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Depression and Chronic Diseases in Old Age : = Understanding their Interplay for Better Health.

紀錄類型:	書目-語言資料,手稿 : Monograph/item
正題名/作者:	Depression and Chronic Diseases in Old Age :/
其他題名:	Understanding their Interplay for Better Health.
作者:	Triolo, Federico.
面頁冊數:	1 online resource (97 pages)
附註:	Source: Dissertations Abstracts International, Volume: 85-08, Section: A.
Contained By:	Dissertations Abstracts International85-08A.
標題:	Psychology. -
電子資源:	click for full text (PQDT)
ISBN:	9798381459807

Depression and Chronic Diseases in Old Age : = Understanding their Interplay for Better Health.
Triolo, Federico.

Depression and Chronic Diseases in Old Age :Understanding their Interplay for Better Health. - 1 online resource (97 pages)

Source: Dissertations Abstracts International, Volume: 85-08, Section: A.

Thesis (Ph.D.)--Karolinska Institutet (Sweden), 2023.

Includes bibliographical references

Late-life depression is intricately linked with somatic diseases. This thesis aimed to systematically explore this complex interplay. Specifically, we investigated: 1) the symptom-level interconnectedness between depression and somatic diseases, 2) the association of depression with somatic multimorbidity accumulation, 3) the role of somatic disease burden in depression development, and 4) the association of somatic burden with transitions across depressive states in older adults. Data were gathered from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), a populationbased study comprising 3,363 individuals aged 60+ years who underwent clinical assessments over a 15-year follow-up.Study I.Using a network approach, we aimed to describe the interconnectedness between depressive symptoms and somatic disease burden in older people. We found that sadness, pessimism, anxiety, and suicidal thoughts were central to the network, whereas somatic symptoms of depression appeared peripherally with fewer interconnections. When examining the association between depressive symptoms and measures of somatic disease burden, we found that suicidal thoughts, reduced appetite, and cognitive difficulties were bridge symptoms, linking late-life depression with somatic health.Study II.We investigated the impact of depression severity and phenotypes (i.e., affective, anxiety, cognitive, and psychomotor) on the progression of somatic multimorbidity over 15 years. Compared to those without depression, individuals with major (β*year: 0.33, 95%CI: 0.06-0.61) and subsyndromal depression (β*year: 0.21, 95%CI: 0.12-0.30) presented an accelerated accumulation of somatic multimorbidity. An increase in the cognitive phenotype burden (and not in the other three) was associated with faster accumulation of somatic diseases in old age (β*year: 0.07, 95%CI: 0.03-0.10).Study III.We aimed to examine the association between quantitative and qualitative measures of somatic disease burden and the incidence of depression in older adults. Each additional somatic disease was associated with an increased hazard of depression over a 15-year follow-up (HR 1.16, 95%CI: 1.08-1.24). Individuals presenting with disease patterns of sensory/anemia (HR 1.91, 95%CI: 1.03-3.53), thyroid/musculoskeletal (HR 1.90, 95%CI: 1.06-3.39), and cardiometabolic patterns (HR 2.77, 95%CI: 1.40-5.46) had higher depression hazards compared to those without multimorbidity. In the subsample of multimorbid participants, the cardiometabolic pattern remained associated with a higher depression risk (HR 1.71, 95%CI: 1.02-2.84) compared to the unspecific pattern.Study IV. We examined the course of old-age depression by investigating 15-year transitions along the depressive continuum and exploring time-varying factors associated with specific transition patterns. Over the follow-up, 19.1% had ≥1 transitions across depressive states (no depression, subsyndromal depression [SSD], depression), while 6.5% had ≥2 transitions. A higher number of somatic diseases was associated with progression from no depression to both SSD (HR 1.09, 95%CI: 1.07-1.10) and depression (HR 1.06, 95%CI: 1.04-1.08), and with lower recovery rates from SSD (HR 0.95, 95%CI: 0.93- 0.97) and depression (HR 0.96, 95%CI: 0.93-0.99). A richer social network was linked to lower transition rates to depressive states (HRNoDep-SSD 0.81, 95%CI: 0.70-0.94; HRNoDep-Dep 0.58, 95%CI: 0.46-0.73; HRSSD-Dep 0.66, 95%CI: 0.44-0.98), and higher recovery rates (HRSSD-NoDep 1.44, 95%CI: 1.26-1.66; HRDep-NoDep 1.51, 95%CI: 1.34-1.71). Being physically active was associated with higher recovery rates (HRSSD-NoDep 1.49, 95%CI: 1.28-1.73; HRDep-NoDep 1.20, 95%CI: 1.00-1.44).Conclusions.Our findings suggest that several dimensions of complexity characterize the interconnection of depression and somatic disease burden in old age. A symptomlevel characterisation of depression, along with a consideration of subsyndromal severity, may help clarify the comorbidity of depression and somatic diseases, as well as predict health decline in people with depressive symptoms. Similarly, recognizing disease patterns may help improve risk stratification for depression development in clinically complex older adults. Last, the natural course of depression in late life is dynamic and involves complex patterns of transitions through symptom severities, which can be influenced by the time-varying burden of somatic diseases. Developing person-centered care that integrates these complexities could enhance resilience and contribute to better health in old age.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024

Mode of access: World Wide Web

ISBN: 9798381459807Subjects--Topical Terms:

555998
Psychology.
Index Terms--Genre/Form:

554714
Electronic books.

Depression and Chronic Diseases in Old Age : = Understanding their Interplay for Better Health.
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520 $a Late-life depression is intricately linked with somatic diseases. This thesis aimed to systematically explore this complex interplay. Specifically, we investigated: 1) the symptom-level interconnectedness between depression and somatic diseases, 2) the association of depression with somatic multimorbidity accumulation, 3) the role of somatic disease burden in depression development, and 4) the association of somatic burden with transitions across depressive states in older adults. Data were gathered from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), a populationbased study comprising 3,363 individuals aged 60+ years who underwent clinical assessments over a 15-year follow-up.Study I.Using a network approach, we aimed to describe the interconnectedness between depressive symptoms and somatic disease burden in older people. We found that sadness, pessimism, anxiety, and suicidal thoughts were central to the network, whereas somatic symptoms of depression appeared peripherally with fewer interconnections. When examining the association between depressive symptoms and measures of somatic disease burden, we found that suicidal thoughts, reduced appetite, and cognitive difficulties were bridge symptoms, linking late-life depression with somatic health.Study II.We investigated the impact of depression severity and phenotypes (i.e., affective, anxiety, cognitive, and psychomotor) on the progression of somatic multimorbidity over 15 years. Compared to those without depression, individuals with major (β*year: 0.33, 95%CI: 0.06-0.61) and subsyndromal depression (β*year: 0.21, 95%CI: 0.12-0.30) presented an accelerated accumulation of somatic multimorbidity. An increase in the cognitive phenotype burden (and not in the other three) was associated with faster accumulation of somatic diseases in old age (β*year: 0.07, 95%CI: 0.03-0.10).Study III.We aimed to examine the association between quantitative and qualitative measures of somatic disease burden and the incidence of depression in older adults. Each additional somatic disease was associated with an increased hazard of depression over a 15-year follow-up (HR 1.16, 95%CI: 1.08-1.24). Individuals presenting with disease patterns of sensory/anemia (HR 1.91, 95%CI: 1.03-3.53), thyroid/musculoskeletal (HR 1.90, 95%CI: 1.06-3.39), and cardiometabolic patterns (HR 2.77, 95%CI: 1.40-5.46) had higher depression hazards compared to those without multimorbidity. In the subsample of multimorbid participants, the cardiometabolic pattern remained associated with a higher depression risk (HR 1.71, 95%CI: 1.02-2.84) compared to the unspecific pattern.Study IV. We examined the course of old-age depression by investigating 15-year transitions along the depressive continuum and exploring time-varying factors associated with specific transition patterns. Over the follow-up, 19.1% had ≥1 transitions across depressive states (no depression, subsyndromal depression [SSD], depression), while 6.5% had ≥2 transitions. A higher number of somatic diseases was associated with progression from no depression to both SSD (HR 1.09, 95%CI: 1.07-1.10) and depression (HR 1.06, 95%CI: 1.04-1.08), and with lower recovery rates from SSD (HR 0.95, 95%CI: 0.93- 0.97) and depression (HR 0.96, 95%CI: 0.93-0.99). A richer social network was linked to lower transition rates to depressive states (HRNoDep-SSD 0.81, 95%CI: 0.70-0.94; HRNoDep-Dep 0.58, 95%CI: 0.46-0.73; HRSSD-Dep 0.66, 95%CI: 0.44-0.98), and higher recovery rates (HRSSD-NoDep 1.44, 95%CI: 1.26-1.66; HRDep-NoDep 1.51, 95%CI: 1.34-1.71). Being physically active was associated with higher recovery rates (HRSSD-NoDep 1.49, 95%CI: 1.28-1.73; HRDep-NoDep 1.20, 95%CI: 1.00-1.44).Conclusions.Our findings suggest that several dimensions of complexity characterize the interconnection of depression and somatic disease burden in old age. A symptomlevel characterisation of depression, along with a consideration of subsyndromal severity, may help clarify the comorbidity of depression and somatic diseases, as well as predict health decline in people with depressive symptoms. Similarly, recognizing disease patterns may help improve risk stratification for depression development in clinically complex older adults. Last, the natural course of depression in late life is dynamic and involves complex patterns of transitions through symptom severities, which can be influenced by the time-varying burden of somatic diseases. Developing person-centered care that integrates these complexities could enhance resilience and contribute to better health in old age.
520 $a Sambandet mellan depression hos aldre och somatiska sjukdomar ar komplext. Syftet med denna avhandling var att systematiskt utforska det komplexa samspelet mellan dessa tva tillstand. Mer specifikt undersokte vi: 1) sambandet mellan depressiva symptom och somatiska sjukdomar, 2) sambandet mellan depression och ackumulering av somatisk multimorbiditet, 3) vilken roll somatisk sjukdomsborda spelar i utvecklingen av depression, och 4) sambandet mellan somatisk sjukdomsborda och overgangar mellan olika depressiva tillstand hos aldre vuxna. Data samlades in fran "the Swedish National study on Aging and Care in Kungsholmen" (SNAC-K). SNAC-K ar en populationsbaserad studie dar 3,363 personer som var 60 ar eller aldre genomgick kliniska bedomningar under en 15-arig uppfoljningsperiod.Studie I.Med hjalp av natverksanalys undersokte vi sambandet mellan depressiva symptom och somatisk sjukdomsborda hos aldre personer. Vi fann att sorg, pessimism, angest och sjalvmordstankar var centrala i det depressiva natverket. Somatiska symptom pa depression forekom mer perifert i natverket och med farre samband till de andra depressiva symptomen. Nar vi undersokte sambandet mellan depressiva symptom och somatisk sjukdomsborda identifierades sjalvmordstankar, nedsatt aptit och kognitiva svarigheter som symptom som kopplade samman depressiva tillstand med somatisk halsa.Studie II.Vi undersokte effekten av depressionens svarighetsgrad och fenotyper (dvs. affektiva, angest, kognitiva och psykomotoriska fenotyper) pa progressionen av somatisk multimorbiditet over 15 ar. Jamfort med de utan depression, uppvisade personer med egentlig (β*ar: 0.33, 95%CI: 0.06-0.61) och subsyndromal depression (β*ar: 0.21, 95%CI: 0.12-0.30) en accelererad utveckling av somatisk multimorbiditet. Gallande de depressiva fenotyperna var det endast den kognitiva fenotypen som var associerad med en snabbare ackumulering av somatiska sjukdomar hos aldre (β*ar: 0.07, 95%CI: 0.03-0.10).Studie III.Vi syftade till att undersoka sambandet mellan kvantitativa och kvalitativa matt pa somatisk sjukdomsborda och forekomsten av nya fall av depression hos aldre. For varje tillkommande somatisk sjukdom okade risken for depression under en 15-arig uppfoljningsperiod (HR 1.16, 95%CI: 1.08-1.24). Individer med sensoriska/anemiska (HR 1.91, 95%CI: 1.03-3.53), skoldkortel/muskuloskeletala (HR 1.90, 95%CI: 1.06-3.39), och kardiometabola sjukdomar (HR 2.77, 95%CI: 1.40-5.46) hade en hogre risk for depression jamfort med de utan dessa sjukdomar. Hos individer som lider av multimorbiditet var det kardiometabola monstret fortsatt kopplat till hogre risk for depression (HR 1.71, 95%CI: 1.02-2.84), jamfort med det ospecifika sjukdomsmonstret.Studie IV. Vi undersokte det dynamiska sjukdomsforloppet av depression genom att analysera olika overgangar av depressiva tillstand hos aldre over en 15-arig period. Vidare utforskade vi aven faktorer som var kopplade till specifika overgangsmonster over tid. Under uppfoljningsperioden hade 19.1% minst en overgang mellan depressiva tillstand (ingen depression, subsyndromal depression [SSD], depression), medan 6,5% hade minst tva overgangar. En hogre forekomst av somatiska sjukdomar var associerat med en hogre progression fran ingen depression till bade SSD (HR 1.09, 95%CI: 1.07-1.10) och depression (HR 1.06, 95%CI: 1.04-1.08), samt med lagre remission fran SSD (HR 0.95, 95%CI: 0.93- 0.97) och depression (HR 0.96, 95%CI: 0.93-0.99). Ett rikare socialt natverk var kopplat till en lagre risk for att utveckla depressiva tillstand samt svarare former av depression (HRNoDep-SSD 0.81, 95%CI: 0.70-0.94; HRNoDep-Dep 0.58, 95%CI: 0.46-0.73; HRSSD-Dep 0.66, 95%CI: 0.44-0.98). Det var aven kopplat till en hogre grad av remission (HRSSD-NoDep 1.44, 95%CI: 1.26-1.66; HRDep-NoDep 1.51, 95%CI: 1.34-1.71). Att vara fysiskt aktiv var associerat till en hogre sannolikhet att uppna remission (HRSSD-NoDep 1.49, 95%CI: 1.28-1.73; HRDep-NoDep1.20, 95%CI: 1.00-1.44).
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