研究背景 憂鬱症狀會出現在情緒、生理、行為、認知等層面，影響了個體在各層面的表現。而近期國內的調查顯示，大專院校學生有達輕度憂鬱以上的比率已超過了50%。因此對於大學生憂鬱症狀的研究是具有非常重要的意義。根據過去文獻，家庭功能與憂鬱症狀有關，可能是造成個體容易憂鬱的傾向或是使目前憂鬱症更惡化，但其機制未明。近期研究發現，五大性格理論中的神經質、外向性、親和性、和嚴謹性與憂鬱症狀有關，而也有研究支持此些性格與家庭功能有關。因此，本研究根據文獻回顧，假設家庭功能會影響個體的性格差異，造成神經質、外向性、親和性、與嚴謹性的改變，此些性格的改變又進一步地導致憂鬱症狀的變化
研究目的 本研究試圖驗證性格為家庭功能與憂鬱症狀間關係的中介角色的模型。
研究方法 本研究採縱貫式設計。參與者：樣本為從南區大專院校中採分層與叢集抽樣而得的大學生。研究工具：以柯氏憂鬱量表、家庭功能量表簡版、五大因素量表中文化簡版，以團體施測的方式分別測量大學生的憂鬱症狀、五大性格以及家庭功能。研究程序：在2003年與2004年時皆對同一群大學生進行研究說明、同意書填寫與問卷填答。統計分析：利用結構方程模型分析，驗證性格中介家庭功能對憂鬱症狀關係的模型。
結果與討論 2003年的問卷回收率為72.86%，而隔年的追蹤率為47.20%。最後有效樣本人數為1,208人。在根據對假設模型分析後的結果以及文獻中所提出的理論，將假設模型做一修改，剔除外向性為整體家庭功能與憂鬱症狀的中介因子。修改後的性格中介家庭功能與憂鬱症狀間關係的模型，符合大多數基本適配、整體適配、精簡適配、增值適配的標準。內在適配度雖在多項指標上呈現需要修改，但多與理論或測量時間關係不符，故本修改模式有可接受的內在品質。修改後結構方程模式分析結果，不支持神經質、親和性、與嚴謹性中介整體家庭功能對憂鬱症狀的影響，但個體的不良好家庭功能以及神經質各自獨立地可以預測隔年的憂鬱症狀。在新模式中，第二年憂鬱的變異可被解釋的部份佔了35%。研究限制：(1)問卷回收率與追蹤率過低，造成樣本代表性的問題。但比較年齡、性別、第一階段的各量表分數後發現，分析樣本與未追蹤或被排除的樣本之間無需要重視的差異存在；(2)因家庭功能與性格皆在同一個階段被測量，因此無法排除受試者在兩份量表上的反應可能有關；(3)缺乏客觀資料，如第三者評量、臨床診斷等；(4)對憂鬱症狀的預測，可能未包含其他可能變項。
結論與建議 結論：本研究利用縱貫式大樣本資料，驗證了性格非為家庭功能對憂鬱症狀的關係的中介因子模型，即整體家庭功能對日後憂鬱症狀的影響非透過神經質、親和性、與嚴謹性的改變來產生作用，而是屬於直接效果。建議：未來研究可以嘗試釐清家庭功能與性格間的因果關係，並加入觀察者評量或臨床診斷以增加觀察資料的客觀性。在臨床應用上，可對家庭功能與性格的衡鑑，來篩選出潛在的憂鬱症狀危險族群，以達到預防效果。並且可利用性格改變技巧以及家族治療方式，以改善其性格與家庭功能，減少其對憂鬱症狀的惡化效果，以達到治療效果。

Background
Depressive symptoms manifested in emotional, physiological, behavioral, and cognitive facets, influenced individuals’ various abilities. Recent domestic surveys showed that the rate of minor to severe depression in the college student population was over 50%, emphasizing the importance to study college students’ depressive symptoms. According to past researches, an association was found between family functioning and depressive symptoms; a dysfunctional family might cause an individual to become depress or worsen concurrent depression. However, little was known about the underlying mechanisms between the variables. Recent researches found relationships between depressive symptoms and Neuroticism, Extraversion, Agreeableness, and Conscientiousness in the Five-Factor Model and there personalities were relevant to family functioning. Therefore, the present study made the assumption that family functioning influenced individual personality changes, which further caused the development of depressive symptoms.
Objective
The present study intended to prove the mediation role of personality in the relationship between family functioning and depressive symptoms.
Methods
A longitudinal design was taken. Participants: The sample was recruited by a stratified and cluster sampling from Southern Taiwan university students. Inventories: Ko’s Depression Inventory, Shortened Family Function Inventory, and Shortened Chinese Version of Five-Factor Inventory were administered. Procedures: In 2003 and 2004, research statements and informed consents were given to the same participants, followed by inventory-administering. Statistical Analyses: Structural Equation Model Analysis was used to examine the mediation model.
Results and Discussion
Retrieval rate of inventories was 72.86% in 2003 and follow-up rate was 47.20% during the following year. The final valid sample totalled 1,208. The hypothesis model was modified according to preliminary results and past researches; Extraversion was removed as a mediator. The modification model met most standards of fit indexes. The analysis results of the modification model did not support the mediation roles of Neuroticism, Agreeableness, and Conscientiousness between family functioning and depressive symptoms. Instead, after controlling for concurrent depressive symptoms, family dysfunctions and Neuroticism independently predicted the depressive symptoms in the next year. Thirty five percent of the variance in depressive symptoms during the second year could be explained by those study variables. Limitation 1) The low retrieval rate and follow-up rate raised the concern of representability. However, no notable differences were found between the valid sample and those who were excluded or not followed. 2) The family functioning and personality were assessed in the concurrent phase so the causality could not be established. 3) There was no objective information, e.g. observer reports or clinical diagnoses. 4) Other relevant variables to depressive symptoms were not incorporated.
Conclusion and Suggestion
Conclusion: In the present study, the longitudinal data supported that personality did not mediate the relationship between family functioning and depressive symptoms, and instead, family dysfunction and Neuroticism independently and directly increased individuals’ future depressive symptoms. Suggestion: Future researches can explore the direction of causality between family functioning and personality or take objective information into account. In clinical application, we can locate potential risk groups of depressive symptoms by assessing family functioning and personality and introducing them to prevention programs. Treatment can be done via improving personality and family functioning.

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