arXiv subjects

Samuel Iddi

Publications and source records attributed to Samuel Iddi.

6 recordsLinked to original sources

arXiv2026

Marginalised Poisson Hurdle Model for Cross-Sectional Count Data with Excess Zeros

Count data with excess zeros arise frequently in health economics and epidemiology. The standard Poisson Hurdle Model (PHM) parametrises the underlying Poisson rate directly, so its count-component coefficients are log-rate ratios rather than log-ratios of the marginal mean. Consequently, the incidence density ratio (IDR) from the PHM is neither exact nor constant across covariate profiles, complicating applied reporting. We propose the Marginalised Poisson Hurdle Model (MPHM), which reparametrises the count component so that the coefficient vector beta directly governs the marginal mean E[Y]. A nonlinear connector equation links the structural Poisson rate to this parametrised mean. We prove existence and uniqueness of the connector solution, develop a vectorised Brent's-method solver, derive the score equations and block-diagonal Fisher information, establish asymptotic normality, and prove that exp(beta) is exactly constant across all covariate values. A simulation study with n in {100, 250, 500, 1000}, zero proportion pi in {0.2, 0.4, 0.6, 0.8}, and R = 200 replications confirms consistency, near-zero bias, and 95% Wald coverage of 0.905-0.975 across all 16 scenarios. Applied to the NMES1988 physician visit data (n = 4,406), the MPHM yields IDR = 1.163 (95% CI: 1.150-1.177) per additional chronic condition - an exact, population-wide effect not derivable from the PHM. The MPHM resolves the non-constant IDR problem by directly parametrising E[Y]. The resulting IDR holds for every individual and the whole population without further marginalisation, substantially simplifying the reporting of covariate effects in health utilisation research.

stat.ME↗

arXiv2021

Modelling COVID-19 Transmission Dynamics in Ghana

In late 2019, a novel coronavirus, the SARS-CoV-2 outbreak was identified in Wuhan, China and later spread to every corner of the globe. Whilst the number of infection-induced deaths in Ghana, West Africa are minimal when compared with the rest of the world, the impact on the local health service is still significant. Compartmental models are a useful framework for investigating transmission of diseases in societies. To understand how the infection will spread and how to limit the outbreak. We have developed a modified SEIR compartmental model with nine compartments (CoVCom9) to describe the dynamics of SARS-CoV-2 transmission in Ghana. We have carried out a detailed mathematical analysis of the CoVCom9, including the derivation of the basic reproduction number, $\mathcal{R}_{0}$. In particular, we have shown that the disease-free equilibrium is globally asymptotically stable when $\mathcal{R}_{0}<1$ via a candidate Lyapunov function. Using the SARS-CoV-2 reported data for confirmed-positive cases and deaths from March 13 to August 10, 2020, we have parametrised the CoVCom9 model. The results of this fit show good agreement with data. We used Latin hypercube sampling-rank correlation coefficient (LHS-PRCC) to investigate the uncertainty and sensitivity of $\mathcal{R}_{0}$ since the results derived are significant in controlling the spread of SARS-CoV-2. We estimate that over this five month period, the basic reproduction number is given by $\mathcal{R}_{0} = 3.110$, with the 95\% confidence interval being $2.042 \leq \mathcal{R}_0 \leq 3.240$, and the mean value being $\mathcal{R}_{0}=2.623$. Of the 32 parameters in the model, we find that just six have a significant influence on $\mathcal{R}_{0}$, these include the rate of testing, where an increasing testing rate contributes to the reduction of $\mathcal{R}_{0}$.

q-bio.PE↗

arXiv2020

The Alzheimer's Disease Prediction Of Longitudinal Evolution (TADPOLE) Challenge: Results after 1 Year Follow-up

We present the findings of "The Alzheimer's Disease Prediction Of Longitudinal Evolution" (TADPOLE) Challenge, which compared the performance of 92 algorithms from 33 international teams at predicting the future trajectory of 219 individuals at risk of Alzheimer's disease. Challenge participants were required to make a prediction, for each month of a 5-year future time period, of three key outcomes: clinical diagnosis, Alzheimer's Disease Assessment Scale Cognitive Subdomain (ADAS-Cog13), and total volume of the ventricles. The methods used by challenge participants included multivariate linear regression, machine learning methods such as support vector machines and deep neural networks, as well as disease progression models. No single submission was best at predicting all three outcomes. For clinical diagnosis and ventricle volume prediction, the best algorithms strongly outperform simple baselines in predictive ability. However, for ADAS-Cog13 no single submitted prediction method was significantly better than random guesswork. Two ensemble methods based on taking the mean and median over all predictions, obtained top scores on almost all tasks. Better than average performance at diagnosis prediction was generally associated with the additional inclusion of features from cerebrospinal fluid (CSF) samples and diffusion tensor imaging (DTI). On the other hand, better performance at ventricle volume prediction was associated with inclusion of summary statistics, such as the slope or maxima/minima of biomarkers. TADPOLE's unique results suggest that current prediction algorithms provide sufficient accuracy to exploit biomarkers related to clinical diagnosis and ventricle volume, for cohort refinement in clinical trials for Alzheimer's disease. However, results call into question the usage of cognitive test scores for patient selection and as a primary endpoint in clinical trials.

q-bio.PE↗

arXiv2019

The relative efficiency of time-to-progression and continuous measures of cognition in pre-symptomatic Alzheimer's

Pre-symptomatic (or Preclinical) Alzheimer's Disease is defined by biomarker evidence of fibrillar amyloid beta pathology in the absence of clinical symptoms. Clinical trials in this early phase of disease are challenging due to the slow rate of disease progression as measured by periodic cognitive performance tests or by transition to a diagnosis of Mild Cognitive Impairment. In a multisite study, experts provide diagnoses by central chart review without the benefit of in-person assessment. We use a simulation study to demonstrate that models of repeated cognitive assessments detect treatment effects more efficiently compared to models of time-to-progression to an endpoint such as change in diagnosis. Multivariate continuous data are simulated from a Bayesian joint mixed effects model fit to data from the Alzheimer's Disease Neuroimaging Initiative. Simulated progression events are algorithmically derived from the continuous assessments using a random forest model fit to the same data. We find that power is approximately doubled with models of repeated continuous outcomes compared to the time-to-progression analysis. The simulations also demonstrate that a plausible informative missing data pattern can induce a bias which inflates treatment effects, yet 5% Type I error is maintained.

stat.AP↗

arXiv2018

Bayesian latent time joint mixed effect models for multicohort longitudinal data

Characterization of long-term disease dynamics, from disease-free to end-stage, is integral to understanding the course of neurodegenerative diseases such as Parkinson's and Alzheimer's; and ultimately, how best to intervene. Natural history studies typically recruit multiple cohorts at different stages of disease and follow them longitudinally for a relatively short period of time. We propose a latent time joint mixed effects model to characterize long-term disease dynamics using this short-term data. Markov chain Monte Carlo methods are proposed for estimation, model selection, and inference. We apply the model to detailed simulation studies and data from the Alzheimer's Disease Neuroimaging Initiative.

stat.AP↗

arXiv2015

Statistical model for overdispersed count outcome with many zeros: an approach for direct marginal inference

Marginalized models are in great demand by most researchers in the life sciences particularly in clinical trials, epidemiology, health-economics, surveys and many others since they allow generalization of inference to the entire population under study. For count data, standard procedures such as the Poisson regression and negative binomial model provide population average inference for model parameters. However, occurrence of excess zero counts and lack of independence in empirical data have necessitated their extension to accommodate these phenomena. These extensions, though useful, complicates interpretations of effects. For example, the zero-inflated Poisson model accounts for the presence of excess zeros but the parameter estimates do not have a direct marginal inferential ability as its base model, the Poisson model. Marginalizations due to the presence of excess zeros are underdeveloped though demand for such is interestingly high. The aim of this paper is to develop a marginalized model for zero-inflated univariate count outcome in the presence of overdispersion. Emphasis is placed on methodological development, efficient estimation of model parameters, implementation and application to two empirical studies. A simulation study is performed to assess the performance of the model. Results from the analysis of two case studies indicated that the refined procedure performs significantly better than models which do not simultaneously correct for overdispersion and presence of excess zero counts in terms of likelihood comparisons and AIC values. The simulation studies also supported these findings. In addition, the proposed technique yielded small biases and mean square errors for model parameters. To ensure that the proposed method enjoys widespread use, it is implemented using the SAS NLMIXED procedure with minimal coding efforts.

stat.ME↗