Decreased cognition is associated with altered cardiovascular autonomic functions and decreased baroreflex sensitivity in women with premenstrual syndrome

Premenstrual syndrome (PMS) is a clinical entity of concern in women of reproductive age group with its onset during the late luteal phase of the menstrual cycle that typically resolves within a few days after the onset of menstruation. Female reproductive hormones stimulate the gene promotor region of Gonadal steroids, which are modulators of the hypothalamic-pituitary axis, in association with the autonomic nervous system (ANS), form the stress system, which regulates the homeostatic mechanisms of the body. Disruption of this mechanism can lead to sympathovagal imbalance and cognitive deficits. Objectives: This study was aimed to compare the autonomic functions and cognition between PMS and control group. Methodology: This cross-sectional study was conducted as a pilot study with 20 subjects in each group. Autonomic function test and P300 were recorded. Study participants were also asked to answer Montreal cognitive assessment (MOCA) questionnaire. Results: On comparison of the test results between the two groups, individuals in PMS group were found to have increased sympathetic activity and reduced cognition when compared to the no PMS (control) group. Conclusion: The findings from this study proves a detrimental effect of gonadal steroids on autonomic nervous system and cognition

Decreased baroreflex sensitivity is associated with cardiometabolic risks and prehypertension status in early-postmenopausal women

Objective We studied the link of decreased baroreflex sensitivity (BRS) to cardiometabolic risks and prehypertension status in postmenopausal women during their early menopausal phase. Methods Premenopausal women (n = 55) and early-postmenopausal women (n = 50) of age group between 40 and 55 years were recruited for the study, and their anthropometric parameters, complete battery of autonomic function tests (AFT), BRS, hormone levels, and cardiometabolic risk parameters were measured and compared between two groups. Correlation analysis of BRS with various physiological and biochemical parameters in these two groups were performed. Multiple regression analysis of BRS with various other associated factors in postmenopausal subjects and bivariate logistic regression analysis for assessing prediction of prehypertension status by BRS in postmenopausal group were performed. Results There was a significant difference in AFT and metabolic parameters between premenopausal and postmenopausal women. Sympathovagal imbalance (increased sympathetic and decreased parasympathetic) was prominent in early-postmenopausal women. Decreased BRS, the marker of cardiovascular (CV) risk was found to be significant (P < .001) and correlated with various cardiometabolic parameters in early-postmenopausal subjects. Multiple regression analysis demonstrated that decreased BRS is independently linked to parameters of decreased vagal activity, inflammation, and oxidative stress in early-postmenopausal group. Decreased BRS could predict prehypertension status in early-postmenopausal subjects as confirmed by bivariate logistic regression analysis. Conclusion Sympathovagal imbalance, decreased BRS and considerable metabolic derangements were observed in women in their early phase of menopause. Decreased BRS appears to be associated with the cardiometabolic risks in these women. Prehypertension status in early-postmenopausal subjects could be predicted by decreased BRS

Effect of honey and insulin treatment on oxidative stress and nerve conduction in an experimental model of diabetic neuropathy Wistar rats.

Diabetic neuropathy is the most common complication affecting more than 50% of patients with longstanding diabetes. Till date, there are no reports to explain the scientific basis of alternative medicine as an adjunct therapy for treating diabetic neuropathy. Hence, we studied the effect of honey and insulin treatment on hyperglycemia, dyslipidemia, oxidant and anti-oxidant status and nerve conduction in experimental diabetic neuropathy Wistar rats. In this experimental study, forty healthy male Wistar albino rats of 10-12 weeks age, weighing between 150 to 200g were obtained from our institute central animal house. After acclimatization, the rats were divided into control (n = 8) and experimental (n = 32) groups randomly. In the experimental group, type 2 diabetic neuropathy was induced with high fat and high sugar diet for 8 weeks followed by streptozotocin at a dose of 35 mg/kg body weight. Three days after streptozotocin injection, blood glucose levels of rats were measured from fasting samples to confirm diabetes. After the development of diabetes, rats were given standard rodent chow and allowed four more weeks to remain diabetic and to develop neuropathy. Every second week, nerve conduction study was done to confirm neuropathy. All the diabetic rats of experimental group developed neuropathy after 4 weeks of developing diabetes, which was confirmed by significant reduction in conduction velocity of sensory and motor nerve when compared to non-diabetic control group. After the development of neuropathy, these rats were randomly divided into diabetic neuropathy with no treatment group (n = 8) and three treatment groups (n = 8, each). The rats of treatment group were administered with either honey or insulin or honey+insulin for six weeks. After six-weeks of intervention, there was significant decrease in blood glucose and lipids in honey, insulin and honey+insulin treated neuropathy rats, when compared with no treatment group. Malondialdehyde was reduced and total anti-oxidant status improved in all the three treatment groups. There was no significant increase in conduction velocity of sciatic tibial motor nerve in treatment groups when compared with no treatment group. However, the sensory nerve conduction velocity improved significantly in honey+insulin treated neuropathy rats. In conclusion, six-week honey treatment helped in reducing dyslipidemia and oxidative stress. Honey given along with insulin for six-weeks improved sensory nerve conduction velocity in experimental diabetic neuropathy Wistar rats

Attenuation of baroreflex sensitivity and heart rate variability is linked to reduced levels of nitric oxide in pregnant women having risks of developing gestational hypertension

Purpose: Decreased baroreflex sensitivity (BRS) and sympathovagal imbalance (SVI) have been reported as a cardiovascular (CV) risk in gestational hypertension (GH). Nitric oxide (NO) has been implicated in pathophysiology of GH. In the present study, we assessed the link of CV risks (decreased BRS and SVI) to the plasma levels of NO in women having risk of developing GH. Materials and Methods: A total of 96 pregnant women having risk factors for GH were recruited for the study. The blood pressure variability (BPV), heart rate variability (HRV), plasma NO, marker of insulin resistance (HOMA-IR), lipid risk factors, inflammatory markers (hsCRP, interleukin-6), and malondialdehyde (MDA), the marker of oxidative stress (OS) were measured at 16th and 36th week. Link of various parameters to NO was assessed by correlation and multiple regression analysis. Results: Of HRV indices, parasympathetic components were decreased and sympathetic components were increased, BRS was decreased, NO was decreased, HOMA-IR, lipid risk factors, hsCRP, interleukin-6, and MDA were increased significantly at 36th week compared to 16th week of pregnancy. Most of the markers of cardiometabolic risk were correlated with NO. However, only the markers of CV risk (SVI and reduced BRS) were independently associated with decreased level of NO, but not the metabolic markers except interleukin-6. The independent contribution of BRS (β = 0.334, P < .001) to NO was found to be most significant. Conclusion: It was concluded that decreased BRS, SVI, and increased interleukin-6 are associated with reduction in NO in GH, which may possibly be linked to the development of CV risks in GH

Contribution of insulin resistance to decreased baroreceptor sensitivity & cardiometabolic risks in pre-obesity & obesity

Background & objectives: Although insulin resistance (IR) is a known complication in obesity, the physiological mechanisms linking IR with cardiometabolic risks in obesity have not been well studied. This study was conducted to assess the difference in cardiovascular (CV) risk profile in IR and non-IR (NIR) conditions, and contribution of IR to cardiometabolic risks in pre-obese and obese individuals. Methods: Basal CV, blood pressure variability, autonomic function test and cardiometabolic parameters were recorded in pre-obese (n=86) and obese (n=77) individuals during 2012 and 2015. The association of altered cardiometabolic parameters with homeostatic model for IR (HOMA-IR) in pre-obese and obese groups and with baroreceptor sensitivity (BRS) in IR and NIR groups was calculated by appropriate statistical analysis. Results: Decreased BRS, a known CV risk and cardiometabolic parameters were significant in IR (pre-obese and obese) group compared to the NIR group. Sympathovagal imbalance in the form of increased sympathetic and decreased parasympathetic activities was observed in individuals with IR. There was no significant difference in the level of independent contribution of HOMA-IR to cardiometabolic parameters in pre-obese and obese groups. Adiponectin and inflammatory markers had an independent contribution to BRS in IR group. Interpretation & conclusions: Findings of the present study demonstrated that the intensity of cardiometabolic derangements and CV risk were comparable between IR, pre-obese and obese individuals. Pro-inflammatory state, dyslipidaemia and hypoadiponectinaemia might contribute to CV risk in these individuals with IR. IR could possibly be the link between altered metabolic profile and increased CV risks in these individuals independent of the adiposity status

Sympathovagal imbalance contributes to prehypertension status and cardiovascular risks attributed by insulin resistance, inflammation, dyslipidemia and oxidative stress in first degree relatives of type 2 diabetics.

BackgroundThough cardiovascular (CV) risks are reported in first-degree relatives (FDR) of type 2 diabetics, the pathophysiological mechanisms contributing to these risks are not known. We investigated the association of sympathovagal imbalance (SVI) with CV risks in these subjects.Subjects and methodsBody mass index (BMI), basal heart rate (BHR), blood pressure (BP), rate-pressure product (RPP), spectral indices of heart rate variability (HRV), autonomic function tests, insulin resistance (HOMA-IR), lipid profile, inflammatory markers, oxidative stress (OS) marker, rennin, thyroid profile and serum electrolytes were measured and analyzed in subjects of study group (FDR of type 2 diabetics, n = 72) and control group (subjects with no family history of diabetes, n = 104).ResultsBMI, BP, BHR, HOMA-IR, lipid profile, inflammatory and OS markers, renin, LF-HF (ratio of low-frequency to high-frequency power of HRV, a sensitive marker of SVI) were significantly increased (pConclusionSVI in FDR of type 2 diabetics occurs due to sympathetic activation and vagal withdrawal. The SVI contributes to prehypertension status and CV risks caused by insulin resistance, dyslipidemia, inflammation and oxidative stress in FDR of type 2 diabetics

Multiple regression analysis of LF-HF (as dependent variable) with various parameters (as independent variables) in study group subjects.

<p>P values<0.05 considered significant. BMI: Body mass index; HOMA-IR: homeostatic model assessment of insulin resistance; AI: Atherogenic index; IL6: Interleukin 6; hsCRP: high-sensitive C reactive protein; TNFα: Tumor necrosis factorα; TBARS: Thiobarbituric acid reactive substance; PHTN status: Prehypertension status.</p