. In other words, a diet that offers plenty of good tasting and healthy choices, banishes few foods, and doesn't require an extensive and expensive list of groceries or supplements.

Resistant Hypertension - High Blood Pressure That's Hard to Treat

These approaches have been used extensively in various rodent models of hypertension, including L-NAME rats, SHRs, stroke-prone SHRs, salt-sensitive rats, renovascular models, Ang II—induced hypertension, and transgenic mice, and they have contributed enormously to elucidating the vascular phenotype as a cause and target of hypertension. In addition to impaired endothelial function, hyperreactivity, and structural remodeling, hypertension-induced vascular damage may involve rarefaction, which is characterized by a decrease in microvascular density.

Cardiac injury is a major consequence of persistent, uncontrolled hypertension.

Elevated BP culminates in myocardial strain, resulting in LVH, an independent risk factor for cardiovascular mortality. Disruption in cardiac architecture with LVH is associated with aberrant electrical conduction, leading to atrial or ventricular arrhythmias and sudden death. When the heart can no longer sustain normal function in the face of elevated afterload, persistent hypertension leads to diastolic and ultimately systolic heart failure. Accordingly, hypertension is a leading cause of congestive heart failure in humans.

In many rodent models of hypertension, approximating human stage 2 hypertension leads to LVH within 2 to 4 weeks, measured by augmented ratios of heart to body weight or heart to tibia length. The level of BP measured by radiotelemetry correlates with the extent of cardiac hypertrophy, making heart weight a possible surrogate for hypertension when direct measurements are unavailable. Rodent echocardiography allows direct assessment of changes in cardiac filling patterns and left ventricular wall thickness.

These detailed measurements allow discrimination between signaling pathways that favor physiological versus pathogenic cardiac hypertrophy. After 1 month, hypertensive cardiac injury in rodents is marked at the histological level by myocyte damage, mild perivascular fibrosis, and sparse mononuclear cell infiltrates, which nonetheless modulate cardiac injury during hypertension. At the molecular level, cardiac hypertrophy is characterized by recapitulation of fetal gene expression in experimental hypertension.

Scarring disrupts electric conduction in the heart with consequent discrete dysrhythmias that can be captured and quantified with current radiotelemetry monitoring systems. Hypertension-induced renal damage comprises at least 3 patterns: benign nephrosclerosis, malignant nephrosclerosis, and hypertension-accelerated kidney disease. The individual risk of end-stage kidney disease from benign nephrosclerosis is surprisingly small, but the net effect of benign hypertension is significant because hypertension itself is so common.

In contrast, malignant hypertension, which itself is uncommon, typically leads to kidney damage, often associated with fibrinoid necrosis and thrombosis of small vessels and glomeruli. Hypertension-induced renal damage most commonly occurs in the setting of underlying kidney disease, in which hypertension accelerates the progression, for instance, of diabetic kidney disease. The 3 subtypes of hypertension-induced renal damage have been replicated in animal models.

Rodent models like the SHR develop kidney damage very slowly. This appears to reflect preserved renal vascular autoregulation, with normal pressure-induced afferent vasoconstriction, preventing high arterial pressure from being transmitted to the glomerular capillaries. In contrast, when arterial pressure rises above a critical threshold, for example, in stroke-prone SHR rats exposed to high salt intake, renal damage develops rapidly, with lesions characteristic of malignant hypertension. This causes proteinuria and rapidly progressive renal dysfunction resulting from glomerular damage.

These characteristic features of human malignant hypertension can also be observed in Ren2 transgenic rats. In the setting of underlying renal disease, the relationship between arterial pressure and kidney damage shifts, and BPs that do not normally lead to progressive damage do so. Mechanisms involved are controversial and depend on the models used.

Many studies use five-sixths nephrectomy see the Renoprival Hypertension section. Kidney damage has been suggested to result from resultant dilation of the afferent arteriole with efferent vasoconstriction, which together increase glomerular capillary pressure independently of changes in arterial pressure.

Weight control and diet

In contrast, a surgical approach to reduce renal mass without generating hypertension showed that systemic hypertension is required for renal damage. Rodent models of diabetic kidney disease, for example, that are induced by streptozotocin on a SvE background, have been used to demonstrate the impact of superimposed hypertension on baseline kidney damage. Hypertension is a major risk factor for cerebrovascular diseases such as stroke ischemic and hemorrhagic and vascular dementia but also for neurodegenerative diseases, including Alzheimer disease.

Lacking energy reserves, the brain is highly susceptible to alterations in blood supply, and hypertension can promote both acute and chronic ischemic brain injury. Distinctive alterations, similar to those observed in the kidney lipohyalinosis , are observed in penetrating arterioles of the brainstem and basal ganglia. Functionally, hypertension alters myogenic tone and cerebrovascular autoregulation, induces endothelial dysfunction, impairs the ability of neural activity to increase cerebral blood flow neurovascular coupling , and damages the blood-brain barrier.

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Higher sodium, lower blood pressure. You read that right.

These structural and functional alterations promote vascular occlusions, leading to acute ischemic brain injury and chronic vascular insufficiency, causing white matter damage. A major consequence of the hypertensive white matter damage is cognitive impairment. Indeed, hypertension is the major cause of cognitive impairment on a vascular basis, the most common cause of dementia after Alzheimer disease. Several animal models of hypertension have been used to investigate the effects of hypertension on the brain Table 4. Although these models do not fully recapitulate the harmful effects of hypertension, they have provided valuable knowledge of the potential mechanisms underlying the susceptibility of the brain to hypertension.


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Most of the models used for cerebrovascular research have been in rodents, although there have been studies in larger animals, mainly pigs and monkeys. As noted, models based on administration of pharmacological agents have the advantage that the cause of hypertension is known and hypertension can be induced in a defined time frame and in transgenic animals, allowing the study of early mechanisms of disease at the molecular level, as well as cognitive dysfunction.

A disadvantage is that the hypertension is limited in time usually weeks and does not mimic the long-lasting impact on the brain of the human disease. Nevertheless, these models have been some of the most commonly used. Table 4. Genetic models based on intercrossing and selecting for the hypertensive phenotype, for example, stroke-prone SHRs and blood pressure high-2 BPH2 mice, exhibit lifelong hypertension and provide insight into the effects of hypertension on the brain, including cognitive dysfunction, over the life course.

However, the precise cause of the hypertension remains unknown, raising the possibility that the cerebrovascular alterations are not attributable to hypertension but to unrelated genetic factors. For example, the increased susceptibility to ischemic brain injury in SHRs and stroke-prone SHRs could be related, in part, to an inherited vulnerability of neurons to excitotoxicity. Some hypertension models that produce brain lesions infarcts, hemorrhages, or white matter lesions usually require the combination of pharmacological, dietary, genetic, and surgical manipulations to enhance the effects of hypertension on the brain Table 4.

Although this mimics the neuropathological impact of hypertension, the time when lesions develop cannot be predicted, and the location of the lesions is highly variable. Of particular interest are models in larger animals such as pigs and monkeys, in which brain size, gray-white matter ratio, vascular topology, cognitive testing, and cardiovascular function have greater translational relevance.

However, these models are expensive, not well suited to high-throughput investigations, and less amenable to genetic manipulations. In summary, although investigations into target-organ damage in animal models of human hypertension have focused mainly on vessels, the heart, and the kidney, there is a paucity of information on the brain effects in these models.

This is particularly evident in renovascular hypertension and low-renin hypertension. Considering the devastating impact of hypertension on the brain and its vessels and its pathogenic role in a wide variety of brain diseases, there is a strong rationale for expanding application of state-of-the-art cerebrovascular and neurovascular investigative tools to delve deeper into the mechanisms through which hypertension promotes neurovascular and neurodegenerative diseases.

Great insight has been gained from the genetic study of human hypertension. Studies of monogenic forms of hypertension have revealed the molecular basis of several related syndromes. More recently, GWAS analyses uncovered common variants of modest effect and low-frequency variants that contribute to BP variation in patients. These studies provide important insight into human disease, which can be complemented by animal studies, often in models exhibiting phenotypic characteristics observed in human hypertension, which can provide mechanistic biological insight into gene function and underlying cardiovascular risk.

Of the different inbred species used for genetic studies of hypertension, the rat has been widely used for the identification of QTL with linkage analysis approaches. This has been driven by the large number of rat genetic models of hypertension, the relatively low cost of rat experimentation, and the ease and accessibility of techniques for assessing cardiovascular phenotypes in rats.

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The functional validation of QTL has been enabled by the generation of congenic or consomic strains, in which defined segments of DNA from 1 strain are introgressed onto the genetic background of a second strain with a genetic marker—assisted breeding strategy. With this approach, phenotypic differences detected between the parental and congenic strains can indicate that a gene or genes within a particular substituted region of genomic DNA have an influence on the functional trait of interest.

The subsequent identification of genes within these QTL has been difficult and depends on complementary approaches, including transcriptomic analyses, gene sequencing, and gene editing. Rodent models have served as excellent platforms to validate the impact of deletion or overexpression of individual genes associated with hypertensive traits in GWASs or other linkage studies. In addition to their value for genetic and genomic studies, these models have contributed to recognition of the influence of environmental factors on disease phenotypes, including hypertension, fueling the study of epigenetics.

Epigenetics refers to the effects of environmental factors that induce changes in an organism resulting from modifications in gene expression rather than a direct alteration of DNA sequence. These modifications commonly occur through DNA methylation, posttranslational histone modifications, and noncoding RNAs.

Of these factors, DNA methylation has been most studied. For example, elevated methylation of the promoter region of HSd11b2 has been correlated with reduced activity of the enzyme and hypertension in patients. RNAs that do not code for proteins can influence disease pathogenesis by regulating the effectiveness of gene expression through modulation of mRNA levels and repression of mRNA translation.