Hypertension or high blood pressure is one of the most common chronic conditions and can be classified as either primary (or essential) hypertension or secondary hypertension [1]. The etiology of primary hypertension is considered indeterminate but multifactorial, while secondary hypertension results from an overt cause such as some form of kidney or adrenal gland disease, or the use of oral contraceptives [2]. High blood pressure is conventionally defined as a systolic measure of greater than or equal to 140 mmHg or a diastolic measure of greater than or equal to 90 mmHg [3]. A systolic measure ranging between 120 and 139 mmHg or a diastolic measure ranging between 80 and 89 mmHg is considered prehypertensive. Compensatory mechanisms exist for the homeostatic regulation of blood pressure, so in order for blood pressure to remain elevated, the compensatory mechanisms in place must be persistently overburdened or dysfunctional [4].
Arterial blood pressure is normally a variable powerfully controlled by baroreceptors (such as those found in the carotid arteries and aortic arch) and the renin-angiotensin-aldosterone system (RAAS). The RAAS is powered by the kidneys, liver, and adrenal glands, and involves the protein renin, the peptide hormone angiotensin 2, and the steroid hormone aldosterone. The kidneys convert prorenin into renin and secrete renin into circulation. The liver supplies angiotensinogen which renin converts into angiotensin 1. Angiotensin 1 is largely inert and thus must be transformed into angiotensin 2 by angiotensin-converting enzyme (ACE), found predominantly in the lungs. Angiotensin 2 is a potent vasoconstrictor, but it also triggers the adrenal glands’ release of aldosterone, which raises blood pressure by upping sodium and water reabsorption (as well as the excretion of potassium). Problems in any of the steps or components of the RAAS can disrupt electrolyte and fluid balance or blood pressure modulation [5]. The most commonly identified factor in the onset of hypertension is an excessive intake of dietary sodium, wherein the kidneys become unable to excrete the ingested sodium unless the blood pressure is increased [6]. Evidence suggests that our ancient ancestors consumed a diet that provided around 1,000 milligrams of sodium per day, whereas the average intake in the United States is greater than 3,000 milligrams [7]. Investigations into populations with a low daily intake of salt have found little or no hypertension with little or no rise in blood pressure with age [8]. On the other hand, a 30-year study of 144 Italian nuns demonstrated that the hypertensive effect of dietary salt can be blunted by a low-stress lifestyle [9]. An uptick in the sympathetic nervous system’s stimulation of the kidneys can boost renin secretion and renal sodium reabsorption, and heightened sympathetic nervous system activity is a frequent finding in those with primary hypertension [10]. Mental and emotional stress then, can activate the sympathetic branch and prevent urinary sodium loss through sparking the RAAS [11]. Relatedly, inflammation and oxidative stress in the kidneys can easily promote renal dysfunction and the onset of renal artery stenosis (stenosis meaning abnormal narrowing), also resulting in a boost in renin secretion and activation of the RAAS [12]. Also note that caffeine strongly stimulates the HPA axis and can stiffen the aorta and elevate blood pressure [13]. The hypothalamus is a key element in central blood pressure control and serves as an interface between the nervous and endocrine systems [14]. It has been proposed that more than half of primary hypertension cases can be categorized as neurogenic, and lessening inflammatory signaling within the hypothalamus has attenuated angiotensin 2-induced hypertension [15]. Accordingly, ongoing inflammation and free radical marauding in the brain can be a major factor in the sustainment of high blood pressure. Furthermore, angiotensin 2 can impair the integrity of the blood-brain barrier and drive hypertensive signal transduction in the hypothalamus [16]. So the more permeable the blood-brain barrier from whatever cause (e.g., gluten, toxins, EMFs, and heavy metals), the more blood pressure will be pushed upward. A high concentration of leptin in the blood can rouse the sympathetic nervous system and excite the RAAS in much the same way as mental or emotional stress, and hyperleptinemia can be triggered by proinflammatory cytokines as well as high insulin and fasting glucose [17] [18]. Leptin is a hormone crafted mainly by adipose or fat tissue that signals satiety. Generally speaking, greater fat mass equals greater leptin production which equals greater RAAS stimulation [19]. Elevated leptin can also directly exert oxidative stress upon the endothelial cells of arteries, contributing to vascular pathology and hypertension [20]. Note that renin, angiotensinogen, angiotensin 1, and angiotensin 2 can all be manufactured by fat tissue too, so through multiple means reducing excess adiposity can better blood pressure values [21]. Angiotensin 2 can instigate the generation of reactive oxygen species in vascular cells and enhance the oxidation of low-density lipoproteins (LDLs) by macrophages [22] [23]. Such LDL oxidation engenders foam cell accumulation and the onset of atherosclerosis [24]. As free radical numbers build in the endothelium, nitric oxide counts fall, encouraging endothelial dysfunction and atherogenesis [25]. As atheromas grow, blood vessels become blocked, blood flow becomes impeded, and blood pressure rises [26]. Though vitamin A, vitamin C, and vitamin E can scavenge free radicals in blood vessels and help thwart vascular injury from oxidant stress (vitamin E also helps dilate blood vessels and block platelet aggregation via the making of prostacyclin) [27] [28]. Similarly, vitamin D deficiency can induce hypertension by upping the crafting of renin and enhancing the progress of atherosclerosis [29]. Heightened free radical concentrations along with lessened nitric oxide and antioxidant concentrations in the cardiovascular system is a popular feature in the pathology of hypertension [30]. Again, escalated reactive oxygen species or free radical formation in arterial walls fosters endothelial dysfunction, vascular inflammation, and negative remodeling of the heart [31]. The tripeptide glutathione (made from glycine, cysteine, and glutamic acid) stands as one of the major gatekeepers between oxidative stress and hypertension, and in addition to its antioxidant roles, helps to maintain nitric oxide availability via the making of S-nitrosothiols which dilate blood vessels [32]. Nitric oxide normally exerts an anti-inflammatory effect in blood vessels by inhibiting the adhesion of leukocytes or white blood cells too [33]. So a draining of glutathione by toxins and free radicals can sap nitric oxide availability and weaken the body’s ability to manage blood pressure [34]. Indeed, glutathione depletion has been clearly observed in hypertensive subjects [35]. In remediation, augmenting the body’s supply of glutathione by supplementing with N-acetylcysteine or alpha-lipoic acid can notably slash blood pressure (vitamin C administration can help in much the same way) [36] [37] [38] [39]. In the same vein, mitochondrial dysfunction can lead to abnormal upregulation of the RAAS and foster insulin resistance, which in turn can further damage mitochondria and perpetuate a vicious cycle of mitochondrial injury, insulin resistance, hyperleptinemia, and hypertension [40]. A resistance to insulin can decrease the making of nitric oxide in endothelial cells and amplify its destruction [41]. In countering insulin resistance, supplementation with L-carnitine can be used to improve fatty acid oxidation by mitochondria and glucose utilization in skeletal muscle tissue [42]. Bettering insulin resistance with L-carnitine can improve nitric oxide availability, vascular cell function, and blood pressure [43]. The presence of chronic inflammation can be described as the prime facet of most hypertension cases. And inarguably hypertensive patients tend to exhibit a high plasma measurement of C-reactive protein (an inflammatory marker) [44]. Persistent inflammation can overstimulate the RAAS, and it is important to understand how immune cells have been implicated in the development of hypertension. As insightfully explained by Dinh et al.: “Hypertensive stimuli, including salt, overactivity of the RAAS, oxidative stress, and inflammation lead to an initial elevation in blood pressure (mainly because of central actions but also due to endogenous hormones such as Ang II and aldosterone), which results in protein modifications. These altered proteins are no longer recognized as self (i.e., they serve as neoantigens), and T cells are activated. T cell-derived signals promote entry of macrophages (and other inflammatory cells) into the vasculature and kidney which results in cytokine release. In the vasculature, activated T cells promote vasoconstriction and remodeling. Together with the promotion of sodium and water retention in the kidney, more severe hypertension can result” [45]. The conjuring of inflammation represents the body’s chief approach to the elimination of pathogens and the repair of damaged tissue, and inflammatory processes normally continue until the targeted pathogens are destroyed or the wounded tissue is healed. Ergo, if inflammation is ongoing, then pathogen subsistence and/or continual tissue injury is fanning its flame and must be resolved if hypertension is to be reversed. Appropriately, let us now turn our attention to the gastrointestinal tract, the most frequent source of inflammation in the human body. Compared with healthy controls, hypertensive patients have been seen to exhibit decreased microbial diversity in the GI tract and a Prevotella-dominated gut enterotype [46]. An overgrowth of gram-negative Prevotella and Klebsiella bacteria characterizes the gut dysbiosis associated with high blood pressure, and it has been found that hypertension can be transferred via fecal transplant (meaning the transfer of stool from a human with high blood pressure to a mouse, begetting high blood pressure in the mouse). Importantly, lipopolysaccharide or endotoxin from gram-negative bacteria in the gut can elicit a strong immune response and increase blood pressure by stoking the fire of systemic inflammation [47]. Indeed, lipopolysaccharide-triggered inflammation is the cardinal expression of pathogenicity from Prevotella and Klebsiella bacteria, and has been identified as a significant contributor to the manifestation of high blood pressure [48]. Fortunately, dysbiosis can be treated with probiotics, and probiotic supplementation with multiple strains has been shown to lower blood pressure in humans through multiple means [49]. Lastly, thyroidopathies can markedly alter blood pressure regulation and it is common to see hypothyroidism accompanying hypertension. The thyroid hormone triiodothyronine (T3) relaxes smooth muscle in blood vessels so a lack of functional T3 can drive blood pressure up by worsening arterial compliance and thus increasing systemic vascular resistance [50]. T3 is also needed for the proper development of a population of parvalbuminergic neurons in the hypothalamus that play a role in blood pressure management [51]. Now that we understand that inflammation, prooxidation, nervous system stress, and immune system strain are the chief ingredients in hypertension’s etiology, we can list some natural treatment options and agents. - In those who are overweight, weight loss can effectively lower blood pressure by calming the sympathetic nervous system and bringing down renin, aldosterone, and angiotensinogen release [52]. - A diet low in potassium induces sodium retention and a rise in blood pressure while potassium supplementation promotes natriuresis (the excretion of sodium in the urine via the kidneys) and a fall in blood pressure [53]. Therefore, consuming more potassium-rich foods like winter squash, radishes, broccoli, kale, bananas, cantaloupe, nectarines, lima beans, blackstrap molasses, salmon, tomatoes, and avocados can be helpful for those with hypertension [54]. - Consuming additional garlic and omega-3 fatty acids can also aid blood pressure values [55] [56]. Anti-inflammation and vasodilation appear to be the main effects exerted by fish oil and garlic [57]. - Meditation and appropriate exercise can lower blood pressure and the activity of renal sympathetic nerves [58] [59]. - Coenzyme Q10 can be a wonderful aid for hypertension as it not only supports mitochondria and ATP production, but also inhibits LDL oxidation, dilates blood vessels, reduces proinflammatory cytokines, and lessens blood viscosity [60]. - Overgrowth of the fungal species Candida albicans can exacerbate inflammation in the gut, worsen intestinal permeability, and fan inflammation outside the gut [61]. Many natural agents can be used to treat this popular aggravator of systemic inflammation, the beneficial yeast Saccharomyces boulardii being one of them [62]. - Aberrant methylation status or a deficiency of methyl donors (from methyl consumers like pesticides, toxic metals, food additives, and pharmaceuticals) can encourage high blood pressure via the generation of reactive oxygen species and vascular injury [63]. Eating more foods containing choline, betaine, or methionine (think eggs, chicken, spinach, carrots, cauliflower, Brussels sprouts, beets, mustard seeds, and shrimp) as well as supplementing with methylated folate (vitamin B9) or methylated cobalamin (vitamin B12) can augment your supply of methyl donors [64]. Fun fact: the simple act of sweating can help curb oxidative stress and methyl depletion by assisting the excretion of xenobiotics. - The enzyme nattokinase can function as an excellent tonic for the cardiovascular system and is capable of potent fibrinolytic, antihypertensive, antiatherosclerotic, and neuroprotective effects [65]. Nattokinase is available in isolated supplement form. - The amino acid taurine is capable of effectively lowering blood pressure and improving insulin resistance, while the shrub hawthorn is a time-tested hypotensive [66] [67]. - Calcium amplifies sodium excretion (preventing sodium retention) while sodium amplifies calcium excretion (pushing calcium deficiency). Hence, too much sodium or too little calcium can give rise to high blood pressure via the parathyroid hormone-incited outflow of calcium from bone into soft tissue (like blood vessels which harden as a result), the lack of sympathetic nervous system modulation by calcium, and the loss of arterial relaxation betterment by calcium [68] [69] [70]. - Magnesium can increase insulin sensitivity and bring down blood pressure by modulating vascular tone and prompting the release of both nitric oxide and prostacyclin [71]. Undeniably many Americans are deficient in magnesium. - The herb Indian snakeroot has a long history of use and can be beneficial for treating hypertension because of its ability to systemically lower sympathetic tone [72]. Reishi mushroom has demonstrated similar efficacy [73]. - Bark from the Terminalia arjuna tree is widely employed in Ayurveda for cardiovascular ailments and has documented antioxidant, hypolipidemic, antiatherogenic, and antihypertensive properties [74]. Ayurveda has also utilized the herb Coleus forskohlii for some time, which has the ability to combat inflammation, bring down blood pressure, block the aggregation of platelets, and relax smooth muscle in blood vessels [75]. - Olive leaf extract is another safe and effective antihypertensive that possesses antioxidant, antiatherogenic, anti-inflammatory, hypoglycemic, and hypocholesterolemic qualities [76]. The herb yarrow can notably lower blood pressure and blood lipids too [77]. - Lastly, black cumin seed oil has significantly decreased blood pressure without any adverse effects [78]. In conclusion, with natural medicine we can treat the causes of hypertension and restore health to the body long-term. As stated by Woolf and Bisognano, “For many patients, maximal medical therapy [meaning pharmaceutical prescription] is insufficient to adequately treat refractory hypertension” [79]. Conventional medicine struggles with treating high blood pressure because hypertension is usually multifactorial and pharmaceuticals ignore its root causes. But by taking a sensical approach and improving the diet, cleaning up the gut and liver, exercising more, reducing stress, detoxifying, and healing the circulatory system with natural tools, high blood pressure can be made a thing of the past. References:
1 Comment
|
AuthorDenton Coleman is an Exercise Physiologist and Medical Researcher. Archives
October 2023
Categories |