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The microcirculation: a key player in obesity-associated cardiovascular disease

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It is increasingly recognized that obesity is a risk factor for microvascular disease, involving both structural and functional changes in the microvasculature. This review aims to describe how obesity impacts the microvasculature of a variety of tissues, including visceral adipose tissue, skeletal muscle, heart, brain, kidneys, and lungs.

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These changes involve endothelial dysfunction, which in turn (i) impacts control of vascular tone, (ii) contributes to development of microvascular insulin resistance, (iii) alters secretion of paracrine factors like nitric oxide and endothelin, but (iv) also influences vascular structure and perivascular inflammation. In concert, these changes impair organ perfusion and organ function thereby contributing to altered release and clearance of neurohumoral factors, such as adipokines and inflammatory cytokines. Global microvascular dysfunction in obese subjects is therefore a common pathway that not only explains exercise-intolerance but also predisposes to development of chronic kidney disease, microvascular dementia, coronary microvascular angina, heart failure with preserved ejection fraction, chronic obstructive pulmonary disease, and pulmonary hypertension.


A large body of evidence has accumulated over the years, from both clinical and experimental studies, indicating that obesity is associated with endothelial dysfunction and development of atherosclerosis, and that obesity has become one of the most important risk factors for cardiovascular disease including coronary artery disease, heart failure, and stroke. In addition to atherosclerosis in the larger arteries, obesity is also a risk factor for microvascular disease. Interestingly, a single high fat meal already perturbs endothelial function in the brachial artery, and reduces flow reserve in the coronary vasculature, illustrating how a single exposure to a high circulating lipid load has an impact, albeit transient, on the microvasculature. Regular exposure to high circulating lipid loads, even prior to the onset of overt obesity, leads to an inflammatory response that is accompanied by microvascular dysfunction, the severity of which correlates with the amount of visceral adipose tissue present in the body. Eventually, obesity and the associated inflammation not only impact function, but also structure of the microvasculature (Figure 1).

Figure 1

Proposed mechanisms of obesity-related microvascular dysfunction predisposing to multi-organ disease. High fat diet on a regular basis changes the composition of visceral adipose tissue, and induces a low grade local inflammatory response, which together modify the secretion of adipokines. Simultaneously, high fat diet results in endothelial dysfunction throughout the body, which not only alters vascular tone, and contributes to development of microvascular insulin resistance, but also influences vascular structure and perivascular inflammation. In concert, these microvascular changes impair organ perfusion and organ function thereby further contributing to altered release and clearance of metabolites and neurohumoral factors, like adipokines, inflammatory cytokines as well as (cardio)myokines. Global microvascular dysfunction in obese subjects therefore is a common pathway that contributes to exercise-intolerance and predisposes to development of chronic kidney disease, microvascular dementia, coronary microvascular angina, COPD and pulmonary hypertension. CKD, chronic kidney disease; HFpEF, heart failure with preserved ejection fraction; COPD, chronic obstructive pulmonary disease.

Two main types of adipose tissue can be distinguished in the body, which have distinctly different functions both in healthy and obese subjects being white and brown adipose tissue (WAT and BAT respectively). WAT is the primary site of fat accumulation, and not only allows efficient fat storage, but also quick mobilization of fat stores to meet energy demands of the body. WAT comprises both subcutaneous and visceral adipose tissue (VAT). The main role of BAT is thermogenesis. Thermogenesis in BAT is activated by the sympathetic nervous system. High expression of uncoupling protein-1 on the inner membrane of BAT mitochondria results in uncoupling of mitochondrial respiration so that heat is generated instead of ATP. In adult humans, BAT is mainly located in cervical, supraclavicular, mediastinal, paravertebral, suprarenal, and peri-renal areas. In addition, epicardial and perivascular adipose tissue have a phenotype that more closely resembles BAT than WAT. Both WAT and BAT contain dense microvascular networks, but microvascular density is higher in BAT as compared to WAT, with 3 vs. 1 capillary per adipocyte, respectively. The microvasculature in WAT serves as the exchange site for fat deposition and mobilization, while in BAT it is required for both delivery of fuel for and dissipation of heat produced during thermogenesis. Metabolism, perfusion and function of both WAT and BAT are affected by obesity.

Obesity, by definition an excessive accumulation of fat mass, results in expansion of particularly WAT. Ingestion of a single high fat meal induces upregulation of P-selectin on the venular side of the visceral adipose microvasculature, thereby forming an anchoring point for leucocytes. The leucocytes infiltrate the VAT and initiate an inflammatory response. Hence, low grade inflammation particularly in visceral adipose tissue may precede excessive fat accumulation, increase oxidative stress, and cause chronic microvascular dysfunction. Interestingly, blood flow to VAT increases following meal ingestion in lean but not obese subjects. Moreover, diet-induced obesity is accompanied by decreased eNOS-expression and activity, while eNOS overexpression protects against diet-induced obesity . These observations suggest a key role for microvascular function in adipose tissue homeostasis. Besides this paracrine interaction between adipocytes and the microvasculature, it should be noted that fat accumulation in VAT results in an increase in adipocyte-size from 50 μm up to 150–200 μm, which is beyond the diffusion distance for oxygen, while the accompanying reduction in capillary density will further decrease adipose tissue oxygenation. Indeed, chronic hypoxia has been shown to be present in expanded VAT. Similar to WAT, brown adipocytes hypertrophy in obesity. Intriguingly, it has recently been shown that capillary rarefaction, leading to focal hypoxia in BAT, is sufficient to induce ‘whitening’ of BAT, which is associated with reduced beta-adrenergic signaling, mitochondrial dysfunction, loss of thermogenic capacity and further accumulation of lipid droplets.

Hypoxia per se induces a reduction in adiponectin and an increase in leptin release from isolated adipocytes. Moreover, chronic hypoxia results in sustained inflammation thereby further modulating the secretion of adipokines from both WAT and BAT and contributing to metabolic derangement in obesity. In healthy subjects, the secretion of the anti-inflammatory adipokine adiponectin predominates, whereas in obese subjects, there is a shift toward pro-inflammatory adipokines such as leptin, resistin, TNFα, IL-6, and IL-18 (Table 1).  Thus, adipose tissue hypoxia and inflammation are centrally involved in the pathophysiology of obesity, and can, through release of vasoactive and/or inflammatory adipokines, modulate microvascular function throughout the body (Figure 1).

Although some studies in young adult humans suggest that skeletal muscle blood flow is relatively well-maintained in obesity  even during exercise,  others show a reduction in flow normalized for muscle mass both at rest and during exercise. These findings seem to be independent of age and vascular bed, as the reduction in flow is present in children,  and adults,  both in the forearm and upper leg. Similarly, the exercise-induced increase in systemic vascular conductance is blunted in obese swine as compared to lean swine, consistent with a decrease in flow to exercising muscle. This decrease in flow is compensated by an increase in oxygen extraction to fulfill the oxygen-requirement of skeletal muscle. 

In skeletal muscle, close coupling of blood flow to metabolic activity is required and besides substances released from nerve terminals, the endothelium and the contracting muscle, also involves mechanical interaction between the contracting muscle and the vasculature. The nervous system contributes to exercise hyperemia in skeletal muscle via activation of sympathetic vasodilator fibers, vasodilation elicited by acetylcholine spillover from active motor nerves as well as functional sympatholysis in active muscle. Resting muscle sympathetic nerve activity (MSNA) is significantly higher in obese patients with metabolic syndrome, but it does not further increase during exercise. Interestingly, in the presence of β-blockade, exercise resulted in larger increase in forearm blood flow and conductance in obese as compared to lean men. Together with the observation that the exercise-induced increase in skeletal muscle blood flow is reduced or at best preserved in obesity, these data suggest that β-adrenergic vasodilation is reduced in obesity. Furthermore, in the presence of β-blockade, α2– but not α1-stimulation resulted in a larger decrease in forearm vascular conductance in obese vs. lean subjects at rest and during exercise. Similarly, there was a tendency towards a larger increase in conductance with α-blockade with phentolamine at rest in obese vs. lean subjects, but a reduced increase in conductance upon α-blockade during exercise. These data suggest that obesity results in a shift in the balance of neurogenic control of skeletal muscle blood flow, with increased α-adrenergic constriction at rest, that is withdrawn during exercise, thereby compensating for a loss of β-adrenergic vasodilation .

In humans, endothelium-dependent skeletal muscle microvascular vasodilation in response to acetylcholine is either preserved or reduced in obesity, while eNOS expression is unaltered. However, the contribution of both NOS- and cyclooxygenase (COX)- dependent vasodilator mechanisms to acetylcholine-induced vasodilation is reduced, which is compensated by NOS- and COX-independent vasodilator mechanisms, potentially an increase in endothelium-derived hyperpolarizing factors such as EETs and/or H2O2.  An increase in H2O2 may result from superoxide dismutase (SOD)-mediated conversion of superoxide, particularly in more active obese individuals. In addition, a reduction in NO-bioavailability has been shown to be counterbalanced by reduced phosphodiesterase 5 (PDE5) activity, as well as by a reduced vasoconstrictor influence of ET. The latter is mediated through a reduction in ET-sensitivity of the skeletal muscle arterioles together with a decrease in circulating ET, reflecting a decrease in local ET production. Interestingly, a study in rodents suggests that basal differences exist in endothelial cell phenotype between arteries perfusing slow-twitch and those perfusing fast-twitch muscle fibers, with the former being less susceptible to endothelial dysfunction.

Alterations in endothelial function may also play a role in insulin-dependent modulation of microvascular tone. In healthy individuals, insulin-induced vasodilation serves to facilitate glucose delivery and uptake in skeletal muscle. As outlined in the introduction, insulin resistance is associated with a shift from insulin-induced vasodilation to vasoconstriction. Indeed, the change in femoral vascular conductance upon glucose ingestion is smaller in obese as compared to lean women, which is associated with impaired body glucose uptake. Moreover, flow to the quadriceps muscle of obese men is lower in the presence of insulin both at rest and during exercise, and insulin-induced vasodilation is converted into vasoconstriction in skeletal muscle arterioles isolated from obese women. The latter is mediated, at least in part, by alterations in perivascular adipose tissue (PVAT), that displays a pro- inflammatory phenotype in obesity. 

Although low grade inflammation may lead to an increase in oxidative stress, TBARS (as index of systemic oxidative stress) do not appear to be different between normal and obese young adults. Conversely, ROS production by NADPH-oxidase and Xanthine oxidase in skeletal muscle is increased in overtly obese, but not mildly obese individuals. In accordance with this observation, infusion of the NADPH-oxidase inhibitor and antioxidant apocynin augmented the acetylcholine-induced increase in flow to skeletal muscle in obese but not lean subjects. However, despite a significant inverse correlation between TBARS and vasodilator responses, the antioxidant ascorbic acid augmented acetylcholine-induced vasodilation to a similar extent in normal and obese subjects under resting conditions. Nevertheless, the significant correlation between waist-to-height ratio and TBARS post-exercise, together with a negative correlation between catalase and BMI, suggests that anti-oxidant capacity may fall short during stress in obese subjects.

The obesity-induced decrease in exercise capacity (VO2max) closely correlates with capillary density in skeletal muscle, indicating that besides functional, also structural changes in the skeletal muscle microvasculature are present. A study in rodents suggests that capillary rarefaction in obesity occurs in two phases, of which the first one is mediated by an increase in oxidative stress, and the second one by a decrease in NO-bioavailability. 

Taken together, obesity moderately reduces skeletal muscle blood flow at rest. The mechanisms of this reduction are incompletely understood but may involve factors released from perivascular fat that modulate insulin sensitivity and endothelial function as well as an increased vasoconstrictor influence caused by an increase in MSNA. In addition, structural changes in the skeletal muscle microvasculature may contribute to the decreased resting blood flow. Because exercise hyperemia involves many redundant regulatory mechanisms, it is relatively well-maintained. However, the impairments in blood flow and its distribution are likely to become more severe when the metabolic disturbance persists for a longer time or when other co-morbidities such as hypertension, hyperlipidemia, and hyperinsulinemia co-exist in the same patient, which may contribute to exercise intolerance in obese people.

Similar to skeletal muscle, coronary microvascular function plays an important role in coupling of myocardial perfusion to cardiac metabolism.54 Clinical studies have shown that in conditions such as obesity and hypercholesterolemia the coupling of coronary blood flow to the myocardial metabolic demand is altered.2 Thus, coronary flow velocity of obese patients during dobutamine stress-echo is impaired, with the impairment becoming even more evident when obesity is associated with other risk factors.55 Also, myocardial blood flow measurements with PET indicate that increases in myocardial blood flow in response to cold-pressor testing are diminished in obese patients.56 Interestingly, female sex and the volume of visceral fat are associated with a reduction in myocardial perfusion at peak dose of dobutamine, as measured by MRI.57 These clinical observations are supported by studies in obese Ossabaw swine with metabolic syndrome and swine with severe familial hypercholesterolemia (FH), demonstrating that coronary blood flow regulation and myocardial oxygen balance are altered in particular during treadmill exercise.58,59

Several studies have reported reduced coronary flow reserve and increased minimal vascular resistance in patients with obesity and hypercholesterolemia as assessed by either PET, Doppler echocardiography or MRI.60–64 Such abnormalities can be the result of either changes in microvascular function, i.e. the regulation of vascular tone, or structural changes within the coronary microcirculation, such as vascular rarefaction or inward remodeling.54,65 Alterations in control of coronary microvascular tone are generally characterized by a loss of endothelial vasodilator influence (such as NO) as well as by increased neurohumoral (angiotensin II) and endothelium-derived vasoconstrictor (ROS, ET, prostanoids) influences resulting in a shift in the vasomotor balance towards increased vasoconstriction (Table 1).2,3,66 Indeed, several studies in humans and animal models have demonstrated that obesity is associated with alterations in the vasodilator-vasoconstrictor balance controlling coronary microvascular tone.2–4,67 Thus, hyperoxia-induced vasoconstriction in the coronary microvasculature is enhanced in obese adolescents,68 while bradykinin-induced vasodilation is impaired in isolated coronary arterioles from obese patients due to increased tissue angiotensin-converting enzyme activity.69 Similarly, in swine with hypercholesterolemia, endothelial dysfunction of isolated small coronary arteries due to impaired NO biovailability is noted early in the disease process (2.5 months after start of the high fat diet).70 In contrast, at 15 months of diet, NO signaling is restored but the constriction to ET-1 is exacerbated, this response being mediated by ETB-mediated vasoconstriction, indicating that disturbances in the balance between vasodilators and vasoconstrictors are modulated during progression of the disease (Table 1).71 The observations that eNOS activity is impaired by adipokines secreted by perivascular fat72 and that coronary microvascular dysfunction correlates with increased inflammation62 suggest that inflammation and fat-derived cytokines in obesity are also important determinants of coronary microvascular dysfunction. This is consistent with the correlation of fat deposits with the decline in coronary microvascular function.57,63

In addition to the functional changes in the control of vascular tone, obesity can also result in structural remodeling of the coronary microcirculation. Histological analysis of left ventricular tissue biopsies obtained during coronary bypass surgery show significantly lower capillary densities in obese patients (Table 1).73 Importantly, both arteriolar remodeling and capillary rarefaction likely contribute to the reduced coronary flow reserve in obese patients as reported in several,60–62 though not all studies.66 Similarly, hypertrophic inward remodeling of coronary arterioles, increased stiffness as well as capillary rarefaction are reported in animal models of obesity and hypercholesterolemia.58,71,74

It is increasingly recognized that the factors released by the coronary endothelium also impact the function of the surrounding cardiomyocytes in a paracrine fashion. Loss of NO, increased oxidative stress and the ensuing tissue inflammatory response are thought to play a key role in development of left ventricular diastolic dysfunction through altering relaxation of the cardiac myocytes and increasing collagen fraction in the extracellular matrix.75,100

In conclusion, both clinical and experimental evidence indicate that obesity is an independent risk factor for coronary microvascular dysfunction, with both functional and structural alterations in the coronary microcirculation contributing to the impairments in coronary flow regulation and having a negative impact on the coronary flow reserve in these patients. Some, but not all, of these changes can be alleviated by weight loss and physical exercise.68,76 However, in order to be able to specifically address the different aspects the obesity-associated coronary microvascular dysfunction, future studies should focus on revealing the underlying mechanisms that drive the obesity-associated coronary microvascular abnormalities.

Similar to the heart, the brain relies on a continuous supply of blood flow, with regional alterations in brain activity requiring corresponding changes in brain flow distribution via metabolic vasodilation, which is referred to in the brain as neurovascular coupling. Obesity-induced changes in brain microvascular structure and function have been proposed to result in disruptions in neurovascular coupling, thereby leading to vascular cognitive impairment.20,77 Importantly, the brain microvasculature is only surrounded by neurons and glia as there is no perivascular adipose tissue. Therefore, the effects of obesity likely manifest as the result of changes in neural/glia-vascular (metabolic) interactions, and hemodynamic (i.e. blood pressure) or circulating factors (hyperglycemia and dyslipidemia) that have a direct vasoactive effect or act indirectly via influencing neurons and glia.

Both pre-clinical78,79 and clinical80,81 obese human populations exhibit reduced brain blood flow and impaired vasodilation during hypercapnia. The mechanisms responsible likely relate to microvascular rarefaction,19,20,82 decreased contribution of NO to basal cerebral microvascular tone control, altered release of vasodilator prostanoids, and/or a direct effect of H+ on vascular smooth muscle ion channels.83 Impaired cerebral vasoreactivity in obesity occurs independently of clinical insulin resistance,78,84 but may also worsen with accompanying hypertension and poor glycemic control.80,81 Obese Zucker rats display impaired endothelium-dependent NO-mediated middle cerebral artery (MCA) vasodilation as well as depressed insulin-stimulated vasodilation, potentially due to increased PKC- and MAPK-activation, combined with eNOS uncoupling resulting in augmented superoxide production.82,85 Indeed, depressed vasodilator responses to hypoxia and NOS-dependent dilators, as well as enhanced constrictor responses to 5-hydroxytryptophan1 reflect potential pathological adaptations that impair neurovascular coupling. Decreased insulin-mediated vasodilation potentially contributes to impaired microvascular insulin delivery in the brain (Table 1).86 The physiological significance of this remains incompletely understood, but similar to skeletal muscle, altered insulin signaling in the brain (i.e. brain insulin resistance) can link microvascular and metabolic dysfunction, thereby leading to cognitive impairment. Collectively, the data from humans81 and rodents82,85 suggest that obesity induces endothelial dysfunction with impaired NO production/bioavailability, resulting in altered cerebral vasoreactivity.

Obesity also affects the structure of small arteries, arterioles and capillaries in the brain, with many of these changes reflecting the development of cerebral microvascular disease.20,77 Indices of cerebral microvascular disease, including cerebral microbleeds, lacunas and microlacunas, increase the vulnerability to neurodegeneration,20,77 and occur more commonly in obese individuals with insulin resistance,87 dyslipidemia,87 and central adiposity.88 In addition, genetic predispositions may also contribute to this relationship.77 Beyond these preliminary observations, the underlying mechanisms responsible for obesity-induced cerebrovascular remodeling in humans remain elusive. However, cortical microvascular density decreases,89 and the MCA undergoes eutrophic inward remodeling and progressive arterial stiffening during the progression of metabolic syndrome in obese Zucker rats.82 In diet-induced obesity in Sprague–Dawley rats, similar MCA adaptations are observed in conjunction with increased MMP-2 activity, collagen I expression, and reduced MMP-13 expression, suggesting that increases in collagen deposition contribute to vascular stiffening (Table 1).90 In the aforementioned studies,82,89,90 inward MCA remodeling coincided with the development of hypertension, while pharmacological treatment of hypertension ameliorated the remodeling.82 This suggests that obesity-induced hypertension, and not metabolic dysfunction,91 serves as the primary stimulus responsible for inducing inward remodeling of the MCA.

Although pharmacological treatment of hypertension ameliorates MCA remodeling, it does not improve cortical microvascular rarefaction in obese Zucker rats.89 Also in Rhesus monkeys, diet-induced obesity causes cortical capillary rarefaction, but without concurrent changes in blood pressure.92 In the latter study, cortical capillary rarefaction occurred alongside decreased VEGF, increased von Hippel-Lindau protein (which degrades HIF-1α) and (paradoxically) increased expression of FOXO3, eNOS, and eNOS uncoupling. In contrast to inward remodeling in the MCA, it appears that obesity-induced metabolic dysfunction and oxidative stress, and not hypertension, is responsible for the observed microvascular/capillary rarefaction (Table 1). Therefore, while inward remodeling may prevent hypertension-induced cerebral hyperperfusion, inward remodeling and microvascular rarefaction may limit cerebrovascular reserve and impair brain blood flow control.

Functional and structural microvascular deficits resulting in impaired neurovascular coupling likely reflect an acquired, and not programmed feature of obesity, suggesting that these abnormalities can be environmentally induced, prevented or even reversed.93–95 Indeed, short-term diet-induced obesity reduces prefrontal cortex blood flow in mini-pigs,94 and impairs metabolic vasodilation and precedes neuronal loss in rodents.95 Furthermore, individuals with an elevated BMI exhibit reduced basal flow79 and post-prandial vasodilation93 in the prefrontal cortex, but formerly obese individuals do not display this defect.93 Reversal of such adaptations is of growing importance as the early signs of cerebral microvascular disease can manifest very early in life, as seen in an obese 2-year-old child.96

In conclusion, the cumulative effect of cerebral inward remodeling, microvascular rarefaction, and impaired vasodilator capacity, likely contribute to obesity-related impairments in brain flow control and neurovascular coupling. Such obesity-induced changes can occur rapidly and in young individuals, but it appears these pathological adaptations are modifiable. Gathering more knowledge about mechanisms of obesity-related changes in brain microvascular structure and function along the (micro)vascular tree is essential in understanding the pathology of disease progression and developing effective prevention and treatment strategies.

Obesity is associated with an increased risk for chronic renal failure. In a Swedish case-control study, particularly diabetic nephropathy, nephrosclerosis, and glomerulonephritis were associated with obesity,97 suggesting that obesity negatively impacts the renal microvascular bed. Indeed, clinical studies show that in obesity, afferent arteriolar vasodilation results in an increased renal blood flow (RBF), that causes a state of hyperfiltration.98 Results in experimental animals are equivocal with some laboratories showing that RBF and glomerular filtration rate (GFR) are increased 3–4 months99,100 of high fat diet, whereas others show no change in RBF and GFR.101–105 The reported increase in RBF is mostly due to an increase in renal cortical volume, vascular volume fraction and cortical perfusion, whereas filtration fraction, medullary size, and medullary perfusion showed no difference.99,100,106

Obesity is linked to increased peri-renal fat deposition,100,107 which in turn leads to low grade inflammation and renovascular endothelial dysfunction. Indeed, endothelium-dependent vasodilation to acetylcholine was impaired both in vivo98,102,103,108 and in vitro in renal arteries of obese swine,100 while endothelium-independent vasodilation to the NO donor sodium nitroprusside (SNP) was unaltered in vitro (Table 1).100 Although renal eNOS-expression may initially increase,99 prolonged exposure to high fat diet reduces expression of eNOS and promotes eNOS-uncoupling and activation of xanthine oxidase resulting in impaired bioavailability of NO in obese swine.102 Antioxidant capacity in obesity is further reduced by a decrease in SOD activity.103,108 Moreover, increased NAD(P)H-oxidase and LOX-1 expression further contribute to increased oxidative stress, which together with upregulation of iNOS, may have led to increased nitrotyrosine levels.99,102,104,105,108,109 ROS in turn, induce upregulation of renal pre-pro ET-1 and ETA receptors thereby promoting vasoconstriction (Table 1).102–104

Interestingly, incubating renal arteries of lean swine with peri-renal fat of obese animals transferred the impaired endothelial function to those arteries.100 This response appears to be the result of fat derived inflammatory molecules, and not of oxidative stress, as the endothelial dysfunction could only be reversed by neutralizing TNF-α, but not by the free radical scavenger Tempol, in vitro.100 Furthermore, anti-inflammatory treatment with thalidomide in vivo, abolished the renal increase in TNF-α, and improved endothelial function without altering oxidative stress, suggesting that increased levels of TNF-α play a vital role in impaired function of the endothelium.102

In addition to renovascular dysfunction, structural alterations in the kidney produced by obesity have also been reported (Table 1). Interestingly, obesity is associated with a change in the balance of angiogenic and anti-angiogenic factors in the kidney that favors angiogenesis. Thus, VEGF and its receptor Flk-1108 as well as Angpt2110 are increased. Moreover, protein expression of the angiogenesis inhibitor TSP-1 is decreased as a result of increased oxidative stress,99 although this is not a unanimous finding.104 Indeed, both arteriolar and capillary density in the outer cortex of the kidney are increased in animals with obesity.99,108 However, these newly formed vessels are more tortuous and erythrocyte exudation has been shown, suggesting that the newly formed vessels are leaky and immature.99,102,103,108,109 Furthermore, glomerular density is decreased in animals with metabolic derangement,109 while glomerular hypertrophy due to matrix hyperplasia and glomerular swelling are also observed in obese swine.99,109–111 Taken together, these data suggest that the newly-formed microvasculature does enhance glomerular filtration, but is rather damaged and dysfunctional. Vascular remodeling in obesity is facilitated by dynamic processes in the extracellular matrix, as an increased MMP expression, which promotes extracellular matrix (ECM) degradation was noted at 10 weeks,99 but not at 16 weeks104 of high fat diet. Furthermore, in obese swine, renal expression of tissue transglutaminase is increased, causing extracellular matrix crosslinking and vascular remodeling especially in conditions of sustained vasoconstriction.103 Moreover, microvascular media-to-lumen ratio is increased,104,108 and perivascular as well as tubulointerstitial fibrosis is observed in obese swine.104,108 The increased presence of renal M1-macrophages, and increased NF-κB expression, plasma/renal levels of TNF-α as well as activation of the TGFβ-system in the kidneys of obese animals, suggests that inflammatory cells play a central role in these processes.98–100,103,104,106

In conclusion, the increased fat or lipid deposition in and around the kidney acts as a promotor of a pro-inflammatory state with oxidative stress, endothelial dysfunction and microvascular remodeling as a consequence. Although these changes are initially reversible by switching to a healthy life style,104 as well as by interventions that lower lipids and/or oxidative stress,105,108 modulate the immune-system102 or prevent vasoconstriction,98,103 prolonged exposure results in irreversible alterations in the renal microvasculature. Indeed, although diabetes mellitus and hypertension are still the main causes of chronic kidney disease (CKD),112 it has been shown that obesity independently increases the risk of CKD and end-stage renal disease even in the absence of these known cardiovascular risk factors or nephropathy.113 As the kidney is important in clearing waste products and adipokines from the body, renal dysfunction in obesity and the ensuing increase in so-called uremic toxins, can further contribute to microvascular dysfunction in other organs and thereby contribute to development and aggravation of cardiovascular disease.114

Functional and structural changes in the pulmonary microvasculature as a result of obesity are less well studied as compared to their systemic counterparts. The comparison of the effect of obesity in the pulmonary and systemic microvasculature is of interest as the pulmonary vasculature receives the same cardiac output as the systemic vasculature and is exposed to the same circulating factors, such as glucose, cholesterol, adipokines, and inflammatory factors. Indeed, obesity is also associated with a variety of lung diseases including obstructive sleep apnea, hypoventilation syndrome, chronic bronchitis, asthma, and pulmonary embolism. Many of these diseases have an inflammatory component and it is likely that the change in circulating adipokines with obesity facilitates this pulmonary inflammation. Adiponectin exerts anti-inflammatory and protective effects against inflammatory lung diseases. In contrast, leptin is pro-inflammatory and leptin receptors are present on all inflammatory cell-types in the lung. An increase in leptin primes leucocytes for increased secretion of inflammatory cytokines and reactive oxygen species. However, exactly how a change in adipokine profile impacts pulmonary microvascular structure and function remains to be established.

An autopsy study in 1982 revealed a strong correlation between the size of atherosclerotic plaques in the aorta and the pulmonary artery. In rabbits on a high fat diet, the rate of cholesterol accumulation in the pulmonary artery exceeded that in the aortic arch initially, but at later stages of atherogenesis, the rate of cholesterol accumulation slowed in the pulmonary artery ultimately falling below accumulation rates in the aortic arch. Obesity is also associated with structural changes in the pulmonary microvasculature (Table 1). Increased medial thickness of both pulmonary small arteries and veins, and increased muscularization of pulmonary arterioles were observed in obese humans compared to controls at autopsy. Similarly, an increased wall to lumen ratio was found in pulmonary arterioles of obese rats as compared to lean control rats. Interestingly, adiponectin deficiency has been shown to result in pulmonary microvascular remodeling, with an increased muscularizaton of pulmonary microvessels.

These structural pulmonary microvascular changes in obesity resemble those found in post-capillary pulmonary hypertension. Indeed, the prevalence of pulmonary hypertension (PH) is increased in obese subjects, and is associated not only with sleep apnea and hypoxemia, but also with left ventricular diastolic dysfunction, resulting in increased left atrial pressure. The association between obesity and elevated pulmonary artery pressures has also been found in both obesity prone and overtly obese Zucker rats on a high fat diet and in obese FH-swine. Similar to humans, the elevated pulmonary artery pressure in the obese swine was mainly due to an increase in left atrial pressure as pulmonary vascular resistance was only mildly elevated. However, despite the mildly elevated pulmonary artery pressure and pulmonary vascular resistance at rest, the pulmonary vasodilator response to exercise was preserved in swine with hypercholesterolemia, at a time when systemic vasodilation was reduced.

The effect of obesity and high fat diet on pulmonary vascular function has only been assessed in experimental animals and may depend on the duration of exposure and the stimulus used to assess vascular function. Thus, pulmonary artery vasodilation in response to methacholine is enhanced in rabbits given a 2% cholesterol diet over a period of 2 weeks. Exposure of Zucker rats to high fat diet for 18 weeks has no effect on eNOS expression or acetylcholine-induced NO production in either conductance or resistance pulmonary arteries. Similarly, the increase in pulmonary vascular resistance in response to eNOS inhibition is comparable in healthy swine and in FH-swine on a high fat diet for 6 months, both at rest and during exercise, although ATP-induced NO mediated vasodilation was reduced. Also, the pulmonary vasodilator response to SNP is maintained in both obese Zucker rats and FH-swine exposed to high fat diet. In the latter group, vasodilation to PDE5-inhibition is also preserved. Altogether, these data suggest that pulmonary vasodilation through the NO pathway is well-preserved in obesity (Table 1).

In general, vasoconstrictor responses in the pulmonary microvasculature are reduced in obesity. Thus, vasoconstriction to KCl, phenylephrine, serotonin, and hypoxia are reduced in pulmonary resistance, but not conductance arteries of obese Zucker rats. In FH swine, endothelin receptor blockade did not reduce pulmonary vascular resistance, while it produced pronounced vasodilation in normal swine (Table 1). This loss of ET-mediated vasoconstriction was accompanied by slightly lower plasma ET-levels. These data suggest that reducing the effect of vasoconstrictors may serve as an early compensatory mechanism to maintain pulmonary vascular resistance as low as possible, to limit the workload of the right ventricle.

The term obesity paradox refers to the observation that although obesity is a well-known risk factor for the development of cardiovascular disease, mortality rate in many cardiovascular disorders, once established, is lower in obese patients. Thus, there is evidence suggesting that when CKD is present, mortality is higher in underweight patients and lower in patients with obesity class I, but not with class II or III. Similarly, in patients with established coronary artery disease, heart failure, or stroke, there are large cohort studies suggesting that mortality is reduced in patients with obesity class I, particularly in the short term. Also in patients with established PH, a recent study shows a strong inverse correlation between obesity and mortality, in that both in pre-capillary and out-of proportion post-capillary PH, obese patients had a significantly lower mortality (46% vs. 10% mortality in pre-capillary and 40% vs. 11% in post-capillary PH for lean and obese subjects). Moreover, BMI was the strongest predictor of mortality in a COX hazard analysis, followed by NYHA functional class.

However, there is also concern about selection bias, insufficient control for cardiorespiratory fitness, inadequate determination of body fat localization (i.e. visceral vs. subcutaneous), and underweight vs. normal weight subjects, in these studies. Indeed the overall consensus is that losing weight by for example exercise trainings confers protection against mortality in cardiovascular disease. A large part from these benefits of exercise training can be ascribed to improved microvascular function, and reduced inflammation. Another intriguing possibility is that exercise training results in secretion of ‘myokines’ from skeletal muscle and ‘cardiomyokines’ from cardiac muscle such as FGF21 and irisin, that act in an endo- and/or paracrine fashion on perivascular and epicardial adipose tissue, and induce a ‘browning’ phenotype.

Summary and conclusion

Obesity is a well-established risk factor for microvascular dysfunction throughout the body (Figure 1). This microvascular dysfunction is likely initiated by transient elevations of circulating free fatty acids, and perpetuated by changes in adipokines and inflammatory cytokines released from visceral as well as perivascular adipose tissue. These factors contribute to endothelial dysfunction as well as insulin resistance in the microvasculature, thereby affecting function of different organs not only by impairing tissue perfusion, but also through altering the release of paracrine factors from the endothelial cells. Thus, although the mechanisms can differ between regional vascular beds (Table 1), microvascular dysfunction is a central common pathway that may explain exercise-intolerance as well as the higher prevalence of chronic kidney disease, microvascular dementia, coronary microvascular angina, heart failure with preserved ejection fraction, and pulmonary hypertension in obese subjects.

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Yusuf Myers; a regular on the Dr. Oz Show on working out from home

In the middle of a global pandemic, prioritizing your health and wellness is one of the smartest moves you can make. That’s true for everyone, but for Black Americans, it’s critical as this group faces a disproportionate rate of COVID-19 hospitalizations and death, according to the Centers for Disease Control and Prevention.

Reduce unwanted doctor visits, recommended and ranked top by experts!

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Laila Ali Gives Her Tips for Eating Clean and Being Thoughtful

It’s no secret that Americans struggle with diet and lifestyle. Almost 75 percent have too few vegetables and fruits in their diet, and most eat too much sugar, fat, and salt. Living through a global pandemic isn’t making things any easier.

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Laila Ali wants to inspire us all to be healthier. The daughter of legendary boxer Muhammad Ali, Laila carved out her own legend as the most successful female boxer of all time, and has since created her own lifestyle brand ( focused on building healthy relationships with food.

“I look at health and wellness holistically,” Ali said. “Physically, mentally, and spiritually. I can be in control of my own health by being intentional about my lifestyle choices. My routine is to eat well, exercise, pray, meditate, and practice gratitude.”

For Ali, the secret is knowing what you’re putting into your body.

“Eating clean, NON-GMO whole foods and purchasing the highest-quality ingredients that your budget allows are big factors for wellness,” she said. “Investing in high-quality supplements and vitamins is also key.”

As a mother of two, Ali has a lot of experience encouraging her family to make healthy choices.

“I have been focused on making sure my family was healthy way before the pandemic, but now more than ever, I remind them of why I always make it a point to make them drink smoothies, take vitamins, and eat organic NON-GMO foods,” she said. “We can feel confident in our immune systems and not be fearful because we are strong, and our bodies were created to fight sickness.

“Fear alone can weaken your immune system. So again, being in control of your health and mindset is powerful and healing in itself.”

Ali knows everyone moves at their own speed. “I encourage everyone to think about what they can add to their daily routine as opposed to what needs to be taken away,” she said. “The less overwhelming and forceful making good wellness choices can be, the more successful and long-lasting the changes will be.”

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Why Use D'OXYVA?

Experts trust D’OXYVA® — the advanced solution for fast, painless, and comprehensive athletic performance boost and injury recovery. It promotes benefits related to significantly improved blood circulation, including significantly increased cardiac activity, physical fitness, metabolism, endurance, energy balance and a healthy weight.

D’OXYVA® delivers ultra-purified CO2, the latest non-irritating, non-toxic, and fully non-invasive skin delivery infusion technology to help lose weight, recover from injury, and improve your performance.

Reduce unwanted doctor visits, recommended and ranked top by experts!

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Yusuf Myers; a regular on the Dr. Oz Show on working out from home

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In the middle of a global pandemic, prioritizing your health and wellness is one of the smartest moves you can make. That’s true for everyone, but for Black Americans, it’s critical as this group faces a disproportionate rate of COVID-19 hospitalizations and death, according to the Centers for Disease Control and Prevention.

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Yusuf Myers, the founder, creator, and owner of PRX Workouts, emphasized the importance of self-care, like fitness, at a critical time like this. After all, some research suggests exercise may help reduce the risk of a severe respiratory complication called acute respiratory distress syndrome.

“I do not believe the problem is a lack of understanding of the importance of exercise, [because] Black people are very physical in their everyday lives and work,” he said. “However, there is a lack of viable, affordable resources and options for the Black community.”

Staying fit at home

Fortunately, you don’t need professional workout equipment to give your immune system a lift. Myers recommends starting small with simple exercises like burpees, jumping jacks, high knees, and standing up and sitting down on the couch or a chair.

“All these movements you can do from anywhere,” he said. “You do not need to be in a gym to practice them.”

He added that the goal is to get your heart rate up. “Other great examples include HITT training, walking outside with a mask on, taking the stairs, changing your rituals, and adding movement to your rituals.”

If you’re looking for a specific routine to get started, Myers recommended the following:

“Try doing 30 seconds of jumping jacks, then 30 seconds of an active rest, and then 30 seconds of jumping jacks again,” Myers said. “As you start to build your cardiovascular endurance and increase blood flow, you can continue to increase the time to 45 seconds, then to a minute.”

Nutrition-wise, he suggested cutting back on saturated fats and watching your caloric intake.

Finding support

Finally, he recommended building — and then leaning on — your support system, whoever that may be.

“I have created a platform and community filled with unity, trust, integrity, and a positive outlet to learn and grow for oneself and for others,” Myers said. “Not only during a trying time like COVID-19, but always.”

To stay motivated, Myers said you should seek out a virtual workout buddy or join an online program you think you’d enjoy. If you’re new to working out, trust the process.

“My job as a fitness leader in my community and virtually, touching people around the country and the world on social media, is to get people to realize nothing is impossible with hard work and consistency,” Myers said.



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Why Use D'OXYVA?

Experts say D’OXYVA® can help patients find relief. Overwhelming published medical data shows people with preexisting conditions, including diabetes may experience serious complications with COVID-19. D’OXYVA significantly helps people and their pets by gently and quickly spraying a patented and patent-pending ultra-purified, supersaturated solution on the skin surface to achieve major health benefits for well over 90% of users. Experts call D’OXYVA a game-changer biotech.

“Studies with D’OXYVA have shown unmatched results in noninvasive wound care,” Dr. Michael McGlamry. Anyone with an underlying condition should know this option is available.

Reduce unwanted doctor visits, recommended and ranked top by experts!

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These are the fittest US cities in 2020: Report

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The American Fitness Index found that Arlington, Virginia, is the fittest US city this year. For the third year in a row, Arlington, Virginia, is the fittest city in the U.S., according to a recent report.

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On Tuesday, the American College of Sports Medicine (ACSM) and the Anthem Foundation published the annual American Fitness Index, which put Arlington in the top spot on its list of the 100 largest U.S. cities.

To determine the ranking, the American Fitness Index analyzed those cities based on 33 measurements, including “health behaviors, chronic diseases and community infrastructure indicators,” according to a release about the report.

Arlington took the top spot because of its healthy behaviors and community infrastructure, the release said.

Aside from getting the overall top spot, Arlington was also found to be the city with the lowest rate of adults with obesity and the city with the highest rate of residents who meet aerobic and strength activity guidelines, according to the release.

The report also found that all 100 cities saw improvements in several areas including the rate of residents exercising, the number of residents who smoke, and the number of parks within a 10-minute walk.

However, in all 100 cities, only 22 percent of adults met guidelines for aerobic and strength activities.

“It should be of national concern that only one in four Americans meets national physical activity guidelines and more than 30 million have diagnosed heart disease,” American Fitness Index Advisory Board chair Barbara Ainsworth, a fellow of the American College of Sports Medicine, said in a statement.

“Sedentary lifestyles across the United States cost more than $117 billion annually in sick care services, adversely impacting both our nation’s health and economic well-being,” Ainsworth added. “This challenge has local solutions, and the Fitness Index is a prescription for communities to bring about positive change.”

According to the report, the coronavirus pandemic shows how important it is for cities to give residents the opportunities to have healthy lifestyles.

“We know from research that physical activity can build a healthier immune system and overall wellness, which help minimize harmful effects of illness and disease,” Ainsworth said. “This pandemic shows the need to have local parks, trails and connected sidewalks in all neighborhoods that allow people to exercise safely. City leaders and planners need to act boldly and decisively to enact policies and funding to promote physical activity, better health and stronger communities.”

To see what other cities made it to the top ranking, here are the top 10 fittest U.S. cities in 2020, according to the American Fitness Index.

10. Boston

9. Boise, Idaho

8. Denver, Colorado

7. Irvine, California

6. Washington, D.C.

5. San Francisco

4. Madison, Wisconsin

3. Minneapolis, Minnesota

2. Seattle, Washington

1. Arlington, Virginia


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Why Use D'OXYVA?

Expert say D’OXYVA can help COVID-19 patients find relief. Preliminary medical data shows people with preexisting conditions including diabetes may experience serious complications from COVID-19.

D’OXYVA helps by delivering transdermal ultra-purified medical gas directly to the blood stream delivering major outcomes for well over 90% of users. Experts call D’OXYVA a game changer.

“Studies with D’OXYVA have shown unmatched results in noninvasive woundcare,” Dr. Michael McGlamry. Anyone with an underlying condition should know this option is available.

Reduce unwanted doctor visits, recommended and ranked top by experts!

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Company shares shocking model of future remote worker as pandemic continues

Millions of American workers became remote employees overnight when the coronavirus pandemic hit earlier this year, and the future isn’t looking too bright for those who fail to maintain healthy habits while working from home in the long-term, new findings claim.

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Job discovery platform DirectlyApply recently unveiled a visual model for what future remote workers might look like in 25 years if they don’t reform bad habits now, in a figure they’ve named Susan.

Suffering from digital eye strain, poor posture, “tech neck,” obesity, increased stress due to lack of human contact and more, Susan dramatically exemplifies the physical repercussions remote workers may suffer if they fail to prioritize their physical and mental health beyond their 9 to 5.

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Suffering from digital eye strain, poor posture, tech neck, obesity, increased stress due to lack of human contact and more, Susan dramatically exemplifies the physical repercussions remote workers may suffer if they neglect to keep healthy habits.

Susan was created in partnership with a team of clinical psychologists and fitness experts to highlight the effects that isolated working can have on the body, according to DirectlyApply.

“With lockdown having forced people across the globe into what has been the world’s largest remote working experiment, our usual interpretation of the perk has been transformed forever,” a spokesperson for the job-searching site said in a statement shared with Fox News. “Whilst your bed-to-desk commute may allow for more free time and independence, will the physical repercussions to your mind and body be worth it in the future?”

With that being said, the London-based job searching site, which also operates in the U.S. and Canada, shared positive tips for improving physical and mental health while working remotely, amid an uncertain future.

To improve health and wellness during this time, remote workers are encouraged to stick to a routine to optimize productivity, nurture (virtual) social connections with colleagues, exercise outside, clearly delineate between working and living spaces to promote a healthy work-life balance and use free time wisely to support emotional health.


D’OXYVA is the only fully noninvasive, completely painless over-the-skin microcirculatory and nerve stimulant solution that has been validated to significantly improve microcirculation.The improvement of microcirculation, i.e., blood flow to the smallest blood vessels, benefits one’s health, immune system and overall sense of well-being in a variety of ways, including but not limited to weight loss, recover from injury, improved performance, besides diabetes and heart health.

Reduce unwanted doctor visits, recommended and ranked top by experts!

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Non-Invasive Treatments: What No One Is Talking About

D'OXYVA | Cardiovascular, Diabetes Care, Pain Reliever in CA.

Sometimes it seems like the best way to guess a person’s age is by how much medicine they take daily. This system is not perfect, as some people start medications early in life, but we all seem to accumulate pills and creams as we age. That is why it can be a relief to discover an application that can be used for multiple health disorders.

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Alexa, a 58-year-old woman from Texas, United States, has suffered from type 2 diabetes for more than 6 years. She has been taking multiple medications and treatments such as inhibitors, metformin, pain relievers and antibiotics for her diabetic foot wound. After discovering D’OXYVA, a non-invasive application that significantly helped with her pain and wound management after 5 weeks of twice-daily application, she shared that she saved so much when she started decreasing the intake of other medications and avoided a possible amputation just by using this non-invasive application.

D’OXYVA, for example, can be applied for a variety of conditions related to poor circulation. This multi-application product helps consumers save money, space, and time while simplifying everyday life.

Here are a few things about non-invasive treatments that people seem unwilling to discuss.

In layman’s terms, non-invasive treatments do not break the skin or enter beyond the surface of body openings. Invasive treatments include surgery and injections. Because the needles actually penetrate the skin, acupuncture is also considered an invasive procedure. Certain procedures may be considered minimally invasive if they do not penetrate deeply into the body or only require a small incision.

Non-invasive procedures include massage and gas delivery systems such as D’OXYVA.

By nature, an invasive procedure can be hazardous. Even under a doctor’s care, for example, minimally invasive surgical procedures carry risks (Mayo Clinic). Patients can experience unforeseen complications related to anesthesia, infections, or bleeding. While these risks are mitigated with less serious regular treatments, any invasive procedure carries the potential for infections or bleeding complications.

While you should always trust your medical professional’s advice, many non-invasive treatments can be safer. Most doctors will attempt to find the least invasive, most effective treatment.

Although the human body contains many different cells and functional systems, most of them share the same basic processes. For example, every cell in the body depends on a healthy circulation system to receive nutrients and oxygen. Therefore, when a person has circulation problems, it can manifest as a number of issues. Your doctor may be able to recommend one product like D’OXYVA for multiple circulation-related issues.

Examples of Circulation Related Issues

  • Slow-healing wounds, especially those related to diabetes or other cardiovascular issues
  • Septic shock related to a severe infection or a compromised immune system
  • Many forms of chronic pain
  • Varicose veins and other blemishes


D’OXYVA is the only fully noninvasive, completely painless over-the-skin microcirculatory and nerve stimulant solution that has been validated to significantly improve microcirculation.The improvement of microcirculation, i.e., blood flow to the smallest blood vessels, benefits one’s health, immune system and overall sense of well-being in a variety of ways.

If you suffer from symptoms related to poor circulation, end your suffering in silence now!

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Improving Microcirculation for Weight Reduction in Obesity

weight loss obesity

Obesity, by definition, is a Body Mass Index (BMI) of 30 kg per square meter or greater. The prevalence of obesity has increased and is now thought to affect more than one third of the adult population.[1] Recent studies have shown that obesity has an adverse effect on microcirculation and is an important risk factor for the development of many health problems, such as metabolic syndrome (insulin resistance, elevated lipid levels, high blood pressure and increased abdominal girth), ischemic heart disease, heart failure, and other cardiovascular diseases.[2]

The following case demonstrates how improving microcirculation can help with weight reduction in obese people.

Brenda V was a 39-year-old white female patient with severe obesity and a BMI of 52.4 kilograms per square meter. Brenda’s past medical history was significant because it included a history of morbid obesity, high cholesterol, high blood pressure, diabetes mellitus, gout, and depression. She revealed that she could only walk for one block without severe shortness of breath and had to sleep on 2 pillows at night.

On physical examination, her weight was 340 pounds, and her height was 5 feet, 1 inch. Her blood pressure was 180/105, and her cardiovascular exam revealed severe pitting edema of both legs.

Brenda’s abdomen was distended and morbidly obese with decreased bowel sounds. Her laboratory exam showed a hemoglobin A1C level of 12.5% (normal is less than 5.7%) and a triglyceride level of 600 mg/dl (normal is less than 150 mg/dl).

Brenda was put on a regimen of diet, increased exercise, and the use of the peripheral deoxyhemoglobin vasodilator D’OXYVA[3] for 5 minutes per day, 5 times a week, for a 3 month period. After the regular applications, she had the following improvements:

  • Increased physical activity
  • Decreased blood sugar levels
  • Decreased blood pressure
  • Decreased triglyceride levels
  • Decreased HgbA1C levels
  • Increased cardiac function
  • Increased endurance
  • Increased physical fitness
  • Decreased depression
  • Massively decreased weight
  • Increased mobility


How Does Obesity Affect Microcirculation?

Microcirculation[4] refers to the body’s smallest branching blood vessels (arterioles, venules, and capillaries with internal diameters less than 100 microns) that supply oxygen to and remove wastes products from the body’s tissues.

Microcirculation responds to changes in metabolic demands or sympathetic nervous system activation by either expanding or contracting to increase or decrease perfusion levels.

Early in the course of obesity, dysfunctional changes begin to appear in microcirculatory endothelial lining cells”.

These changes are caused by oxidative stress and inflammation of the microcirculation[5] and are now thought to lead to both insulin resistance and hypertension.


Obesity has been found to lead to microcirculatory dysfunction, which causes severe health problems, such as metabolic syndrome, diabetes mellitus and various cardiovascular diseases. Reducing obesity through a program of strict dietary control, increased exercise and the use of D’OXYVA to enhance microcirculation can significantly improve general health and reduce the risk of potentially lethal health complications.



D’OXYVA is the only fully noninvasive, completely painless over-the-skin microcirculatory solution that has been validated to significantly improve microcirculation.The improvement of microcirculation, i.e., blood flow to the smallest blood vessels, benefits one’s health, immune system and overall sense of well-being in a variety of ways.
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Healthy Choices and Technology Equals Better Diabetes Management

D'OXYVA | Cardiovascular, Diabetes Care, Pain Reliever in CA.

By Justin Bennet

According to the American Diabetes Association, 1.5 million people are diagnosed with diabetes every year, 84.1 million Americans are considered prediabetic, and diabetes is in the top 10 causes of death in the US. These are alarming statistics, which can be unsettling if you have diabetes. However, living with a chronic condition in the 21st century means that you have access to technology and information that wasn’t available even as recently as the 1990s.

Smart Tech for Diabetics

Technology has done so much for medicine. There are now robots that can assist with surgery and devices you can wear to monitor everything from your heart rate to how much you sleep at night. Apple’s Series 4 smartwatch, for example, can output an ECG directly on the screen. It will also let you call for help via an emergency SOS function if you get into a bad situation.

Perhaps more importantly, this and other fitness trackers, such as the Fitbit, can help you keep tabs on your exercise routine by counting your steps and calculating your average active time each day. Knowing how much movement you get is paramount to keeping your body fit and healthy. Exercise, according to EndocrineNet, can help you manage your blood glucose levels.

Technology can go one step further by allowing you to take your exercise routines with you no matter where you are. Apps such as MyFitnessPal and 8Fit can encourage you to make healthy exercise choices, and they can also help you monitor what you eat, which is another crucial element related to diabetes management.

Your Actions Matter

While technology can give you the tools to take control of your health, ultimately, it is your actions that direct the path of your well-being.

A few things you can do to stay healthy are:

  • Maintain a relationship with your doctor. Your primary care provider will likely be the one to diagnose you with diabetes. Once the condition is established, they will refer you to an endocrinologist, who may work at an independent office, the hospital, or at a diabetes care center. Make sure to keep your appointments with both, and don’t be afraid to ask questions about caring for yourself. If you have yet to find an endocrinologist, sites like HealthGrades can help you make an informed decision.
  • Exercise and eat right. We’ve already mentioned how technology can help you exercise and eat right, but both of these deserve special emphasis. When you have diabetes, it is not enough to simply eat the right foods; you also have to avoid the wrong ones. Things like white bread, French fries, and sports drinks might seem innocent enough, but they can send your blood sugar skyrocketing while expanding your waistline. You’ll also want to enhance your diet with diabetes-safe supplements to help you manage your weight and keep it within an acceptable range. Nutrition is what gives your body the energy to function, and adding polyphenols and other lesser-known nutrients to your daily intake is an important step in managing your condition.
  • Take your medicine on time. If your doctor has put you on a prescription for your diabetes, it’s important to take it at the same time every day. This is another area where technology can enhance your self-care efforts via medication reminder apps. Pharmacist Christina Tarantola lists several of her favorites and also cautions that around half of all prescriptions are taken incorrectly.

When it comes to diabetes management, technology can get you halfway there. However, what you choose to do with it and the lifestyle decisions you make mean the difference between living with your condition and letting your condition rule your life.



Do you own a wearable fitness tracker? Is it really a fitness technology or just more of a fad? If your wearable records heart rate, blood pressure, blood sugar, blood flow (perfusion index), blood oxygen (SpO2), blood pH, we challenge you to prove that you have the best wearable by testing its efficiency with D’OXYVA.D’OXYVA is the only fully noninvasive, completely painless transdermal (over-the-skin) microcirculatory solution that has been validated to significantly improve microcirculation.Results of improved blood flow (perfusion index) is visible in just after 5 minutes of D’OXYVA and at its peak at about 60 minutes!Are you up for the challenge? Register below to get further details! Amazing prizes await!
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A Success Story: Enjoying the stage again after years of chronic pain

chronic pain success story

Rachel shares how her healthcare professionals, along with the use of D’OXYVA, have helped her every step of the way. My story started 2 years ago when I severely injured my ankle. At that time, I was working hard preparing for a dance presentation. I am a professional ballet dancer; my injury happened after a grand jeté, when I landed badly on my right foot. I needed to undergo surgery and rehab.

It was so painful that I had a hard time sleeping. Luckily, I got some pain meds so I could fall asleep. The nights were rough. I would wake up every two hours to call the nurses and ask for more medicine.According to the doctors, this fracture could leave me limping for life. When I heard those words, my world just fell apart. I didn’t know how to accept my situation. I wouldn’t be able to dance again? I wouldn’t be able to walk again? I started to view life differently; I was hopeless.I had to undergo months of rehab and physical therapy. Luckily, I had my friends and family to support me all the way. I slowly noticed I was feeling better; I could slowly stand up and take a few steps.A few weeks before Christmas, due to my eagerness to recover so I could dance again, I once again aggravated my ankle after forcing it. The pain was excruciating; it felt like the first time I fractured it. That time I thought, “I’m done. I’m giving up; I will never really be able to dance again.” I had to undergo surgery and rehab for the second time, but this time, I didn’t feel like doing it; I thought it was useless, much more so after the doctor told me that the chances I could dance again were small.

One month later, I met Janina, my co-ballet dancer, at the rehab center undergoing the same physical therapy as I was. She told me she had just fractured her ankle about 4 weeks earlier; I was amazed at how fast she seemed to be recovering. I couldn’t help but ask what she had been doing or what medications she had been taking.

She then pulled a device from her bag and said, “This is D’OXYVA. This helped me with my recovery really well.” I was intrigued. Janina told me that her mother, who is diabetic, had been using D’OXYVA to manage her neuropathy and her diabetic wound, so she thought it might help her, too. Indeed, it helped her recover quickly, and she barely felt any pain from her injured ankle.

When I arrived home, I turned on my computer and did my research on D’OXYVA. Their customer support was very helpful with all the questions I had.

After almost 4 weeks of twice daily D’OXYVA therapy with the help of my orthopedic doctor and therapist, I was walking; after 5 weeks, the pain was almost gone. Now, it’s been almost 8 weeks, my D’OXYVA therapy has been reduced to 4 times a week, and I’m back at the rehearsal studio. It was an unexpected turn of events. I went from hopeless to hopeful!

I am still continuing my D’OXYVA therapy at least 3 times a week and working my way to becoming fully recovered. I’d like to thank Janina for introducing me to D’OXYVA. It gave me hope and positive vibes during my recovery stage. As for the D’OXYVA support staff, my orthopedic doctor, and my physical therapist, I couldn’t ask for a more professional, caring, and extremely helpful group. They are just plain AMAZING, all of them!


D’OXYVA improves oxygenation-balanced circulation of blood flow. Oxygen is one of the body’s natural healers. If you have ever taken deep breaths to help reduce your stress or pain, you know that increasing oxygen flow throughout your body can help with healing and minimizing pain.In various clinical studies, D’OXYVA® (deoxyhemoglobin vasodilator) has achieved over 90%* elimination of all sorts of chronic pain in 100% of subjects either the same day or in a few days, such as from a very high 8 to a very low 1 on the Visual Analog Scale (VAS).
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Under Armour developing ‘smart’ sneaker that reads blood pressure

D'OXYVA | Cardiovascular, Diabetes Care, Pain Reliever in CA.

Under ArmourOpens a New Window. is developing a “smart” sneaker that would track the blood pressure of its wearer, according to a patent filing this week.

The sports apparel brand’s filing with the U.S. Patent and Trademark Office details two versions of a sneaker currently in development. The first version of the sneaker would link to a wearable device and transmit blood pressure that would then be used to adjust the sneaker’s fit for optimal blood flow. The second version of the sneaker contains a “blood pressure detector.”

In the patent filing, Under Armour said the sneaker is meant to help its wearer recover after a “strenuous workout.”

“There exists a need for a device and method to effectively pump blood through the plantar venous plexus and support recovery after engaging in athletic activity,” the company wrote in its filing, dated June 25.

Under Armour representatives did not immediately respond to a request for comment. Baltimore Business Journal was first to report on the filing.

The filing comes as Under Armour and other sports apparel companies seek to integrate technology into their products.

The Baltimore-based company unveiled its first smart shoe, the “HOVR Connected Series,” in 2018. The footwear line measures a runner’s gait and other workout data.


D’OXYVA is the only fully noninvasive, completely painless transdermal (over-the-skin) microcirculatory solution that has been clinically tested to significantly improve microcirculation.

D’OXYVA promotes benefits related to significantly improved blood circulation, including significantly increased cardiac activity, physical fitness, metabolism, endurance, energy balance and a healthy weight by significantly improving Microcirculation that is detectable real-time with high quality diagnostics.

The improvement of microcirculation, i.e., blood flow to the smallest blood vessels, benefits one’s health, immune system and overall sense of well-being in a variety of ways.