Cancer and diabetes represent two of the most significant public health challenges worldwide. In 2022 alone, nearly 20 million new cases of cancer were diagnosed globally, and estimates suggest hundreds of millions of adults live with diabetes. Given this prevalence, it is common for people to wonder if these diseases are simply hereditary conditions passed down through generations. The true answer is complex, as the terms “hereditary” and “familial” carry distinct meanings in genetics that clarify the risk associated with these common illnesses.
Defining True Hereditary Disease vs. Familial Risk
A truly hereditary disease is one where a specific condition results from a single gene mutation passed directly from parent to child in a predictable pattern, known as Mendelian inheritance. These disorders, such as Huntington’s disease or cystic fibrosis, are rare but carry a high risk of inheritance.
In contrast, most common conditions like cancer and diabetes are considered multifactorial or polygenic diseases, meaning they arise from a complex interplay of multiple genes and environmental factors. The term “familial risk” describes the increased likelihood of contracting a disease due to a shared environment and a shared set of low-risk genes within a family unit.
The Contribution of Genetics to Cancer Development
The majority of cancer cases, approximately 75% to 90%, are classified as sporadic. These cancers develop from acquired, or somatic, genetic mutations that accumulate in a person’s cells during their lifetime. These mutations are not present in the reproductive cells, meaning they cannot be passed on to children. Environmental exposures, aging, and lifestyle choices are the primary drivers of these somatic mutations.
Only a small fraction, typically 5% to 10% of all cancers, are strictly hereditary. These cases are linked to a harmful mutation, called a germline mutation, that is inherited from a parent and is present in nearly every cell in the body from birth. Individuals with these germline mutations are born with an increased predisposition to develop certain cancers, often at a younger age.
Examples of hereditary cancer syndromes include mutations in the BRCA1 and BRCA2 genes, which increase the lifetime risk for breast and ovarian cancers. Similarly, mutations associated with Lynch syndrome increase the risk for colorectal and endometrial cancers. However, even inheriting a high-risk germline mutation does not guarantee that a person will develop cancer, as other genetic and non-genetic factors still play a role.
The Contribution of Genetics to Diabetes Development
Diabetes also shows a complex relationship with genetics, which differs significantly between its two most common forms, Type 1 and Type 2. Type 1 Diabetes (T1D) is an autoimmune disorder where the immune system mistakenly attacks insulin-producing beta cells in the pancreas. This form has a strong genetic predisposition linked primarily to variations in the human leukocyte antigen (HLA) genes, which are involved in immune system function.
Genetic factors account for about half of the heritability of T1D, with certain HLA patterns, such as HLA-DR3 and HLA-DR4-DQ8, carrying the highest risk, particularly in people of European descent. However, T1D is not a simple Mendelian disorder; it is polygenic, meaning multiple genes contribute a small effect, and it requires an environmental trigger for the disease to manifest. Even for an identical twin of someone with T1D, the risk of developing the condition is only 30% to 70%, highlighting the role of non-genetic factors.
Type 2 Diabetes (T2D) is the most common form, accounting for 90% to 95% of cases, and is profoundly polygenic and multifactorial. More than 60 genetic regions have been identified that each contribute a small increased risk of T2D. While T2D often appears to run in families, this clustering is often due to the shared environment and lifestyle, not a single inherited gene. The genetic risk for T2D sets a baseline susceptibility, but the onset of the disease is heavily dependent on lifestyle factors like diet, physical activity, and weight.
Why Lifestyle and Environment Are Critical Modifiers
The common clustering of both cancer and T2D within families is often a reflection of shared environmental and behavioral factors, not just inherited genes. Families typically share similar dietary habits, physical activity, and exposure to environmental carcinogens, all of which act as modifiers of genetic risk. This shared environment is a major component of the “familial risk” seen in these common diseases.
A high genetic predisposition to T2D, for example, can be lowered by maintaining a healthy lifestyle, including regular physical activity and a balanced diet. Conversely, an unhealthy lifestyle can increase the risk for individuals with a high genetic score.
The correlation between obesity, diabetes, and certain cancers (such as endometrial and liver cancer) demonstrates the influence of metabolic and environmental factors. Diabetes and obesity create a pro-cancerous microenvironment through mechanisms like chronic inflammation and insulin resistance, compounding the risk even without a high-risk inherited mutation. The realization of the disease is highly dependent on non-genetic factors that can be actively managed.