PM2.5 and Neurodegenerative Diseases

Epidemiological human and animal studies support the notion that air pollution can affect the central nervous system (CNS) 

and lead to CNS disorders [165,166,167]. 

PM_2.5 and UFPM are of special concern as they can enter the systemic circulation and spread to the brain and other organs

, as well as obtain direct access to the brain via the nasal olfactory mucosa [168,169,170]. 

Decreased cognitive performance, olfactory problems, auditory impairments, depression symptoms, and other negative neuropsychological consequences have been reported in humans in highly polluted areas [171,172].

 Controlled acute diesel exhaust (300 g/m³) exposure has been demonstrated to cause electroencephalogram (EEG) alterations [173].

 Post-mortem examinations of highly exposed people have indicated elevations in the levels of indicators of oxidative stress and neuroinflammation [174]

. Furthermore, research suggests that young people may be especially vulnerable to air pollution-induced neurotoxicity [175]. 

Studies in Mexico City have found heightened levels of neuroinflammatory markers in the brains of children exposed to high levels of air pollution, as well as cognitive impairments and hyperactivity in 7-year-old children linked with early life exposure to traffic-related air pollution [176]

. A retrospective cohort study in Catalonia, Spain, discovered a link between air pollution (defined as residing 300 m from a highway) and the prevalence of attention deficit hyperactivity disorder (ADHD) [177]. 

In contrast, a major study including eight European population-based birth/child cohorts found no link between air pollution exposure and ADHD, similar to a Swedish investigation [178,179]. 

Experimental studies support the hypothesis that air pollution is a developmental neurotoxicant. A study by Ema, Naya, and Kato [180]

 indicated that developmental exposure to diesel exhaust may produce toxicity and neurotoxicity. In male mice, in utero exposure to high doses of diesel exhaust (1.0 mg/m³) resulted in changes in motor activity and coordination, and impulsive behavior [181]. 

Further research in mice revealed that postnatal injection (PND 4–7 and 10–13, for 4 h/day) of diesel exhaust particulate matter (DE-PM) (100 g/m³) induced alterations in GFAP expression in numerous brain areas, whereas UFPM (45 g/m³) caused male-specific learning and memory dysfunctions [182].

 Subsequent research has revealed that embryonic DE exposure in mice impacts motor activity, spatial learning and memory, and new object recognition abilities, and alters gene expression, causing neuroinflammation and oxidative damage [183].

 The effects of air pollution on the nervous system and its possible role in neurodegenerative disorders are illustrated in Figure 5

Ref

Int J Environ Res Public Health. 2022 Jun 19;19(12):7511. doi: 10.3390/ijerph19127511

Recent Insights into Particulate Matter (PM2.5)-Mediated Toxicity in Humans: An Overview

Prakash Thangavel 1, Duckshin Park 2,*, Young-Chul Lee 1,3,*

Editor: Paul B Tchounwou

PM2.5 and cardiovascular Diseases

   Cardiovascular Diseases

Epidemiological studies have shown a clear association between PM2.5 and cardiovascular diseases, including arrhythmia [123],

 cardiac arrest [124], coronary artery disease [125], heart failure [126,127], venous thromboembolism [128], and cerebrovascular disease [129] 

Acute exposure has been linked to such cardiovascular diseases. Individuals presenting with myocardial infarction were more like to have been in traffic 1–2 h prior [130].

 Although it is difficult to control for confounding variables such as noise and stress, correcting for activity intensity had no effect on the connection. The confounding relationship between pollution and cardiovascular health provides a prediction of cardiovascular health, noises, such as railway and air traffic, are highly connected with cardiovascular health [131]. 

However, with respect to considering the health effects of PM2.5, the confounding variables are not included to determine the PM2.5 effects of cardiovascular diseases.

 Subsequent investigations have further corroborated this link, which is independent of the mode of transportation used [132]. 

Epidemiological studies have associated air pollution with various end points underpinning cardiovascular conditions. Atherosclerosis in a variety of arterial beds has been linked to urban air pollution [133].

 Although there is some variation, PM exposure is linked to a slight but significant increase in blood pressure (typically 5 mmHg for an interquartile increase due to PM2.5) [134]. 

The constriction or reduced vasodilation of resistance arteries, which occurs after exposure to PM, elevates blood pressure. Although not all studies have identified significant connections, exposure to PM2.5 and traffic (e.g., distance from major road to residential address) has been related to increased arterial stiffness [135,136,137].

 Oxidative stress is the primary hierarchical response to PM exposure in humans, followed by other variables. Toll-like receptors (TLR2/TLR4) and nucleotide binding receptors are involved in this response and may be directly or indirectly activated by secondary mediators, including ROS [138,139,140]. 

The induction of ROS may lead to the activation of MAPK pathways, NF-κb, and AP1, which increases the synthesis of inflammatory proteins and brings about alterations in membrane permeability and mitochondrial dysfunction [141,142].

 Inflammatory markers induced by PM2.5 directly act on the heart and induce cardiac tissue remodeling and function alteration, leading to the development of cardiac diseases. Current evidence suggests that translocated PM2.5 causes both systemic inflammation and sympathetic activation in the cardiovascular system. PM2.5 causes systemic inflammation and elevates catecholamines, leading to an acute or chronic phase response of hypercoagulable state (suppression of fibrinolysis and activation of coagulation), vasoconstriction, increase in blood pressure, endothelial dysfunction, cardiac electrical changes, imbalance of cardiac ANS [143].

 Sympathetic activation increases catecholamine production, leading to endothelial dysfunction, increase in heart rate, and promotes vasoconstriction and hypertension [144]. The combined effects of systemic inflammation and sympathetic activation on their molecular targets lead to ischemic or thrombotic events, cardiac arrhythmia, and heart failure [145].

 The biological pathways whereby PM2.5 promotes cardiovascular impairments are illustrated (Figure 3). The effects of PM2.5 exposure on catecholamine levels show that PM2.5 exposure is a major disruptor of the cardiac autonomic nervous system (ANS). Little is known about how PM2.5 exposure affects the cardiovascular system, thus further study is needed to discover the negative health consequences linked with PM2.5 exposure [145]

.Changes in inflammatory pathways and ER stress have been identified as the key mechanisms by which PM2.5 promotes IR and T2DM and activates their pathophysiological responses [143,144,145]. 

Modulation of visceral adipose inflammation, hepatic lipid metabolism, glucose utilization in skeletal muscle, and CC-chemokine receptor 2-dependent pathways were discovered to play a significant role in PM2.5-mediated IR. Furthermore, PM2.5 has been shown to activate unfolded protein response (UPR), an intracellular ER stress signal that governs cell metabolism and survival in vivo, by phosphorylating inositol-requiring enzyme 1 alpha in hepatic cells [144]. 

Additionally, UPR or UPR-mediated ER stress has been linked to inflammatory pathways and has been shown to contribute to the generation of inflammatory mediators. Inflammatory mediators might activate or spread intracellular UPR [145].

 As a result of the combination between inflammation

 and ER stress, a positive feedback loop may form, amplifying the effects of PM2.5 on DM.

Ref

Int J Environ Res Public Health. 2022 Jun 19;19(12):7511. doi: 10.3390/ijerph19127511

Recent Insights into Particulate Matter (PM2.5)-Mediated Toxicity in Humans: An Overview

Prakash Thangavel 1, Duckshin Park 2,*, Young-Chul Lee 1,3,*

Editor: Paul B Tchounwou

              PM 2.5 Health Complications

The GBD study estimated the attributable levels of PM2.5 in 195 countries and territories worldwide. 

Ambient PM2.5 and household PM2.5 ranked among the top ten leading global risk factors for disease [48]

. Exposure to environmental PM2.5 has been associated with an increase in the incidence and mortality of many diseases.

 High risk of PM2.5-related death from stroke, ischemic heart disease, chronic obstructive pulmonary disease (COPD), lung cancer, and other diseases around the world has been demonstrated in several studies [49,50,51,52,53,54].

 The lungs, the initial sites of PM2.5 deposition in the airway, are among the primary targets of PM2.5-induced toxicity, which leads to airway inflammation, impairing normal immune responses of the lungs and making them susceptible to various respiratory infections [55]

. It’s been hypothesized that PM2.5 impairs the normal immune responses by various mechanisms.

 Firstly, PM2.5 can damage the bronchial mucociliary system, reducing bacterial clearance [56]. 

Secondly, PM2.5 and PM2.5-induced inflammatory cytokine net disruption may cause the death of lung epithelial cells and fibroblasts, as well as the inhibition of gap junctional intercellular communication between these cells, increasing epithelial barrier permeability and impairing their function as physical barriers for pulmonary innate immunity [57].

 Thirdly, alveolar macrophages are essential inflammation regulators and are required for antibacterial activity in the lower airway [58].

 Recently, increasing evidence has shown that PM2.5 not only inhibits alveolar macrophage phagocytosis by disrupting the normal physical and immunological function of lung surfactants, such as di-palmitoyl-phosphatidylcholine and amino acids related to opsonin proteins [59]

, but they also impair the response of natural killer (NK) cells [60] and inhibit antibacterial capabilities through transferrin-mediated Fe3+ transport [61],

 disrupting the expression of toll-like receptors (TLRs) and microtubule architecture [62,63]. 

Recently, increasing evidence has shown that PM2.5 not only inhibits alveolar macrophages phagocytosis by disrupting the normal physical and immunological function of lung surfactants, such as di-palmitoyl-phosphatidylcholine and amino acids related to opsonin proteins [59], which generally act as opsonins and enhance alveolar macrophages phagocytosis to bacteria, and impairing the response of natural killer (NK) cells [60], 

which also enhance alveolar macrophages phagocytosis, but also directly inhibiting alveolar macrophages antibacterial capabilities through a variety of methods. These methods include influencing transferrin-mediated Fe3+ transport to alveolar macrophages [61], affecting the expression of toll-like receptors (TLRs); disrupting microtubule architecture; and decreasing their phagocytic activities [62,63]. All of these would lead to reduced pulmonary immunity and facilitate infectious illnesses. Recently, chronic exposure to PM2.5 was found to be linked with the development of diabetes mellitus (DM), inducing multiple abnormalities associated with the development of type 2 diabetes mellitus (T2DM), insulin resistance (IR), adipose inflammation, and hepatic endoplasmic reticulum (ER) stress. Alterations in ER stress and inflammatory pathways have been proposed to be the mechanisms by which PM2.5 induces IR and T2DM [64]. Furthermore, PM2.5 exposure not only leads to subclinical changes in cardiovascular function, but also impairs the function of the cardiac autonomic nervous system (ANS), leading to a decline in heart rate variability, which is inevitably related to cardiovascular morbidity and mortality [65]. Epidemiological evidence suggests that PM2.5 is a risk factor for chronic kidney disease (CKD). Moreover, PM2.5 leads to a decrease in glomerular filtration rate (GFR) and is related to the prevalence and incidence of CKD [66]. Protecting the environment and the environmental health of mothers and infants remains a top global priority. Epidemiological evidence suggests that maternal PM2.5 exposure during pregnancy is associated with negative birth outcomes, including preterm birth, low birth weight, and post neonatal infant mortality [67,68,69,70,71]. The health impacts of PM2.5 are summarized (Table 2). In addition, PM2.5 influences several other adverse health effects such as bone damage, liver fibrosis, lung cancer, macrosomia, Alzheimer’s disease, ovarian dysfunction, hormone dysregulation, and compromised antiviral immunity [72,73,74,75,76,77,78].

Ref

Int J Environ Res Public Health. 2022 Jun 19;19(12):7511. doi: 10.3390/ijerph19127511

Recent Insights into Particulate Matter (PM2.5)-Mediated Toxicity in Humans: An Overview

Prakash Thangavel 1, Duckshin Park 2,*, Young-Chul Lee 1,3,*

Editor: Paul B Tchounwou

PM. 2.5 and Airways Inflammation

 5. PM2.5 and Airways Inflammation

The airways and lungs, the initial sites of PM_2.5 entry and deposition, are the primary targets of its toxicity. 

After PM_2.5 inhalation, the fine particles deposit on the surface of the airway and pulmonary bronchi and alveoli before being internalized into lung cells such as epithelial cells and alveolar macrophages [98]. 

Thereafter, PM_2.5 triggers oxidative stress and impairs the normal function of cells or can even induce apoptosis by different mechanisms, 

such as autophagy. Furthermore, PM_2.5 induces inflammatory responses, which play a major role in respiratory damage.

 Epidemiological evidence shows that PM_2.5 can regulate different inflammation-related signaling pathways, as indicated by elevated Th2 cytokine (interleukin (IL)-4, IL-5, and IL-13) levels in bronchoalveolar lavage fluid (BALF),

Ref 

 Int J Environ Res Public Health. 2022 Jun 19;19(12):7511. doi: 10.3390/ijerph19127511

Recent Insights into Particulate Matter (PM2.5)-Mediated Toxicity in Humans: An Overview

Prakash Thangavel 1, Duckshin Park 2,*, Young-Chul Lee 1,3,*

Editor: Paul B Tchounwou 

Particulate Matter (PM2.5) ,& Toxicity in Humans

 

Abstract

Several epidemiologic and toxicological studies have commonly viewed ambient fine particulate matter (PM_2.5), defined as particles having an aerodynamic diameter of less than 2.5 µm, as a significant potential danger to human health. 

PM_2.5 is mostly absorbed through the respiratory system, where it can infiltrate the lung alveoli and reach the bloodstream.

 In the respiratory system, reactive oxygen or nitrogen species (ROS, RNS) and oxidative stress stimulate the generation of mediators of pulmonary inflammation and begin or promote numerous illnesses. 

According to the most recent data, fine particulate matter, or PM_2.5, is responsible for nearly 4 million deaths globally from cardiopulmonary illnesses such as heart disease, respiratory infections, chronic lung disease, cancers, preterm births, and other illnesses. 

There has been increased worry in recent years about the negative impacts of this worldwide danger. The causal associations between PM_2.5 and human health, the toxic effects and potential mechanisms of PM_2.5, and molecular pathways have been described in this review.

1. Introduction

Particulate matter (PM) is made up of solid and liquid particles that are discharged directly into the air as a result of diesel use, road and agricultural dust, and industrial activity. 

The morphological, chemical, physical, and thermodynamic features of PM are diverse.

 Because of its size, density, and thermal conditions, as well as wind speed, PM remains suspended in the air, polluting it [1,2]. The WHO reported that around 7 million people 

die every year due to exposure to polluted air, and that ambient air pollution, especially in low/middle-income countries, caused 4.2 million deaths in 2016 (World Health Organization, 2016). 

Air pollution is caused by a mixture of substances such as gases, particles, and biological components in the earth’s atmosphere. The toxic effects caused by particle pollution on humans are dependent on their size, superficial area, and chemical composition [3]. 

The adverse health effects of gaseous pollutants have been extensively studied in the past few decades; however, despite differences in air pollutants and variations in local atmospheres, the basic features of acute and long-term health effects caused by such pollutants are yet to be explored [4]. 

Epidemiological studies collecting data on concentrations of the main gas pollutants, exposure, and dose for the exposed population have been conducted to determine the specific causes of observed health effects [5].

 Air pollution is the single largest environmental causative agent of various diseases. 

The health effects induced by exposure to air pollution mainly manifest in elderly people with pre-existing cardiopulmonary diseases [6], 

cerebrovascular diseases [7], neurodegenerative diseases [8], bronchitis [9], emphysema [10], increased irritation of the eye and respiratory system [11], asthma attacks [12], respiratory infections [13], and so on

 Air pollution has also been associated with adverse pregnancy outcomes such as preeclampsia and hypertensive disorders [14,15]. 

PM can be classified by its aerodynamic diameter size as PM10 (particles ≤ 10 µm in diameter); PM2.5 (particles ≤ 2.5 µm in diameter), also called fine particles; and PM0.1 (particles ≤ 0.1 µm in diameter),

 called ultrafine particles, which have different health effects, as the particles are strongly linked to particle size, which can deposit in the lung and can navigate through bronchioles and escape lung defense mechanisms [16]

. These particles are extensively found in the atmosphere and are released by various sources such as dust storms, forest fires, and volcanoes, as well as human activities, including transportation, fuel burning, and industrial processes [17]. 

The Global Burden of Disease (GBD) study estimated that 5 million deaths are caused by PM2.5 annually. PM2.5 is characterized by fine particles that have a large surface area.

 Due to their size, they can accumulate more compared to PM10, propagate long distances, become stagnant in the atmosphere, stay in the air longer,

 and travel farther [18]. 

PM2.5 is composed of primary particles that are emitted directly into the atmosphere and secondary particles produced by chemical reactions between precursor gases [19,20]. 

Primary PM2.5 particles which are directly emitted into the atmosphere can originate from both natural sources,

 such as dust storms and forest fires, and anthropogenic sources, such as fossil fuel combustion, cigarette smoke, and biomass burning. Secondary PM2.5 particles are generated by chemical reactions between PM from anthropogenic and biogenic sources [21,22]. The exact mechanisms associated with the impact of PM2.5 on the human body remain unclear. It is hypothesized that inhaled PM accumulates in the lungs and activates inflammatory cells, leading to the release of mediators and the stimulation of alveolar receptors, which causes an imbalance in the autonomic nervous system (ANS) and neuroendocrine pathway [23,24,25]. The other mechanism is translocation of PM via the pulmonary epithelium. The primary pollutants in fine PM enter the blood circulation and affect the whole organism. However, when there is inflammation in the lungs due to PM2.5, the inflammation leads to oxidative stress and causes vascular dysfunction [26,27]. Air pollutant particles, such as PM2.5, have a negative impact on the productivity of agricultural workers, land miners, and sewer employees due to the particles generated during their work [27]. Mineral dusts, such as those containing free crystalline silica (e.g., as quartz); organic and vegetable dusts, such as wheat, wood, cotton, and tea dust; and pollens may be found in the workplace. Dust particles or additives can enter the airway and impair lung function [28,29]. In this review, we discuss the sources of PM2.5 and its health effects on humans based on epidemiological, experimental, and molecular studies.

Ref Int J Environ Res Public Health. 2022 Jun 19;19(12):7511. doi: 10.3390/ijerph19127511

Recent Insights into Particulate Matter (PM2.5)-Mediated Toxicity in Humans: An Overview

Prakash Thangavel 1, Duckshin Park 2,*, Young-Chul Lee 1,3,*

Editor: Paul B Tchounwou

Lung cancer smaller particular matter risk?

 Introduction 

Great health concern has been placed on the severe air pollution in China. Particular matters as the dominant air pollutants in Chinese cities (e.g. PM1, PM2.5 and PM10), have already been recognized as the Group I carcinogenic factor to lung cancer diseases in the world [1]. 

As reported by the State of Global Air 2020, particular matter air pollution has led to the mortality of around 500,000 infants across the world [2].

 Despite considerable efforts on the estimates of particular matter effects, especially for PM2.5 and PM10 [3–5], however, whether finer particular matter has the greater effect on human health has not been well understood in China and across the world.Several potential mechanisms have been proposed

 to explain the varying effects of size-fractioned particular matters. 

Biologically, particular matters including PM1, PM2.5 and PM10, can exert adverse effects on the physical health of human beings by the way of aggregating genetic damage [1]. 

With regards to the difference in health effects, firstly, there

 is high ratio of surface area to volume in finer than in coarser particular matters.

 This enables finer particular matter to more easily approach the deeper places in lung, such as lung alveoli [6, 7]. 

Secondly, the proportion of toxic chemical composition is usually higher in finer than in coarser particular matters. Such physicochemical property makes finer particular matter more easily cause detrimental effects on lung function and epigenetic alteration [8, 9].

Empirically, few attempts have examined the effects of PMs with different particle sizes.

 In general, the argument that smaller particular matters have greater effects on human health, is still debated. 

Many studies tend to support this argument, especially for research investigating the effects of PM1, PM2.5 and PM10 [10–12].

 Particularly, a time-series study performed in 65 Chinese cities between 2014 and 2017 indicated that the association with cardiovascular disease was stronger for PM1 than for PM2.5 and PM10 [7].

Similarly, as reported in the 33 Communities Chinese Health Study, the odds ratio of cardiovascular disease associated with a 10 μg/m3 increase in PMs was 1.12 (95% CI:1.05, 1.20) for PM1, which was higher than 1.06 (95% CI:1.01, 1.11) of PM2.5 [13]. 

By contrast, some studies report the greater effects of particular matters with larger particle sizes [14, 15] 

or the insignificant effects of some size-fractioned particular matters [16, 17]. 

For example, a case–crossover study performed in Barcelona of Spain suggested that the effect on cardiovascular mortality during Non-Saharan dust days was smaller for PM1 than for PM2.5 and PM10 [18].

Apart from inconsistent findings above, more efforts are required 

due to the three reasons.

Firstly, of research investigating the varying effects of particular matters with different particle sizes, most are single- or several-site studies [12, 19–21], 

while nationwide studies are quite limited [7, 22]. 

Hence, findings from previous studies are still not sufficient to

 conclude the greater effects of finer particular matters than those of coarser particular matters.

 Secondly, few studies pay attention to PM1 which is the dominant component of severe PM2.5 air pollution in Chinese cities [23]

. This is partly resulted from the unavailable data on PM1, especially at the national scale [7, 10]. 

Thirdly, it remains unknown whether smaller particular matter has the larger effect on lung cancer which has become the second-order of cancer incidences for the female in China [24], although numerous studies have suggested the effects of PMs (especially for PM2.5 and PM10) 

on lung cancer diseases [3, 25–27].

To fill the aforementioned gaps, this work used 

data collected from 436 Chinse counties between 2014 and 2016 to examine whether finer particular matter has the greater effect on the incidence rate of female lung cancer in China where particular matter air pollution is much more severe than developed countries.

 To answer the research question, three regression models were developed with different controls of time, location and socioeconomic covariates. 

We further investigated whether the findings are sensitive to the controls of smoking and drinking behaviors as well as additional air pollutant. Moreover, we tried to answer whether urban-rural division modifies the association of the incidence rate of female lung cancer with each of three particular matters (i.e. PM1, PM2.5 and PM10).

Ref

BMC Public Health. 2022 Feb 18;22:344. doi: 10.1186/s12889-022-12622-1

Smaller particular matter, larger risk of female lung cancer incidence? Evidence from 436 Chinese counties

Huagui Guo 1, Xin Li 2, Jing Wei 3, Weifeng Li 4,5, Jiansheng Wu 6,7, Yanji Zhang 8,✉

Part 4 Non‐pharmacologic management of Hypertension

4.SODIUM MAGNESIUM AND POTASSIUM INTAKE

There is strong and consistent evidence that reducing sodium intake reduces BP. Adults should be advised to limit their sodium intake to no more than 2,400 mg per day (equivalent to around 5 gm/1 teaspoon of table salt per day). Further reduction of sodium intake to 1,500 mg per day is desirable because it is associated with an even greater reduction in BP. The average BP reduction in patients consuming a sodium‐restricted diet of 2,400 mg per day is 2/1 mm Hg, or 7/3 mm Hg for those restricting sodium to 1,500 mg per day. 33 Reducing baseline sodium intake by at least 1,000 mg per day will lower BP even if the desired daily sodium intake is not yet achieved. Food prepared out of home, canned foods, and prepackaged foods (dry or frozen) tend to contain more sodium than home‐cooked meals or frozen vegetables, so it is best to be avoided. Recent analysis of 15 randomized control trials (RCTs) for potassium supplementation (75‐125 mmol per day) in 917 normotensive and hypertensive patients independent to antihypertensive drugs had a reduction in SBP by 4.7 mmHg and in DBP values by 3.5 mmHg in all patients, an effect that was stronger in hypertensive by 6.8 and 4.6 mmHg for SBP and DBP values, respectively. 34 An analysis of 34 trials involving 2028 normotensive and hypertensive patients showed a positive effect of magnesium supplementation (368 mg/d) for three months, in lowering SBP by 2.0 mmHg and DBP values by 1.78 mmHg. We need more studies to clarify the role of potassium and magnesium supplementation in the management of hypertension. (Table 1)

TABLE 1.

Summarizing the main points/message of the review

1. A reduction of just 5 mm of Hg systolic blood pressure has been found to be associated with mortality reductions of 14% from stroke, 9% from heart disease, and 7% from all‐cause mortality

2. Dietary pattern is a very important part of non‐pharmacologic management of blood pressure as it is influenced by appropriate calorie requirements, personal, cultural food preferences, and nutritional therapy for other medical conditions, such as diabetes mellitus and chronic kidney disease.

3. Both the Mediterranean Diet and the Dietary Approaches to Stop Hypertension diet are relatively easy to adhere to and are palatable, high in fruit, vegetables, whole grains, nuts, and unsaturated oils; moreover, both minimize the consumption of red and processed meat, and are in accordance with dietary recommendations for cardiovascular health.

4. Cardioprotective effects of the alternate‐day fasting diet are associated with a reduction of visceral fat tissue, increased adiponectin, decreased leptin, and low‐density lipoproteins cholesterol. A method of intermittent fasting, like alternate‐day fasting or time restricted meal intake could be adopted by the patient.

5. Adults should be advised to limit their sodium intake to no more than 2,400 mg per day (equivalent to around 5 gm/1 teaspoon of table salt per day).

6. Food prepared out of home, canned foods, and prepackaged foods (dry or frozen) tend to contain more sodium than home‐cooked meals or frozen vegetables, so a hypertensive patient should consciously restrict the intake of such foods.

7. Regular exercise, stopping the use of tobacco, decreased alcohol intake or substitution by non‐alcoholic beverages are helpful in controlling blood pressure.

8. Practising yoga, transcendental meditation, acupuncture, mindfulness‐based stress‐reduction program (MBSRP), Tai chi / taiji / tai chi chuan (origin: China) which combines movement, deep breathing could help in alleviating stress.

9. Home monitoring of blood pressure is highly recommended

10. Quality nutrition, physical activity of few times per week, attaining normal body weight, cessation of alcohol and tobacco, reduction in sodium intake & increasing calcium, magnesium & potassium, stress management and supplementation of certain ingredients may prove beneficial.

Ref  

J Clin Hypertens (Greenwich). 2021 Mar 18;23(7):1275–1283. doi: 10.1111/jch.14236SODIUM MAGNESIUM AND POTASSIUM INTAKE

Non‐pharmacological management of 

hypertension

Narsingh Verma 1,✉, Smriti Rastogi 1, Yook‐Chin Chia 2, Saulat Siddique 3, Yuda Turana 4, Hao‐min Cheng 5, Guru Prasad Sogunuru 6, Jam Chin Tay 7, Boon Wee Teo 8, Tzung‐Dau Wang 9, Kelvin Kam Fai TSOI 

10, Kazuomi Kario 11

Part 3 Non pharmacological management

 

  Part   3. How do these diets actually work?

Both the Mediterranean diet and the Dietary Approaches to Stop Hypertension diet are relatively easy to adhere to and are palatable, high in fruit, vegetables, whole grains, nuts, and unsaturated oils ¹⁷ ; moreover, both minimize the consumption of red and processed meat, and are in accordance with dietary recommendations for cardiovascular health. The difference is that the Dietary Approaches to Stop Hypertension diet is more suitable for recommending a low sodium intake, ¹⁸ , ¹⁹ whereas this is not a feature of the Mediterranean diet. Second, it may well be that the Dietary Approaches to Stop Hypertension diet includes more proteins since it includes poultry and fish and emphasizes the consumption of free‐ or low‐fat dairy products (two or three servings per day). ¹⁸ , ¹⁹ In this regard, either a higher protein intake or protein supplementation has been shown to decrease BP. ²⁰ , ²¹ Concerning dairy products, in particular, the addition of conventional non‐fat dairy products to the routine diet has hypotensive effects. ²² Moreover, a recent systematic review has shown a favorable association between a higher dairy intake and a lower risk of hypertension. ²³ One of the reasons could also be the lower salt consumption associated with vegetables and fruits etc The Dietary Approaches to Stop Hypertension diet reduces high BP by lowering the amount of sodium in your diet to 2300 milligrams (mg) a day. Lowering sodium to 1500 mg a day reduces BP even more. It also includes a variety of foods rich in nutrients that help some people lower BP, such as potassium, calcium, and magnesium. The Mediterranean diet may mediate its effects in part through the maintenance of BP and endothelial function. ²⁴ The consumption of a diet that is high in fruit, vegetables, nuts, and unsaturated oils and low in sodium can lower BP. ²⁵ , ²⁶ In addition, a number of components of a Mediterranean dietary pattern have been shown to improve endothelial function. ²⁷

Intermittent Fasting is another method which can be implemented easily by the patients. There are two major subcategories of intermittent fasting: (a) fasting 1‐4 d per week, that is, alternate‐day fasting or the 5:2 diet [1]; or (b) fasting every day for a 14 to 20 h period, that is, time restricted feeding. ²⁸ Cardioprotective effects of the alternate‐day fasting diet are associated with a reduction of visceral fat tissue, increased adiponectin, decreased leptin and low‐density lipoproteins cholesterol. Intermittent fasting has also shown a beneficial effect on prevention of stroke. ²⁹ In 2018, Erdem et al, 2018 ³⁰ undertook a study with the Cappadocia cohort of 60 prehypertensive and hypertensives, where SBP was 120—139 and ≥ 140; DBP values were 80‐89 and ≥90 mmHg. A decrease in SBP (P < .001) and DBP values (P < .039) was observed. Intermittent fasting inhibits the development of atherosclerotic plaque by reducing the concentration of inflammatory markers IL‐6 (Interleukin −6),

homocysteine, and C‐reactive protein. ²⁰ Intermittent fasting increases brain‐derived neurotrophic factor (BDNF) resulting in lowering BP by activating the parasympathetic system. ³¹ , ³²

Ref

J Clin Hypertens (Greenwich). 2021 Mar 18;23(7):1275–1283. doi: 10.1111/jch.14236SODIUM MAGNESIUM AND POTASSIUM INTAKE

Non‐pharmacological management of hypertension

Narsingh Verma 1,✉, Smriti Rastogi 1, Yook‐Chin Chia 2, Saulat Siddique 3, Yuda Turana 4, Hao‐min Cheng 5, Guru Prasad Sogunuru 6, Jam Chin Tay 7, Boon Wee Teo 8, Tzung‐Dau Wang 9, Kelvin Kam Fai TSOI 

10, Kazuomi Kario 11

उच्च रक्तदाबाचे आहारविषयक आणि औषधविरहित व्यवस्थापन

 

उच्च रक्तदाबाचे आहारविषयक आणि औषधविरहित 

व्यवस्थापन

सारांश

उच्च रक्तदाब हा एक कपटी आजार आहे ज्यामुळे हृदय व रक्तवाहिन्यांसंबंधी गुंतागुंत होण्याचा धोका असतो आणि जर त्यावर योग्य उपचार केले नाहीत तर विविध गंभीर गुंतागुंत होऊ शकतात. आर्थिक मर्यादा,

तसेच कमी किंवा जवळजवळ कोणतेही दुष्परिणाम नसताना अतिरिक्त फायदे मिळत असल्याने, उच्च रक्तदाबाचे औषधविरहित व्यवस्थापन

विकसित आणि विकसनशील दोन्ही देशांमध्ये उच्च रक्तदाबाचा सामना करण्यासाठी एक आकर्षक दृष्टिकोन बनला आहे. या समीक्षा लेखासाठी मूळ अभ्यास, यादृच्छिक नियंत्रित चाचण्या आणि मेटा-विश्लेषणांवर भर देऊन संबंधित संदर्भांसाठी MEDLINE शोध घेण्यात आला. आहार पद्धतीतील बदलांसह जीवनशैलीतील बदल, कमी सोडियम, संतृप्त चरबी आणि उच्च कॅल्शियम, मॅग्नेशियम व पोटॅशियम असलेले विशेष आहार घेणे आणि सर्केडियन लयसोबत सुसंगतपणे काम करणाऱ्या वेळेनुसार मर्यादित जेवणासारख्या नवीन पद्धतींचा अवलंब करणे, हे उच्च रक्तदाबाच्या औषधविरहित व्यवस्थापनाच्या क्षेत्रात नवीन संधी निर्माण करत आहेत. रक्तदाब प्रभावीपणे कमी करणारे जीवनशैलीतील बदल म्हणजे वाढलेला शारीरिक व्यायाम, वजन कमी करणे, मद्यपानावर मर्यादा, योगाची शिथिलीकरण तंत्रे, ॲक्युपंक्चर, ताई ची, माइंडफुलनेस-आधारित तणाव कमी करण्याचा कार्यक्रम आणि ट्रान्सेंडेंटल मेडिटेशन.

आजूबाजूच्या हवेतील वायू प्रदूषण

खराब आरोग्याशी जोडलेले आहे आणि जागतिक आजारांच्या ओझ्यामध्ये त्याचा मोठा वाटा आहे. २.५ μm पेक्षा कमी व्यासाचे सूक्ष्म कण (PM2.5)

हृदय व रक्तवाहिन्यांसंबंधी आजार आणि मृत्यूशी घट्टपणे संबंधित आहेत. पीएमच्या अल्प-मुदतीच्या संपर्कामुळे (तास ते आठवडे) मायोकार्डियल इन्फेक्शन, स्ट्रोक आणि हृदयविकाराचा झटका यासह प्रतिकूल हृदय व रक्तवाहिन्यांसंबंधी घटनांची शक्यता वाढते आणि दीर्घकालीन संपर्क हा धोका अनेक पटींनी वाढवतो. औषधविरहित पद्धती रोगाच्या सुरुवातीच्या टप्प्यात सुरू केल्या पाहिजेत आणि औषधांसोबत सुरू ठेवल्या पाहिजेत.

आहार

रक्तदाब कमी करण्यासाठी, संपूर्ण धान्य, अधिक भाज्या आणि फळे यांचा समावेश असलेला आहार घेण्याची शिफारस केली जाते. (८, ९) इतर शिफारसींमध्ये कमी चरबीयुक्त दुग्धजन्य पदार्थ, कुक्कुटपालन उत्पादने, मासे, कडधान्ये, उष्णकटिबंधीय नसलेली वनस्पती तेल आणि सुका मेवा यांचा समावेश आहे; आणि मिठाई, साखर-युक्त पेये आणि लाल मांस यांचे सेवन कमी करणे. आहाराच्या पद्धतीवर योग्य कॅलरीची आवश्यकता, वैयक्तिक आणि सांस्कृतिक अन्नाची आवड आणि मधुमेह आणि तीव्र मूत्रपिंडाचा आजार यांसारख्या इतर वैद्यकीय स्थितींसाठी पोषण उपचारांचा देखील प्रभाव पडतो. हे विविध आहार योजनांद्वारे साध्य केले जाऊ शकते. हे साध्य करण्याचा एक मार्ग म्हणजे 'डायटरी ॲप्रोचेस टू स्टॉप हायपरटेन्शन' (DASH) आहार, यूएस कृषी विभागाचे अन्न नमुने किंवा अमेरिकन हार्ट असोसिएशनच्या आहारासारख्या योजनांचे पालन करणे.  डायटरी अप्रोचेस टू स्टॉप हायपरटेन्शन (DASH) आहारामध्ये अधिक फळे आणि भाज्या खाण्यावर, परंतु दुग्धजन्य पदार्थ, संतृप्त चरबी, लाल मांस आणि गोड पदार्थ व साखरयुक्त पेये कमी खाण्यावर भर दिला जातो. डॅश आहारामुळे सिस्टोलिक रक्तदाब (SBP) मध्ये ५.५ मिमी एचजी आणि डायस्टोलिक रक्तदाब (DBP) मध्ये ३ मिमी एचजीने घट झाल्याचे दिसून आले. EPIC (युरोपियन प्रॉस्पेक्टिव्ह इन्व्हेस्टिगेशन इन कॅन्सर अँड न्यूट्रिशन) अभ्यासाच्या निष्कर्षांनुसार, ७०६१ उच्च रक्तदाब नसलेल्या महिलांमध्ये (३५-६४ वर्षे), शरीराचे वजन, कमरेचा घेर, बॉडी मास इंडेक्स, प्रक्रिया केलेले मांस आणि वाइन व बटाट्यांचे सेवन यांचा रक्तदाबाच्या मूल्यांशी थेट संबंध होता;  भाज्या, दही आणि अंडी यांचे वाढलेले सेवन एसबीपीशी व्यस्तपणे संबंधित होते (आणि तेलाचा वापर डीबीपी पातळीशी संबंधित होता).१३ एका दुसऱ्या अभ्यासात रक्तदाब पातळी आणि फळे व भाज्यांच्या भूमध्यसागरीय आहारादरम्यान नकारात्मक संबंध दिसून आला.१४ ENCORE (Exercise and Nutritional Interventions for Cardiovascular Health) अभ्यासात, जास्त वजन असलेल्या उच्च रक्तदाबाच्या व्यक्तींमध्ये 'डायटरी अप्रोचेस टू स्टॉप हायपरटेन्शन' (DASH) आहाराच्या दीर्घकालीन परिणामांमध्ये, १६ आठवड्यांच्या उपचारानंतर ८ महिन्यांच्या फॉलो-अपमध्ये, रक्तदाब, व्यायाम आणि शरीराच्या वजनावर काही फायदेशीर परिणाम दिसून आले. तथापि, कायमस्वरूपी जीवनशैलीत बदल घडवून आणणाऱ्या प्रभावी पद्धतींची आवश्यकता आहे.१५ SUN ("Seguimiento Universidad de Navarra") प्रकल्पाच्या अभ्यासात, सहा वर्षे निरीक्षण केलेल्या ९४०८ पुरुष आणि स्त्रियांमध्ये, भूमध्यसागरीय आहाराच्या अंमलबजावणीमुळे एसबीपी आणि डीबीपी मूल्यांमध्ये घट झाल्याचे दिसून आले. भूमध्यसागरीय आहाराच्या मध्यम अंमलबजावणीमुळे एसबीपीमध्ये २.४ mmHg आणि डीबीपीमध्ये १.३ mmHg घट झाली; तर अधिक पद्धतशीर अंमलबजावणीमुळे एसबीपी आणि डीबीपीमध्ये अनुक्रमे ३.१ आणि १.९ mmHg घट झाली.१६ याव्यतिरिक्त, हृदय व रक्तवाहिन्यांसंबंधीच्या आजारांचा उच्च धोका असलेल्या ७७२ व्यक्तींमध्ये (५५-८० वर्षे) भूमध्यसागरीय आहार स्वीकारल्यामुळे एसबीपीमध्ये ७.१ mmHg घट झाली.

डॉक्टरी सल्ला घेणे गरजेचे आहे

Ref 

J Clin Hypertens (Greenwich)

. 2021 Mar 18;23(7):1275–1283. doi: 10.1111/jch.14236

उच्च रक्तदाबाचे गैर-औषधी व्यवस्थापन

नर्सिंग वर्मा १,✉, स्मृती रस्तोगी १, युक-चिन चिया २, सौलत सिद्दीकी ३, युडा तुराना ४, हाओ-मिन चेंग ५, गुरु प्रसाद सोगुनुरु ६, जाम चिन टे ७, बून वी टीओ ८, त्झुंग-डाऊ वांग ९, केल्विन काम फाई त्सोई १०, काझुओमी  कारिओ ११

Ref

J Clin Hypertens (Greenwich). 2021 Mar 18;23(7):1275–1283. doi: 10.1111/jch.14236

Non‐pharmacological management of hypertension

Narsingh Verma 1,✉, Smriti Rastogi 1, Yook‐Chin Chia 

2, Saulat Siddique 3, Yuda Turana 4, Hao‐min Cheng 5, Guru Prasad Sogunuru 6, Jam Chin Tay 7, Boon Wee Teo 8, Tzung‐Dau Wang 9, Kelvin Kam Fai TSOI 10, Kazuomi Kario 11

Part 2 NonPharmacologicalManagement Of Hypertension

Abstract

Hypertension is an insidious disease which predisposes to cardiovascular complications and if not treated properly can lead to various serious complications. Economic limitations, 

having additional benefits with few or almost no side effects have made non‐pharmacological management of hypertension 

an attractive approach for dealing with hypertension, in developed and developing countries alike. A MEDLINE search was done for relevant references with emphasis on original studies, randomized controlled trials, and meta‐analyses for this review paper. Lifestyle modifications including changes in the dietary pattern, adopting special diets with low sodium, saturated fat and high calcium, magnesium and potassium and trying the new methods like time restricted meal intake which work in tandem with the circadian rhythm are opening new vistas in the field of non‐pharmacological management of hypertension. Lifestyle modifications that effectively lower blood pressure are increased physical activity, weight loss, limited alcohol consumption, relaxation techniques of Yoga, Acupuncture, Tai chi, mindfulness‐based stress‐reduction program, and Transcendental Meditation. Air pollution of the

 surrounding air is linked with poor health outcomes and is a major contributor to the global burden of disease. Fine particulate matter <2.5 μm in diameter (PM2.5) is strongly associated with 

cardiovascular morbidity and mortality. Short‐term PM exposure (hours to weeks) increases the likelihood of adverse cardiovascular events including myocardial infarction, stroke, and heart failure, and longer‐term exposure multiplies that risk. Non‐pharmacological methods should be initiated early phase of disease and should be continued with medication

Diet 

To reduce BP, a diet consisting of whole grains, more vegetables, and fruits is recommended. (⁸ , ⁹ )Other recommendations include consuming low‐fat dairy products, poultry, fish, legumes, non‐tropical vegetable oils, and nuts; and reducing intake of sweets, sugar‐sweetened beverages, and red meat. Dietary pattern is also influenced by appropriate calorie requirements, personal and cultural food preferences, and nutritional therapy for other medical conditions, such as diabetes mellitus and chronic kidney disease. This can be achieved by various dietary plans. One way to achieve this is by following plans such as the Dietary Approaches to Stop Hypertension diet, US Department of Agriculture Food Patterns, or the American Heart Association diet. The Dietary Approaches to Stop Hypertension diet emphasized consuming more fruits and vegetables, but less dairy products, saturated fats red meat and less sweets, and sugar‐sweetened beverages. With the Dietary Approaches to Stop Hypertension diet, a lowering of SBP by 5.5 mm Hg and DBP by 3 mm Hg ¹⁰ , ¹¹ , ¹² was seen. Results from the EPIC(European Prospective Investigation into Cancer and Nutrition) study showed that for 7061 non‐hypertensive women (35‐64 years), body weight, waist circumference, body mass index, processed meat, and wine and potatoes consumption correlated directly with BP values; while increased eating of vegetables, yoghurt, and eggs was inversely associated with SBP (and consumption of oil with DBP levels. ¹³ Another study showed a negative association between BP levels and a Mediterranean diet of fruits and vegetables ¹⁴ The long‐term effects of Dietary Approaches to Stop Hypertension diet in overweight hypertensive individuals in the ENCORE Exercise and Nutritional Interventions for Cardiovascular Health study, where a follow‐up 8 months after the end of their 16 weeks treatment, showed some beneficial impact on BP, exercise, and body weight control. However, effective methods that promote permanent lifestyle modification are needed. ¹⁵ In the SUN ("Seguimiento Universidad de Navarra") project study, involving 9408 men and women followed for six years, the implementation of the Mediterranean diet was associated with a decrease in SBP and DBP values. Moderate implementation of the Mediterranean diet showed a decrease of 2.4 mmHg for SBP and 1.3 mmHg for DBP; while more systematic application decreased SBP and DBP by 3.1 and 1.9 mmHg, respectively. ¹⁶ Additionally, the adoption of the Mediterranean diet in 772 subjects (55‐80 years), in high risk for cardiovascular disease, resulted in SBP reduction of 7.1 mmHg

. 2021 Mar 18;23(7):1275–1283. doi: 10.1111/jch.14236

Non‐pharmacological management of hypertension

Narsingh Verma ^1,✉, Smriti Rastogi ¹, Yook‐Chin Chia ², Saulat Siddique ³, Yuda Turana ⁴, Hao‐min Cheng ⁵, Guru Prasad Sogunuru ⁶, Jam Chin Tay ⁷, Boon Wee Teo ⁸, Tzung‐Dau Wang ⁹, Kelvin Kam Fai TSOI ¹⁰, Kazuomi Kario ¹¹

PMCID: PMC8678745  PMID: 33738923