Chapter 29 - The use of family history in public health practice: the epidemiologic view Tables
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Human Genome Epidemiology (2nd ed.): Building the evidence for using genetic information to improve health and prevent disease
“The findings and conclusions in this book are those of the author(s) and do not
necessarily represent the views of the funding agency.”
necessarily represent the views of the funding agency.”
These chapters were published with modifications by Oxford University Press (2010)
Rodolfo Valdez, Muin J. Khoury, and Paula W. Yoon
Table 29-1
Sample of studies reporting the effect of family history on a trait that precedes a condition or disease
| Condition | Precursor Trait | Definition of Family History | Effect Attributed to Family History |
|---|---|---|---|
| Alzheimer disease | Rate of glucose metabolism in the brain | Only mother or father diagnosed with the disease at age 65–80 years | Healthy adults (age: 48–80 years) with a maternal family history had a lower cerebral metabolic rate of glucose than comparable subjects with just paternal or no family history (7). |
| Cardiovascular disease | Endothelium-dependent vasodilation (EDV) | Both parents with type 2 diabetes | Normal adults (average age around 38 years) with a family history had a significantly lower EDV than comparable subjects with no family history (8). |
| Cardiovascular disease | Intimal-medial thickness of the common carotid artery (IMT CCA) | Diabetes family history score that includes only first-degree relatives older than the participant (parents, siblings) | IMT CCA was increased among adult (average age around 40 years) Mexican Americans without diabetes but with a higher burden of the disease among their older first-degree relatives (9). |
| Colorectal | Colorectal polyps | One or more first-degree relatives reported to have had cancer of the colon, rectum, or large bowel | The risk of colon cancer among subjects who reported at least one first-degree relative with colorectal polyps was approximately double the risk of those who did not (10). |
| Diabetes | Insulin action | Both parents with type 2 diabetes | Normoglycemic adults (average age around 30 years) with a family history had significantly reduced indicators of glucose disposal at baseline and developed diabetes, two decades later, at a rate 10–20 times the rate of comparable subjects with no family history (11). |
| Diabetes | Beta cell function and insulin sensitivity | First- or second-degree relative with diabetes, confirmed by treatment or by interview with other relatives if deceased | Healthy children (aged 12–15 years), mostly of Hispanic background, with a family history were more likely to have a lower insulin secretory capacity and a lower rate of glucose disposal than comparable children with no family history (12). |
| Diabetes | Impaired glucose tolerance (IGT) | Type 2 diabetes in at least one parent, a sibling, or a grandparent | About one in three overweight Hispanic children (average age: 11 years) with a family history has IGT. The association is independent of the severity of overweight (13). |
| Diabetes | Insulin sensitivity | Presence of known family members with type 2 diabetes in any of three generations (siblings, parents, or grandparents) | Healthy white children (average age around 12 years) with a family history showed lower insulin sensitivity and insulin clearance capability than comparable children with no family history (14). |
| Obesity, diabetes | Expression of adiponectin receptor genes and the concentration of adiponectin in plasma | At least two known first-degree relatives with diabetes | Healthy adult Mexican Americans (aged 30–40 years) with a family history showed a significantly lower gene expression and lower plasma concentrations of adiponectin than comparable subjects with no family history (15). |
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