The Link between Fetal Programming, Inflammation, Muscular Strength, and Blood Pressure

Abstract

Hypertension affects one billion individuals worldwide and is considered the leading cause of cardiovascular death, stroke, and myocardial infarction. This increase in the burden of hypertension and cardiovascular diseases (CVD) is principally driven by lifestyle changes such as increased hypercaloric diets and reduced physical activity producing an increase of obesity, insulin resistance, and low-grade inflammation. Visceral adipocytes are the principal source of proinflammatory cytokines and systemic inflammation participates in several steps in the development of CVD. However, maternal and infant malnutrition also persists as a major public health issue in low- to middle-income regions such as Latin America (LA). We propose that the increased rates of cardiovascular and metabolic diseases in these countries could be the result of the discrepancy between a restricted nutritional environment during fetal development and early life, and a nutritionally abundant environment during adulthood. Maternal undernutrition, which may manifest in lower birth weight offspring, appears to accentuate the relative risk of chronic disease at lower levels of adiposity. Therefore, LA populations may be more vulnerable to the pathogenic consequences of obesity than individuals with similar lifestyles in high-income countries, which may be mediated by higher levels of proinflammatory markers and lower levels of muscle mass and strength observed in low birth weight individuals.

Identification of High-Risk Pregnancies in a Remote Setting Using Ambulatory Blood Pressure: The MINDI Cohort

“…The nature of the relationship between infection and blood pressure may depend on whether the infection induces a proor anti-inflammatory response. Inflammation modulates blood pressure in pregnancy (22) as evidenced by the association of HDPs with inflammatory markers including C-reactive protein (CRP) (23,24) and with two pro-inflammatory cytokines, interleukin (IL)-6 and tumor necrosis factor (TNF)-α (25). In contrast, down-regulation of the pro-inflammatory response by IL-10 and T-regulatory cells (T-regs) has been shown to reduce the pathology of HDPs (26).…”

Serum pentraxin‐3 levels and flow‐mediated dilation in dipper and non‐dipper hypertension

“…Pentraxin‐3 is a novel biological marker of inflammatory processes. Many diseases which have some inflammatory characteristics and have potential to cause endothelial dysfunction can lead to increased serum PTX3 levels . Pentraxin‐3 is involved in a variety of molecular mechanisms which can eventually lead to endothelial dysfunction, inflammation, and increased arterial stiffness in hypertensive patients .…”

“…Many diseases which have some inflammatory characteristics and have potential to cause endothelial dysfunction can lead to increased serum PTX3 levels. [18][19][20][21] Pentraxin-3 is involved in a variety of molecular mechanisms which can eventually lead to endothelial dysfunction, inflammation, and increased arterial stiffness in hypertensive patients. 21 In a study, it was shown that PTX3 induced dysfunction and morphological changes in the endothelial layer through a P-selectin/matrix metalloproteinase-1 pathway.…”

Prediabetes in Colombia: Expert Consensus

“…There is evidence of clear differences in handgrip strength between populations, whereby low and middle income countries, have lower strength than people in high income countries 85 . Indeed, the important role of muscle mass and strength in the regulation of systemic inflammation and insulin sensitivity has recently been increasingly highlighted 86 , given the cross-talk between muscle and fat mass in the maintenance of an adequate metabolic balance. Alterations in this balance begin during intrauterine life, as proposed by Baker a number of years ago in highlighting the importance of fetal programming and its dependence on maternal nutrition 87 .…”