Sex and gender correlates of sexually polymorphic cognition.

BACKGROUND: Sexually polymorphic cognition (SPC) results from the interaction between biological (birth-assigned sex (BAS), sex hormones) and socio-cultural (gender identity, gender roles, sexual orientation) factors. The literature remains quite mixed regarding the magnitude of the effects of these variables. This project used a battery of classic cognitive tests designed to assess the influence of sex hormones on cognitive performance. At the same time, we aimed to assess the inter-related and respective effects that BAS, sex hormones, and gender-related factors have on SPC. METHODS: We recruited 222 adults who completed eight cognitive tasks that assessed a variety of cognitive domains during a 150-min session. Subgroups were separated based on gender identity and sexual orientation and recruited as follows: cisgender heterosexual men (n = 46), cisgender non-heterosexual men (n = 36), cisgender heterosexual women (n = 36), cisgender non-heterosexual women (n = 38), gender diverse (n = 66). Saliva samples were collected before, during, and after the test to assess testosterone, estradiol, progesterone, cortisol, and dehydroepiandrosterone. Psychosocial variables were derived from self-report questionnaires. RESULTS: Cognitive performance reflects sex and gender differences that are partially consistent with the literature. Interestingly, biological factors seem to better explain differences in male-typed cognitive tasks (i.e., spatial), while psychosocial factors seem to better explain differences in female-typed cognitive tasks (i.e., verbal). CONCLUSION: Our results establish a better comprehension of SPC over and above the effects of BAS as a binary variable. We highlight the importance of treating sex as a biological factor and gender as a socio-cultural factor together since they collectively influence SPC.

Many studies show sex differences in cognitive abilities. In general, women outperform men in verbal tasks and fine motor skills, while men outperform women in spatial orientation and mental rotation tasks. These differences underlie research on sexually polymorphic cognition, a concept influenced by sex hormones (estradiol, progesterone, and testosterone) as well as birth-assigned sex. In addition to these biological factors, socio-cultural gender factors such as gender identity (the gender we feel and embody), gender roles (masculine and feminine expressions based on stereotypes), as well as sexual orientation are all known to influence cognition as well. We provide a broader understanding by accounting for both sex and gender factors. Our team recruited 222 adults separated into 5 sub-groups based on birth-assigned sex, gender identity, and sexual orientation. Each participant completed eight sexually polymorphic cognitive tasks. In this 150-min experimental protocol, saliva samples were collected before, during, and after the test to assess testosterone, estradiol, progesterone, cortisol, and dehydroepiandrosterone. Psychosocial variables were derived from self-report questionnaires. Results showed that spatial cognition was better explained by biological sex factors, while verbal cognition was better explained by socio-cultural gender factors. Taken together, our findings demonstrate the importance of considering sex-based and gender-based factors collectively and, respectively, when studying sex differences in cognition.

Sex/gender differences in cognitive abilities.

Sex/gender differences in cognitive sciences are riddled by conflicting perspectives. At the center of debates are clinical, social, and political perspectives. Front and center, evolutionary and biological perspectives have often focused on 'nature' arguments, while feminist and constructivist views have often focused on 'nurture arguments regarding cognitive sex differences. In the current narrative review, we provide a comprehensive overview regarding the origins and historical advancement of these debates while providing a summary of the results in the field of sexually polymorphic cognition. In so doing, we attempt to highlight the importance of using transdisciplinary perspectives which help bridge disciplines together to provide a refined understanding the specific factors that drive sex differences a gender diversity in cognitive abilities. To summarize, biological sex (e.g., birth-assigned sex, sex hormones), socio-cultural gender (gender identity, gender roles), and sexual orientation each uniquely shape the cognitive abilities reviewed. To date, however, few studies integrate these sex and gender factors together to better understand individual differences in cognitive functioning. This has potential benefits if a broader understanding of sex and gender factors are systematically measured when researching and treating numerous conditions where cognition is altered.

Sex and Gender and Allostatic Mechanisms of Cardiovascular Risk and Disease.

Cardiovascular diseases are leading causes of mortality and morbidity in adults worldwide. Multiple studies suggest that there are clinically relevant sex differences in cardiovascular disease. Women and men differ substantially in terms of prevalence, presentation, management, and outcomes of cardiovascular disease. To date, however, little is known about why cardiovascular disease affects women and men differently. Because many studies do not differentiate the concept of sex and gender, it is sometimes difficult to discriminate sociocultural vs biological contributors that drive observed clinical differences. Female sex has some biological advantages in relation to cardiovascular disease, but many of these advantages seem to disappear as soon as women develop cardiovascular risk factors (eg, type 2 diabetes, hypertension, dyslipidemia). Furthermore, stress and allostatic load could play an important role in the relationship between sex/gender and cardiovascular diseases. In this narrative review, we argue that chronic stress and psychosocial factors might better encompass the patterns of allostatic load increases seen in women, while biological risk factors and unhealthy behaviours might be more important mechanisms that drive increased allostatic load in men. Indeed, men show allostatic load patterns that are more associated with impaired anthropometric, metabolic, and cardiovascular functioning and women have greater dysregulation in neuroendocrine and immune functioning. Thus gender-related factors might contribute to the pathogenesis of cardiovascular disease especially through stress mechanisms. It is important to continue to study the mechanisms by which gender influences chronic stress, because chronic stress could influence modifiable gendered factors to promote cardiovascular disease prevention.

Impact of the 2016 Canadian Lipid Guidelines on Daily Practice at a Community Hospital.

OBJECTIVES: The aim of this study was to determine the impact of the 2016 Canadian cardiovascular society guidelines for the management of dyslipidemia. More specifically, we assessed the use of 1) alternate lipid targets when triglyceride (TG) levels are high; and 2) nonfasting lipid testing. METHODS: Lipid profiles and pharmacy data were obtained from patients with a history of myocardial infarction and from patients ≥40 years of age with a diagnosis of diabetes. RESULTS: As TG increased to >1.5 mmol/L, percent within target for non-high-density lipoprotein cholesterol and apolipoprotein B 18 months after guideline release remained low in both patients with atherosclerotic cardiovascular disease (40%) and patients with diabetes in primary prevention (30%). Approximately 50% of patients were fasting when presenting for lipid testing. Use of high-intensity statin was suboptimal in both groups. CONCLUSIONS: The concept of alternate lipid targets may not be well understood by many physicians, leading to undertreatment of patients. Progress was made in the promotion of routine nonfasting lipid testing.

Impact of the Martin/Hopkins modified equation for estimating LDL-C on lipid target attainment in a high risk patient population.

OBJECTIVE: To evaluate the Martin/Hopkins equation for estimating LDL-C as target in a population composed of high cardiac risk patients. METHODS: Lipid profile data from patients with TG ≤ 4.52 mmol/L (<400 mg/dl) were used. The high cardiac risk group (N 4150) consisted of patients over 40 years of age that had an A1C level of 6.5% or above and patients with a history of atherosclerotic cardiovascular disease (ASCVD). Comparisons were made between the Martin/Hopkins formula (MH-LDL-C), the Friedewald formula (F-LDL-C), Non-HDL-C and ApoB. RESULTS: Higher LDL-C values (0.15 mmol/L or 7.3%) were obtained using MH-LDL-C compared to the F-LDL-C. The % within target (%WT) values for F-LDL-C, MH-LDL-C, Non-HDL-C and ApoB were similar when TG levels were ≤ 1.5 mmol/L with a high degree of concordance as measured by the kappa statistic. When compared to F-LDL-C, Non-HDL-C and ApoB showed a profound decrease in the WT value as TG levels increased from normal (67.7%) to intermediate (39.1%) and high levels (20.8%). MH-LDL-C showed an attenuated decrease in the WT value as TG increased from normal (61.4%) intermediate (43.4%) and high levels (32.7%). Concordance with the alternate target parameters was higher for MH-LDL-C than for F-LDL-C when triglycerides levels were increased. CONCLUSION: The Martin/Hopkins modified equation for estimating LDL-C is a significant improvement on the decade's old Friedewald formula; however it remains an imperfect tool to estimate the atherogenic load in patients with high TG levels.

Comparison of fasting and non-fasting lipid profiles in a large cohort of patients presenting at a community hospital.

OBJECTIVE: To compare the fasting and non-fasting lipid profile including ApoB in a cohort of patients from a community setting. Our purpose was to determine the proportion of results that could be explained by the known biological variation in the fasting state and to examine the additional impact of non-fasting on these same lipid parameters. METHODS: 1093 adult outpatients with fasting lipid requests were recruited from February to September 2016 at the blood collection sites of the Moncton Hospital. Participants were asked to come back in the next 3-4days after having eaten a regular breakfast to have their blood drawn for a non-fasting lipid profile. RESULTS: 91.6% of patients in this study had a change in total cholesterol that fell within the biological variation expected for this parameter. Similar results were seen for HDL-C (94.3%) non-HDL-C (88.8%) and ApoB (93.0%). A smaller number of patients fell within the biological variation expected for TG (78.8%) and LDL-C (74.6%). An average TG increase of 0.3mmol/L was observed in fed patients no matter the level of fasting TG. A gradual widening in the range of change in TG concentration was observed as fasting TG increased. Similar results were seen in diabetic patients. CONCLUSION: Outside of LDL-C and TG, little changes were seen in lipid parameters in the postprandial state. A large part of these changes could be explained by the biological variation. We observed a gradual widening in the range of increase in TG for patients with higher fasting TG. Non-HDL-C and ApoB should be the treatment target of choice for patients in the non-fasting state.

Causes and outcomes of markedly elevated C-reactive protein levels.

OBJECTIVE: To characterize the causes of marked elevation of C-reactive protein (CRP) levels, investigate patient outcomes, and examine factors that might influence the CRP response. DESIGN: Health records were used to retrospectively determine patient characteristics, diagnoses, and outcomes over a 2-year period (2012 to 2013). SETTING: A large referral centre in Moncton, NB. PARTICIPANTS: Adult inpatients and outpatients with a CRP level above 100 mg/L. MAIN OUTCOME MEASURES: Differences among the CRP distributions of various diagnosis categories were examined using Kruskal-Wallis tests, and factors affecting outcomes were examined using Fisher exact tests. RESULTS: Over the 2-year period, 1260 CRP levels (839 patients; 3.1% of all tests) were above 100 mg/L (range 100.1 to 576.0 mg/L). The mean age was 63 years (range 18 to 101) and 50.2% of patients were men. Infection was the most prevalent cause (55.1%), followed by rheumatologic diseases (7.5%), multiple causes (5.6%), other inflammatory conditions (5.4%), malignancy (5.1%), drug reactions (1.7%), and other conditions (2.0%). A diagnosis could not be established in 17.6% of cases. On average, infections caused higher peak CRP levels (W = 34 519, P < .001) and infection was present in 88.9% of cases with CRP levels greater than 350 mg/L. Rheumatologic causes were associated with only 5.6% of CRP levels above 250 mg/L. The overall mortality was 8.6% and was higher in patients with malignancy (37.0%), multiple diagnoses (21.0%), and leukopenia (20.7%, P = .002). CONCLUSION: Most patients had infections and the proportion of patients with infections increased with the level of CRP, although many diagnoses were associated with markedly elevated CRP levels. These data could help guide health care professionals in the evaluation and management of these patients.

The Effect of Triglyceride Concentration on Attainment of Lipid Targets in Patients with Diabetes.

OBJECTIVES: To evaluate the effects of triglyceride (TG) and glycated hemoglobin (A1C) concentrations in the percentage of patients with diabetes who are within target (WT) for low-density lipoprotein-cholesterol (LDL-C), non-high-density lipoprotein-cholesterol (non-HDL-C) and apolipoprotein B (ApoB), as defined by the Canadian Lipid Guidelines, in a cohort of outpatients presenting at a 350-bed community hospital. METHODS: Laboratory samples from 1919 patients, 18 years or older, who had A1C levels of 6.5% or above were used. Fasting lipid profiles were retrieved, and ApoB was measured. RESULTS: We found no significant difference in the percentage of those WT for LDL-C as TG increased from normal to intermediate and high levels. For non-HDL-C, we saw a substantial decrease in the percentage of patients WT as TG levels increased from normal (61%) to intermediate (30.4%) and high levels (14.0%). ApoB showed a similar pattern to non-HDL-C: decreasing from normal (68.8%) to intermediate (40.7%) and high levels (21.0%). No significant difference was seen in the percentage of patients WT for the 3 lipid parameters studied with the increase in A1C levels. CONCLUSIONS: As TG increases, we saw discordance in the percentage of patients WT for LDL-C in relation to non-HDL-C and ApoB. Alternative targets to LDL-C should preferentially be used when the TG concentration is elevated.

Interference of gadolinium-based contrast agents on colorimetric calcium assays.

OBJECTIVE: The aim of this study was to evaluate the potential interference of five gadolinium-based contrast agents (GBCAs), gadodiamide (Omniscan®), gadobenate dimeglumine (Multihance®), gadoxetate disodium (Primovist®), gadobutrol (Gadovist®), and gadoteridol (Prohance®), on three clinical laboratory widely used colorimetric calcium assays including the newly developed 5-nitro-5'methyl-l,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (NM-BAPTA) method. METHODS: Plasma was collected from healthy volunteers aged 23-52, and spiked with varying concentrations of the five GBCAs. Calcium determinations were performed in duplicates using the o-cresolphthalein complexone (OCP), arsenazo-III dye, and NM-BAPTA methods on the Roche Integra 400, Abbott Architect 16000, and Roche Modular P automated analyzers respectively. RESULTS: Gadobenate dimeglumine, gadobutrol, and gadoteridol did not interfere with any of the assays. There was a small positive bias (8%, p<0.01) at a very high concentration (25mmol/L) of gadoxetate disodium when calcium was assayed using the arsenazo-III method. Gadodiamide at a very high concentration (50mmol/L) induced a significant positive bias (16%, p<0.01) on calcium when measured using the NM-BAPTA method; however a much larger bias (90%, p≪0.01) was observed when calcium was measured using the arsenazo-III method. Significant interferences in calcium measurements using the OCP method began at gadodiamide concentrations as low as 0.5mmol/L (-9%, p<0.01). This negative bias was more pronounced at higher gadodiamide concentrations. CONCLUSIONS: Of all 5 GBCAs tested, only gadodiamide showed significant interference on the OCP calcium assay at clinically relevant concentrations. The NM-BAPTA assay showed minimum interference with the five GBCAs and demonstrated equal or better performance than the OCP and the arsenazo-III methods in terms of interference with GBCAs.