Inverse Causality Research Articles

Unification of Mind and Matter through Hierarchical Extension of Cognition: A New Framework for Adaptation of Living Systems.

Living systems (LSs) must solve the problem of adapting to their environment by identifying external states and acting appropriately to maintain external relationships and internal order for survival and reproduction. This challenge is akin to the philosophical enigma of how the self can escape solipsism. In this study, a comprehensive model is developed to address the adaptation problem. LSs are composed of material entities capable of detecting their external states. This detection is conceptualized as "cognition", a state change in relation to its external states. This study extends the concept of cognition to include three hierarchical levels of the world: physical, chemical, and semiotic cognitions, with semiotic cognition being closest to the conventional meaning of cognition. This radical extension of the cognition concept to all levels of the world provides a monistic model named the cognizers system model, in which mind and matter are unified as a single entity, the "cognizer". During evolution, LSs invented semiotic cognition based on physical and chemical cognitions to manage the probability distribution of events that occur to them. This study proposes a theoretical model in which semiotic cognition is an adaptive process wherein the inverse causality operation produces particular internal states as symbols that signify hidden external states. This operation makes LSs aware of the external world.

Role of metabolites in mediating the effect of triacylglycerol on aplastic anemia

ABSTRACT Background Observational studies have found a link between lipid metabolism disorders and aplastic anemia (AA). However, due to confounding variables and reverse causation, it is difficult to conclude such a causal link. The precise mechanism and potential implications of lipid metabolism disorder in AA remain unclear, necessitating further studies in this area. Method This study aimed to examine the causal relationship between 38 different subtypes of triacylglycerols and AA using two-sample Mendelian randomization (MR). Additionally, two-step MR analyses were conducted to investigate the mediating effects of vitamin A to oleoyl-linoleoyl-glycerol (18:1–18:2) ratio. Results MR analysis showed that triacylglycerol (53:3) levels were positively associated with the risk of AA [inverse variance weighting (IVW): odds ratio (OR) = 1.131,95% confidence interval (CI):1.029-1.243, P = 0.011; Bayesian weighted MR (BWMR): OR = 1.137,95% CI:1.031-1.254, P = 0.010]. Triacylglycerol (53:3) level showed no inverse causality with AA (IVW:P = 0.834; BWMR:P = 0.349). Mediation analyses showed that increasing the vitamin A to oleoyl-linoleoyl-glycerol (18:1–18:2) ratio can decrease the risk of AA. Conclusion This study revealed the association between vitamin A to oleoyl-linoleoyl-glycerol (18:1–18:2) ratio, triacylglycerol (53:3) levels and AA, and indicated that lowering triacylglycerol (53:3) levels can reduce the risk of AA.

Association between Psoriasis and Renal Functions: An Integration Study of Observational Study and Mendelian Randomization.

Psoriasis is an autoimmune-mediated disease with several comorbidities in addition to typical skin lesions. Increasing evidence shows the relationships between psoriasis and renal functions, but the relationship and causality remain unclear. We aimed to investigate the associations and causality between psoriasis and four renal functions, including the estimated glomerular filtration rate (eGFR), blood urea nitrogen (BUN), urine albumin to creatinine ratio (UACR), and chronic kidney disease (CKD). For the population-based study, we analyzed the National Health and Nutrition Examination Survey (NHANES) data from five cycles (2003-2006 and 2009-2014) on psoriasis and renal functions. Subgroup analyses were conducted among different categories of participants. Meanwhile, a bidirectional two-sample Mendelian randomization (TSMR) study in European populations was also performed using summary-level genetic datasets. Causal effects were derived by conducting an inverse-variance weighted (MR-IVW) method. A series of pleiotropy-robust MR methods was employed to validate the robustness. Multivariable MR (MVMR) was conducted to complement the result when five competing risk factors were considered. A total of 20,244 participants were enrolled in the cross-sectional study, where 2.6% of them had psoriasis. In the fully adjusted model, participants with psoriasis had significantly lower eGFR (p = 0.025) compared with the healthy group. Individuals who are nonoverweight are more likely to be affected by psoriasis, leading to an elevation of BUN (Pint = 0.018). In the same line, TSMR showed a negative association between psoriasis and eGFR (p = 0.016), and sensitive analysis also consolidated the finding. No causality was identified between psoriasis and other renal functions, as well as the inverse causality (p > 0.05). The MVMR method further provided quite consistent results when adjusting five confounders (p = 0.042). We detected a significant negative effect of psoriasis on eGFR, with marginal association between BUN, UACR, and CKD. The adverse of psoriasis on the renal should merit further attention in clinical cares.

Role of inflammatory cytokines and the gut microbiome in vascular dementia: insights from Mendelian randomization analysis.

Both inflammatory cytokines and the gut microbiome are susceptibility factors for vascular dementia (VaD). The trends in the overall changes in the dynamics of inflammatory cytokines and in the composition of the gut microbiome are influenced by a variety of factors, making it difficult to fully explain the different effects of both on the different subtypes of VaD. Therefore, this Mendelian randomization (MR) study identified the inflammatory cytokines and gut microbiome members that influence the risk of developing VaD and their causal effects, and investigated whether inflammatory cytokines are gut microbiome mediators affecting VaD. We obtained pooled genome-wide association study (GWAS) data for 196 gut microbiota and 41 inflammatory cytokines and used GWAS data for six VaD subtypes, namely, VaD (mixed), VaD (multiple infarctions), VaD (other), VaD (subcortical), VaD (sudden onset), and VaD (undefined). We used the inverse-variance weighted (IVW) method as the primary MR analysis method. We conducted sensitivity analyses and reverse MR analyses to examine reverse causal associations, enhancing the reliability and stability of the conclusions. Finally, we used multivariable MR (MVMR) analysis to assess the direct causal effects of inflammatory cytokines and the gut microbiome on the risk of VaD, and performed mediation MR analysis to explore whether inflammatory factors were potential mediators. Our two-sample MR study revealed relationships between the risk of six VaD subtypes and inflammatory cytokines and the gut microbiota: 7 inflammatory cytokines and 14 gut microbiota constituents were positively correlated with increased VaD subtype risk, while 2 inflammatory cytokines and 11 gut microbiota constituents were negatively correlated with decreased VaD subtype risk. After Bonferroni correction, interleukin-18 was correlated with an increased risk of VaD (multiple infarctions); macrophage migration inhibitory factor was correlated with an increased risk of VaD (sudden onset); interleukin-4 was correlated with a decreased risk of VaD (other); Ruminiclostridium 6 and Bacillales were positively and negatively correlated with the risk of VaD (undefined), respectively; Negativicutes and Selenomonadales were correlated with a decreased risk of VaD (mixed); and Melainabacteria was correlated with an increased risk of VaD (multiple infarctions). Sensitivity analyses revealed no multilevel effects or heterogeneity and no inverse causality between VaD and inflammatory cytokines or the gut microbiota. The MVMR results further confirmed that the causal effects of Negativicutes, Selenomonadales, and Melainabacteria on VaD remain significant. Mediation MR analysis showed that inflammatory cytokines were not potential mediators. This study helps us to better understand the pathological mechanisms of VaD and suggests the potential value of targeting increases or decreases in inflammatory cytokines and gut microbiome members for VaD prevention and intervention.

Associations of genetically predicted circulating levels of cytokines with telomere length: a Mendelian randomization study.

Telomere length (TL) has been regarded as a biomarker of aging, and TL shortening is associated with numerous chronic illnesses. The mounting evidence has shown that inflammatory cytokines are involved in maintaining or shortening TL, the causality of cytokines with TL remains unknown. Therefore, we performed a two-sample Mendelian randomization (MR) analysis to estimate the underlying correlations of circulating inflammatory cytokines with TL. Genetic instrumental variables for inflammatory cytokines were identified through a genome-wide association study (GWAS) involving 8,293 European individuals. Summary statistics of TL were derived from a UK Bio-bank cohort comprising 472,174 samples of individuals with European descent. We employed the inverse-variance weighted (IVW) approach as our main analysis, and to ensure the reliability of our findings, we also conducted additional analyses including the weighted median, MR-Egger, MR pleiotropy residual sum and outlier test, and weighted model. Lastly, the reverse MR analyses were performed to estimate the likelihood of inverse causality between TL and the cytokines identified in the forward MR analysis. Cochran's Q test were employed to quantify the degree of heterogeneity. After applying Bonferroni correction, a higher circulating level of Interleukin-7 (IL-7) was suggestively associated with TL maintaining (OR:1.01, 95%CI:1.00-1.02, P=0.032 by IVW method). The study also revealed suggestive evidence indicating the involvement of Interleukin-2 receptor, alpha subunit (IL-2Rα) level was negatively associated with TL maintaining (OR:0.98, 95%CI:0.96-1.00, P=0.045 by IVW method), and the weighted median approach was consistent (OR:0.99, 95%CI:0.97-1.00, P=0.035). According to the findings of reverse MR analysis, no significant causal relationship between TL and cytokines was explored. Our analysis did not reveal any substantial heterogeneity in the Single nucleotide polymorphisms or horizontal pleiotropy. Our MR analysis yielded suggestive evidence supporting the causality between circulating IL-7 and IL-2Rα and telomere length, necessitating further investigations to elucidate the mechanisms by which these inflammatory cytokines may impact the progression of telomeres.

The causality of physical activity status and intelligence: A bidirectional Mendelian randomization study.

Observational studies suggest physical activity (PA) enhances intelligence, while sedentary behavior (SB) poses a risk. However, causality remains unclear. We extracted genetic instruments from large genome-wide association studies summary data and employed an inverse-variance weighted (IVW) approach within a random-effects model as the primary method of Mendelian randomization (MR) analysis to estimate the overall effect of various physical activity statuses on intelligence. To assess IVW stability and MR sensitivity, we also utilized supplementary methods including weighted median, MR-Egger, and MR-PRESSO. Furthermore, multivariable MR analysis was conducted to examine the independent effects of each physical activity trait on intelligence. The MR primary results indicated that LST was negatively associated with intelligence (β = -0.133, 95%CI: -0.177 to -0.090, p = 1.34×10-9), while SBW (β = 0.261, 95% CI: 0.059 to 0.463, p = 0.011) may have a positive effect on intelligence; however, MVPA and SC did not show significant effects on intelligence. Inverse causality analyses demonstrated intelligence significantly influenced all physical activity states. Our study highlights a bidirectional causal relationship between physical activity states and intelligence.

PPIs and gastric cancer: any causal relationship?

Hydrochloric acid is crucial in gastric physiology. In 1978 cimetidine, the first H2 antagonist of histamine receptors on the gastric parietal cell was introduced into therapy, inducing acid. Lasting the years, several studies focused on the potential relationship between inducing hypo-achlorhydria and risk of developing gastric cancer. In 1988 omeprazole, the first proton pump inhibitor, entered therapy. In 1996, Kuipers underlined the danger of progression of chronic atrophic gastritis in subjects taking PPIs. In 2018, one paper from Korea and an another on from Sweden suggested a possible relationship between long-term PPI therapy and the development of gastric cancer. Over the years, several articles, meta-analyzes and population based focused on relationship between long-term of PPI use and the onset of gastric cancer, with conflicting results. As reported, the presence of bias in the collection of cases, in particular concerning the evaluation of the H.p. status and presence of atrophic gastritis and intestinal metaplasia in subjects treated with PPI, can lead to noticeable errors in the results and conclusions, as demonstrated in the literature by exhaustive methodological studies of pharmacoepidemiology. A possible bias in the collection of case histories is due to the fact that PPIs are often administered to dyspeptic patients, among which there are patients already carriers of gastric neoplasia: the so-called inverse causality. Literature data, amended by methodological bias (sampling errors, lack of comparative assessment of Hp status and atrophic gastritis) NOT support a causal relationship between long-term PPIs therapy and the onset of gastric cancer.

Interakcija financijskog razvitka, nejednakosti i rizika od siromaštva u Republici Hrvatskoj

This paper examines the financial development of the Republic of Croatia as measured by the dimensions of financialization, financial deepening and financial inclusion through interaction with two dimensions of social exclusion, such as income inequality and at-risk-of-poverty rates. The aim of the paper is to determine how financialization, financial deepening and inclusion affect income inequality and the risk of poverty. In terms of financialization, research has shown that the development of the overall financial sector relative to GDP reduces income inequality and at-risk-of-poverty rates, while the growth of banking sector assets relative to GDP increases income inequality and at-riskof-poverty. With financial deepening, the share of corporate loans in GDP has been shown to increase income inequality and the at-risk-of-poverty rate, while loans to households are not significant for inequality, but therefore reduce the at-risk-of-poverty rate. The share of household loans in GDP is not significant for income inequality, but it reduces the at-risk-of-poverty rate. The financial inclusion of households has shown that the three groups of loans (transaction account overdrafts, cash and other loans) depend on the level of inequality and that the opposite causality operates. While cash loans reduce the atrisk-of-poverty rate, the at-risk-of-poverty rate as an inverse causality affects transaction account overdrafts. Key words: financialization, financial deepening, financial inclusion, income inequality, at-risk-of-poverty rate, Croatia.

The Dollar and Gold: Which is the Safest Haven? COVID-19 Evidence

Abstract This paper examines the dynamic correlation between the US dollar and gold prices during the coronavirus pandemic to determine which of the two assets is a safer haven from an investor’s perspective. The research utilises methods of analysis and synthesis of theoretical knowledge from published articles, literature, and official statistics websites. Data covering the period from January 1, 2020 to May 26, 2021, were primarily collected from the latest versions of these websites. The study includes a quantitative analysis of variables, including the Johansen cointegration test, the Granger causality test, and the error correction model. Our empirical analysis reveals a long-term equilibrium relationship between the US dollar and gold price. There is a oneway inverse causality relationship between the dollar and gold price. The results indicate that gold can be considered the safest haven from the investors’ perspective.

An immunometabolic signature of athletes susceptible to respiratory tract illness? Comment on: Evidence of immunometabolic dysregulation and airway dysbiosis in athletes susceptible to respiratory illness.

An immunometabolic signature of athletes susceptible to respiratory tract illness? Comment on: Evidence of immunometabolic dysregulation and airway dysbiosis in athletes susceptible to respiratory illness.

Computation by inverse causality: A universal principle to produce symbols for the external reality in living systems

How can a living system escape the solipsistic self-making process? This problem has been ignored in mainstream biology. This study seeks a reasonable mechanism by which a living system produces symbols that signify external states. To this end, the inverse causality model proposed in previous studies was theoretically improved by refining the core concepts. Inverse causality is an epistemic principle operating in a subject system to produce symbols internally, signifying the past states of the external reality hidden to the subject. Inverse causality yields an important theorem for a system to produce symbols for external states. It asserts that if a system changes from state x to y1 in some instances, and from x to y2 in others (y1 ≠ y2), then x ⟼ y1 produces a symbol that signifies one external state, and x ⟼ y2 produces a different symbol for another state. These symbols are embodied as the states of the system components. The model postulates the equivalence principle in the subject-reality relationship, asserting that inverse causality is equivalent to causality in the external view. Living systems operate with inverse causality using biological devices called measurers, which include membrane receptors, second messengers, and molecular switches in cells, and neurons in multicellular organisms. A measurer is a medium of symbols signifying external states. Biological subsystems functioning as measurers are ubiquitous and essential in contemporary living systems for adaptation to their environments in particular ways by manipulating the symbols they produce. By the inverse causality operation, living systems can reduce the uncertainty of events and manage the probability distribution of future events favorable to survival and reproduction. Due to this function, their measurer systems were sophisticated and diversified in evolution. In philosophy and science, there has been endless debate between determinism and indeterminism. However, surprisingly, contemporary living systems use the inverse causality operation (ICW) to adapt to their environments, which is logically equivalent to the causal principle of determinism.

Determinants of Economic Growth in Nepal: A Johansen Cointegration Analysis

This research study investigates the determinants of Economic Growth in Nepal. GDP growth is the dependent variable and import, export, exchange rate, foreign exchange reserve, gross capital formation and broad money supply are the explanatory variables. Data since 1965 to 2020 are taken from secondary sources of World Bank to find the relationship between them. Augmented Dickey- Fuller Test is run to test stationary condition in the variables. Result of Johansen Cointegration Test supports the existence of cointegration in the model. The coefficient of VECM is negative and significant expresses the long run relationship and Granger Causality Test indicates the two way causality between LNFER and LNM2 with LNGDP and one way causality from LNIMP and LNEXR to LNGDP but inverse causality is seen from LNGDP to LNEXP. Results confirm the variables are the determinants of economic growth in Nepal. So policy makers should consider on these variables for economic growth of the country.

Guide and advances on childhood obesity determinants: Setting the research agenda.

Childhood obesity demands global solutions. Low birth weight and small for gestational age were associated with childhood obesity. Available data do not support prenatal exposure to antibiotics as risk factor for childhood obesity, and posology must be assessed. Prenatal exposure to persistent organic pollutants shows associations with childhood obesity. Gut microbiota composition influences obesity onset in childhood. Despite the unquestionable role of Mediterranean diet on healthy weight, there are only incomplete indications of metabolic benefits in childhood weight after following Mediterranean diet. Negative association between total dairy consumption and childhood obesity has been found, but inverse causality could not be discarded. Ultra-processed food intake is an adverse determinant of childhood obesity. Physical inactivity and sedentarism are critical risk factors of children adiposity; hence, built environment and environmental features will be determinants of childhood obesity. A consistent metabolic pattern of childhood obesity was observed; metabolomics research is needed to assess the role of specific molecules concerning childhood obesity. Epigenetic experiences support association with childhood obesity for DNA methylation of specific genes and miRNAs. Therefore, recent childhood obesity rates cannot only be explained by genetic predisposition and changes in lifestyle habits. It implies gene-environment interactions. It will be the next research.

Intellectual capital on performance: a meta-analysis study enhancing a new perspective of the components

PurposeThe authors examined intellectual capital (IC) components, namely human, structural and relational capital, on firm performance (FP) and innovation performance (IP), while also examining the role of knowledge management (KM) in this context.Design/methodology/approachThe authors employed a meta-analysis using 81 studies from 2006 to 2020 using bivariate analysis, meta-analytic structure equation modeling (MASEM) and fuzzy-set qualitative comparative analysis (fsQCA) to study IC components on FP and IP.FindingsThe MASEM results show that IC affects positively on FP, but not in a significant level and affects positively and significantly on IP. The findings also reveal that the moderation effect of KM affects positively on FP but not on IP. Additionally, the fsQCA analysis shows that KM and its multidimensional role has a positive impact on FP and IP and has a potential to be consistent as a dynamic component for IC.Research limitations/implicationsThe results may be limited by different statistical biases and inverse causality issues or associated with contextualities related to the studies of the sample selected by our criteria.Practical implicationsManagers can identify the appropriate IC elements and act accordingly. The study suggests that mobilizing human, structural, relational and knowledge capital must begin from the firms' birth and continue further during firms' stages of the business.Social implicationsIC is the bridge of evolution for future societies. Knowing how its components impact all levels of corporate environment indirectly influences how societies build up their social bases and policies to fulfill new professional generations.Originality/valueBy using the MASEM and fsQCA, the authors have more detailed insights into the multidimensional context of KM in IC components on firm and innovation performance identifying configurations of intangible resources.

Living Systems Escape Solipsism by Inverse Causality to Manage the Probability Distribution of Events

The external worlds do not objectively exist for living systems because these worlds are unknown from within systems. How can they escape solipsism to survive and reproduce as open systems? Living systems must construct their hypothetical models of external entities in the form of their internal structures to determine how to change states (i.e., sense and act) appropriately to achieve a favorable probability distribution of the events they experience. The model construction involves the generation of symbols referring to external entities. This paper attempts to provide a new view that living systems are an inverse-causality operator. Inverse causality (IC) is an algorithmic process that generates symbols referring to external reality states based on a given data sequence. For applying this logical model involving if–then entailments to living systems involving material interactions, the cognizers-system model was employed to represent the IC process; here, living systems were modeled as a subject of cognition and action. A focal subject system is described as a cognizer composed of sub-cognizers, such as a sensor, a signal transducer, and an effector. Analysis using this model proposes that living systems invented the “measurers” for conducting IC operations through their evolution.

Breast cancer risk in patients with polycystic ovary syndrome: a Mendelian randomization analysis.

The association between polycystic ovary syndrome (PCOS) and breast cancer remains inconclusive. Conventional observational studies are susceptible to inverse causality and potential confounders. With a Mendelian randomization (MR) approach, we aimed to investigate the causal relationship between genetically predicted PCOS and breast cancer risk. Our study included 11 PCOS-associated single nucleotide polymorphisms as instrumental variables identified by the latest genome-wide association study. Individual-level genetic summary data of participants were obtained from the Breast Cancer AssociationConsortium, with a total of 122,977 cases and 105,974 controls. The inverse-variance weighted method was applied to estimate the causality between genetically predicted PCOS and breast cancer risk. To further evaluate the pleiotropy, the weighted median and MR-Egger regression methods were implemented as well. Our study demonstrated that genetically predicted PCOS was causally associated with an increased risk of overall breast cancer (odds ratio (OR) = 1.07; 95% confidence interval (CI) 1.02-1.12, p = 0.005). The subgroup analyses according to immunohistochemical type further illustrated that genetically predicted PCOS was associated with an increased risk of estrogen receptor (ER)-positive breast cancer (OR = 1.09; 95% CI 1.03-1.15, p = 0.002), while no causality was observed for ER-negative breast cancer (OR = 1.02; 95% CI 0.96-1.09, p = 0.463). In addition, no pleiotropy was found in our study. Our findings indicated that PCOS was likely to be a causal factor in the development of ER-positive breast cancer, providing a better understanding for the etiology of breast cancer and the prevention of breast cancer.

237P Breast cancer risk in patients with polycystic ovary syndrome: A Mendelian randomization analysis

The association between polycystic ovary syndrome (PCOS) and breast cancer remains inconclusive. Conventional observational studies are susceptible to inverse causality and potential confounders. With a Mendelian randomization (MR) approach, we aimed to investigate the causal relationship between genetically predicted PCOS and breast cancer risk. Our study included 11 PCOS-associated single nucleotide polymorphisms as instrumental variables identified by the latest genome-wide association study. Individual-level genetic summary data of participants were obtained from the Breast Cancer Association Consortium, with a total of 122 977 cases and 105 974 controls. The Inverse-weighted method was applied to estimate the causality between genetically predicted PCOS and breast cancer risk. To further evaluate the pleiotropy, the weighted median and MR-Egger regression method were implemented as well. Our study demonstrated that genetically predicted PCOS was causally associated with an increased risk of overall breast cancer (odds ratio (OR) = 1.07; 95% confidence interval (CI) = 1.02-1.12, p = 0.005). The subgroup analyses according to immunohistochemical type further illustrated that genetically predicted PCOS was associated with an increased risk of estrogen receptor (ER)-positive breast cancer (OR = 1.09; 95% CI = 1.03-1.15, p = 0.002), while no causality was observed for ER-negative breast cancer (OR = 1.02; 95% CI = 0.96-1.09, p = 0.463). Additionally, no horizontal pleiotropy was found in our study.Table 237PMendelian randomization estimates of the causality between PCOS and breast cancer.OutcomeIVW methodMR-EggerWeighted median methodOR (95% CI)P-valueOR (95% CI)P-valueOR (95% CI)P-valueBreast cancer overall1.0667 (1.0200, 1.1155)0.00471.0450 (0.8351, 1.3077)0.70931.0742 (1.0226, 1.1283)0.0043ER-positive breast cancer1.0881 (1.0318, 1.1474)0.00181.0901 (0.8352, 1.4227)0.54141.0992 (1.0346, 1.1678)0.0022ER-negative breast cancer1.0242 (0.9609, 1.0917)0.46280.8817 (0.6507, 1.1947)0.43761.0063 (0.9275, 1.0919)0.8793 Open table in a new tab Our findings indicated that PCOS was likely to be a causal factor in the development of ER-positive breast cancer, providing a better understanding for the etiology of breast cancer and the prevention of breast cancer.

Wpływ czasu pracy na zdrowie – podejścia badawcze i studium przypadku Francji

In recent decades, many publications devoted to the relationship between working time and health have been written. Available sources characterise different methodological approaches and different research perspectives, and the conclusions presented have not been unequivocal yet. The literature refers to both direct research on the impact of working time on health and to descriptions of wider phenomena indirectly related to the issue. Most studies in this area face a potential bias of the sample and the problem of the inverse causality of the impact of working time on health. Due to the reform of the labour law in France that shortened working time while maintaining a constant income, the analysis of the impact of working time on health carried out on the example of this country has overcome the difficulties faced by previous publications in the area. It has been shown that the reduction in working time has positively contributed to the health of the French.

Prevalence and determinants of poor glycaemic control: a cross-sectional study among Moroccan type 2 diabetes patients.

BackgroundDiabetes remains poorly controlled in a high proportion of diabetes patients. This study examines the prevalence of poor glycaemic control and associated factors in type 2 diabetes patients in the Beni-Mellal Khenifra region in Morocco.MethodsA cross-sectional survey was conducted in 2017 among 1456 diabetes patients attending primary health centres. Demographic and clinical data were collected through face-to-face interviews using structured and pre-tested questionnaires. Anthropometric measurements, including body weight, height and waist circumference were taken using standardized techniques and calibrated equipment. Glycaemic control was assessed in terms of the glycated haemoglobin (HbA1c) level and poor glycaemic control was defined as HbA1c ≥7% and a level <7% reflects good glycaemic control.ResultsOf the total participants, 66.3% had poor glycaemic control. Bivariate analysis showed that sex (p=0.010), education level (p=0.013), body mass index (p=0.048), duration of diabetes (p<0.0001) and type of therapeutic regimen (p<0.0001) were significantly associated with HbA1c level. However, multiple logistic regression analyses revealed that only a longer duration of diabetes (OR 1.525 [95% confidence interval {CI} 1.183–1.967], p=0.001) and receiving insulin therapy alone (OR 1.589 [95% CI 1.157–2.183], p=0.004) or a combination of oral antidiabetics with insulin (OR 2.554 [95% CI 1.786–3.653], p<0.001) were significantly associated with inadequate glycaemic control.ConclusionsDespite the particularities of the region, the findings about glycaemic control and its cross-sectionally associated factors are in line with findings from other regions of Morocco. In this subgroup, the longer duration of diabetes and insulin treatment could constitute a cause leading to poor glycaemic control. However, inverse causality cannot be excluded.

Exploring the causal relationships and allocation puzzle between portfolio investments and real sector growth in Sub-Saharan Africa

This study explores the causal dynamics and allocation puzzles between real sector growth and portfolio investments (equity and private debt) in Sub Saharan (SSA). We use growth in manufacturing, industry, agriculture, and services to capture the real sector and employ the two-step dynamic systems GMM model to establish our empirical relationships over the period 1980–2017. We found no evidence in support of the puzzle at the overall level of the real sector and portfolio investments. However, at a decomposed level, we established a bi-directional relationship of a positive association between debt flows and growth in agriculture and services, with no evidence of an allocation puzzle. Though we found a bi-directional association between debt and industrial growth, the association was detrimental in both directions. Finally, the study established a two-way inverse causality between equity flows and manufacturing growth. The paper provides a strong foundation for an additional source of financing, especially for the growth of the service and agriculture sectors. The findings also indicate complementary reactions between real sector growth and portfolio investments in SSA.