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Understanding variation in disease risk: the elusive concept of frailty.

Aalen OO, Valberg M, Grotmol T, Tretli S - Int J Epidemiol (2014)

Bottom Line: Heterogeneity often manifests itself as clustering of cases in families more than would be expected by chance.We emphasize that apparently moderate familial relative risks can only be explained by strong underlying variation in disease risk between families and individuals.Finally, we highlight the potential impact of frailty variation in the interpretation of standard epidemiological measures such as hazard and incidence rates.

View Article: PubMed Central - PubMed

Affiliation: Oslo Centre for Biostatistics and Epidemiology, Department of Biostatistics, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway and Cancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway o.o.aalen@medisin.uio.no.

No MeSH data available.


Related in: MedlinePlus

Simple illustration of an Armitage-Doll multi-stage model of carcinogenesis. The states represent the stages of the carcinogenic process. State one is the healthy state, state two is an intermediate state, and in state three a malignant cell has developed. State four is a censored state. The s and s are transition rates.
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dyu192-F8: Simple illustration of an Armitage-Doll multi-stage model of carcinogenesis. The states represent the stages of the carcinogenic process. State one is the healthy state, state two is an intermediate state, and in state three a malignant cell has developed. State four is a censored state. The s and s are transition rates.

Mentions: It turns out that changes in epidemiological incidence rates over calendar time also can be wrongly interpreted if one does not take into consideration the possible heterogeneity between individuals. Consider the simple Armitage-Doll multistage model of carcinogenesis, which states that a cell has to go through a certain number of transitions to reach malignancy. As an example, consider the simple version of a multistage model as shown in Figure 8. Assume that the transition rates are not the same for all individuals, but that there is a strong variation in susceptibility. Consider for instance a population where only a small subgroup is susceptible to the cancer in question, and the majority has a zero rate of cancer initiation (transition from a normal cell to an intermediate cell). If the initiation rate increases abruptly at a given point in (calendar) time, the incidence rate may increase to a peak, then drop and stabilize on a higher level. This is illustrated in Figure 9a, for the simple multistage model in Figure 8, with only 1% of the population being susceptible. The same point, with 90% being susceptible, is illustrated in Figure 9b. Although a simplification, the abrupt increase in the initiation rate could be the result of a risk factor that becomes more pronounced in the population at a given time.Figure 8.


Understanding variation in disease risk: the elusive concept of frailty.

Aalen OO, Valberg M, Grotmol T, Tretli S - Int J Epidemiol (2014)

Simple illustration of an Armitage-Doll multi-stage model of carcinogenesis. The states represent the stages of the carcinogenic process. State one is the healthy state, state two is an intermediate state, and in state three a malignant cell has developed. State four is a censored state. The s and s are transition rates.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4588855&req=5

dyu192-F8: Simple illustration of an Armitage-Doll multi-stage model of carcinogenesis. The states represent the stages of the carcinogenic process. State one is the healthy state, state two is an intermediate state, and in state three a malignant cell has developed. State four is a censored state. The s and s are transition rates.
Mentions: It turns out that changes in epidemiological incidence rates over calendar time also can be wrongly interpreted if one does not take into consideration the possible heterogeneity between individuals. Consider the simple Armitage-Doll multistage model of carcinogenesis, which states that a cell has to go through a certain number of transitions to reach malignancy. As an example, consider the simple version of a multistage model as shown in Figure 8. Assume that the transition rates are not the same for all individuals, but that there is a strong variation in susceptibility. Consider for instance a population where only a small subgroup is susceptible to the cancer in question, and the majority has a zero rate of cancer initiation (transition from a normal cell to an intermediate cell). If the initiation rate increases abruptly at a given point in (calendar) time, the incidence rate may increase to a peak, then drop and stabilize on a higher level. This is illustrated in Figure 9a, for the simple multistage model in Figure 8, with only 1% of the population being susceptible. The same point, with 90% being susceptible, is illustrated in Figure 9b. Although a simplification, the abrupt increase in the initiation rate could be the result of a risk factor that becomes more pronounced in the population at a given time.Figure 8.

Bottom Line: Heterogeneity often manifests itself as clustering of cases in families more than would be expected by chance.We emphasize that apparently moderate familial relative risks can only be explained by strong underlying variation in disease risk between families and individuals.Finally, we highlight the potential impact of frailty variation in the interpretation of standard epidemiological measures such as hazard and incidence rates.

View Article: PubMed Central - PubMed

Affiliation: Oslo Centre for Biostatistics and Epidemiology, Department of Biostatistics, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway and Cancer Registry of Norway, Institute of Population-Based Cancer Research, Oslo, Norway o.o.aalen@medisin.uio.no.

No MeSH data available.


Related in: MedlinePlus