History repeats itself. This stands true for family medical history. Indeed, people are likely to encounter the same illness as their parents. The likelihood of sharing health problems is typically higher for first-degree relative, such as a parent, sibling or children. The likelihood of sharing health problems is lower for second-degree relatives, such as a grandparent, grandchildren, aunts, uncles, niece, nephews or cousins. The reason why relatives have similar life expectancy is because they have similar genetic makeup, environments and lifestyles.
Life Expectancy = Genes + Environment + Lifestyle
Genes are the blueprint of our physiology. They are inherited as a combination of our parents genes. The genes we share make us look alike but also more likely to share health problems. For example, close relatives share genes involved in the functioning of the vascular system and blood chemistry which predisposes them to similar cardiovascular disorders. But genes are not the only determinants of health. Environments and lifestyle choices also affect life expectancy.
Like genes, environments and lifestyles are passed down from generation to generation. That is, individuals inherit living environments, lifestyles, cultures and social circles from their parents1 and this inheritance has a significant impact on health. For example, an individual with parents who died from a cardiovascular disease (CVD) inherits the risk of dying from a CVD through genes but also through eating habits, region of residence, income, level of physical activity, tobacco use and alcohol use. Indeed, close relatives have similar dietary habits, physical activity levels, smoking or alcohol consumption patterns and stress levels. That is why they have similar risk of dying from CVD, cancer, respiratory diseases, suicide, homicide, etc. However, unlike genetic factors, environments and lifestyles can be altered by will power. Indeed, environments and lifestyles are external factors. They are not an inherent part of us like genes are. They are subject to change. As such, people may avoid their parents’ fate by changing their own environments and lifestyles.
Genetic Predisposition and Protection
Some genetic variations increase the risk of developing specific diseases. For example, the BRCA1 and BRCA2 gene mutations are associated with hereditary breast and ovarian cancer. Others genetic variations provide protection. For example, the apolipoprotein E (APOE) gene variant ε2 is associated with a lower risk of Alzheimer’s disease.
It is important to note that single-gene variants are rarely the only cause of a condition. That is, body functions rarely depend on a single gene. The human genome also often includes redundant copies of a given gene which confers protection against mutation.2 Moreover, the environment affects how genes are expressed. This is very important as genes’ expressions, not genes alone, define our physiology. Therefore, in most cases, it is wrong to think that carrying a given gene spells your doom.
Lifestyle-Related Predisposition and Protection
Some lifestyles increase the risk of developing specific diseases, regardless of genetic predisposition. For example, using tobacco increases the risk of developing lung cancer. Spending too much time on the sofa increases the risk of developing CVDs. Eating processed food increases the chance of developing inflammatory bowel disease.3 There are many more examples of lifestyles which can negatively affect health. On the other hand, some lifestyles offer protection. For example, engaging in regular physical activity offers a protection against almost all causes of death.
Everything is Connected
It is important to recognize that everything is connected and genetic factors interact with environmental factors and vice-versa. Specifically, environmental exposure influences the expression of certain genes and the expression of certain genes affects how the body deals with the environment. For example, exposure to toxins affects how genes involved in metabolic detoxification pathways are activated and genetic variations in those genes affects the nature of the proteins these genes code for and their efficiency in breaking down and eliminating toxins.
Conditions with Significant Genetic Risk
Conditions for which family history represent a significant risk include cancer, suicide, cardiovascular diseases, Alzeimer’s disease and Chronic lower respiratory diseases. Specifically, compared to individuals that do not have a close relative with a given condition:
- Individuals with a close relative with cancer are 171% more likely to die from cancer4
- Individuals with a close relative that died from suicide are 158% more likely to die from suicide5
- Individuals with a close relative with CVD are 145% more likely to die from CVD6
- Individuals with a close relative with Alzheimer’s disease are 73% more likely to die from Alzheimer’s disease7
- Individuals with a close relative with chronic lower respiratory diseases are 57% more likely to die from Chronic lower respiratory diseases8
We are all dealt a hand of genes and environment that we must work with. The way we play our hand through lifestyle choices ultimately determines how long we play. Although we are at risk of encountering the same fate as our parents, it is not guaranteed. Familial inheritance involves a complex interplay of genetic, environmental and lifestyle factors. Moreover, predicting life expectancy is complex and needs to take many factors into consideration. Youlldie allows to visualize how family medical history interacts with other factors like gender, race, world region, income, education, alcohol, tobacco, physical activity, sleep, blood pressure and body mass index to statistically predict life expectancy.
- Alexander, Karl, et al. Long Shadow, The: Family Background, Disadvantaged Urban Youth, and the Transition to Adulthood. Russell Sage Foundation, 2014. JSTOR, http://www.jstor.org/stable/10.7758/9781610448239. Accessed 9 Aug. 2023.
- Krakauer DC, Plotkin JB. Redundancy, antiredundancy, and the robustness of genomes. Proc Natl Acad Sci U S A. 2002 Feb 5;99(3):1405-9. doi: 10.1073/pnas.032668599. Epub 2002 Jan 29. PMID: 11818563; PMCID: PMC122203. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC122203/
- Narula N, Wong E C L, Dehghan M, Mente A, Rangarajan S, Lanas F et al. Association of ultra-processed food intake with risk of inflammatory bowel disease: prospective cohort study BMJ 2021; 374 :n1554 doi:10.1136/bmj.n1554. https://www.bmj.com/content/374/bmj.n1554
- F. Turati et al. Family history of cancer and the risk of cancer: a network of case–control studies. Annals of Oncology 24: 2651–2656, 2013. doi:10.1093/annonc/mdt280. https://www.annalsofoncology.org/article/S0923-7534(19)37098-X/
- Qin P, Agerbo E, Mortensen PB. Suicide risk in relation to family history of completed suicide and psychiatric disorders: a nested case-control study based on longitudinal registers. Lancet. 2002 Oct 12;360(9340):1126-30. doi: 10.1016/S0140-6736(02)11197-4. PMID: 12387960. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(02)11197-4/fulltext
- Lloyd-Jones DM, Nam BH, D’Agostino RB Sr, Levy D, Murabito JM, Wang TJ, Wilson PW, O’Donnell CJ. Parental cardiovascular disease as a risk factor for cardiovascular disease in middle-aged adults: a prospective study of parents and offspring. JAMA. 2004 May 12;291(18):2204-11. doi: 10.1001/jama.291.18.2204. PMID: 15138242. https://jamanetwork.com/journals/jama/fullarticle/198726
- Cannon-Albright LA, Foster NL, Schliep K, Farnham JM, Teerlink CC, Kaddas H, Tschanz J, Corcoran C, Kauwe JSK. Relative risk for Alzheimer disease based on complete family history. Neurology. 2019 Apr 9;92(15):e1745-e1753. doi: 10.1212/WNL.0000000000007231. Epub 2019 Mar 13. PMID: 30867271; PMCID: PMC6511086. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6511086/
- Li LS, Paquet C, Johnston K, Williams MT. “What are my chances of developing COPD if one of my parents has the disease?” A systematic review and meta-analysis of prevalence of co-occurrence of COPD diagnosis in parents and offspring. Int J Chron Obstruct Pulmon Dis. 2017 Jan 24;12:403-415. doi: 10.2147/COPD.S123933. PMID: 28182144; PMCID: PMC5279828. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5279828/