Individual susceptibility explains why people react differently to the same stimulus, whether it is a pathogen, medication, or environmental toxin. It is the reason one person might develop a serious illness after exposure to a virus while another shows no symptoms. A simple analogy is how two people’s skin reacts to sunlight; one might tan while the other suffers a painful sunburn, which is a direct result of their individual susceptibility.
Genetic Basis of Susceptibility
An individual’s genetic blueprint is a significant determinant of their susceptibility. The human genome contains small variations in the DNA sequence known as polymorphisms. While many have no discernible effect, some can alter the function of the proteins they code for, influencing how the body operates and responds to external factors.
For instance, variations in genes that code for metabolic enzymes can change how quickly a person processes a drug or a toxin, making a medication effective for one individual but toxic for another. Similarly, polymorphisms in genes related to the immune system can affect how the body recognizes and responds to pathogens, making some people more prone to certain infections.
A documented example involves the BRCA1 and BRCA2 genes, where specific inherited mutations are associated with a much higher risk of developing breast and ovarian cancers. Another instance is the apolipoprotein E (APOE) gene, where particular variants are linked to an increased likelihood of developing late-onset Alzheimer’s disease. These examples highlight how differences in DNA can translate into significant variations in health outcomes.
These genetic markers do not guarantee the development of a disease but indicate a predisposition. The presence of a high-risk gene variant means an individual has an increased statistical chance of developing a condition compared to someone without the variant. This inherited risk is a foundational component of an individual’s susceptibility profile.
Influence of Age and Sex
Susceptibility is not a fixed trait and evolves throughout a person’s lifespan. Infants and young children have developing immune systems that have not yet built a memory of many common pathogens, leaving them more vulnerable to new infections. Their immune responses are not as robust or refined as those of a healthy adult.
The elderly experience a natural decline in immune function, a process known as immunosenescence. This aging of the immune system leads to a reduced ability to fight off new infections and a weaker response to vaccinations. As a result, older adults are often more susceptible to severe outcomes from illnesses like influenza and pneumonia.
Biological sex also plays a part in determining susceptibility, rooted in chromosomes and distinct hormonal environments. Hormones like estrogen and testosterone can influence the activity and regulation of immune cells. This hormonal influence is thought to contribute to observed disparities in disease prevalence between sexes.
For example, females have a higher incidence of autoimmune diseases, such as rheumatoid arthritis and lupus, where the immune system mistakenly attacks the body’s own tissues. The female immune system is generally more robust in responding to infections, which may also make it more prone to dysregulation. Conversely, males can be more vulnerable to certain viral infections.
Acquired and Environmental Factors
A person’s health history and environment are major contributors to their current susceptibility. These factors can be broken down into several categories.
Acquired Immunity and Pre-existing Conditions
Previous encounters with pathogens can lead to acquired immunity, where the immune system “remembers” an invader and can mount a rapid defense upon re-exposure. This is the principle behind vaccination. Conversely, chronic conditions like diabetes or heart disease can weaken the body’s defenses, increasing vulnerability to new infections.
Lifestyle Choices
Lifestyle choices continuously modify an individual’s resilience. A balanced diet provides the necessary nutrients for immune cells to function properly, while physical activity can enhance immune surveillance. Habits such as smoking can damage the respiratory tract’s protective linings, and excessive alcohol consumption can impair the function of immune cells, increasing the risk of illness.
Environmental Exposures
Chronic exposure to environmental pollutants, such as fine particulate matter in the air, can provoke inflammation and weaken the body’s ability to handle respiratory pathogens. Occupational exposures to certain chemicals or toxins can also have long-term consequences for health, predisposing individuals to specific diseases.
The Microbiome
A growing area of research is the role of the microbiome—the community of microbes living in and on our bodies. These microbes interact with our immune system and metabolism. A healthy gut microbiome can help regulate immune responses and protect against harmful bacteria, while an imbalanced microbiome may contribute to increased susceptibility to inflammatory conditions and infections.
Gene-Environment Interactions
The influences of genetics and environment do not operate in isolation; they often interact in complex ways. This concept, known as gene-environment interaction, describes situations where the effect of an environmental factor on health differs depending on a person’s genetic makeup. This synergy between “nature” and “nurture” can alter an individual’s risk profile for a disease.
A classic illustration is phenylketonuria (PKU), a rare genetic disorder. Individuals with PKU inherit a faulty gene that prevents them from properly metabolizing an amino acid called phenylalanine. If left untreated through a specific diet, phenylalanine builds up to toxic levels, causing severe intellectual disability. The genetic variant only causes disease when combined with the specific environmental exposure.
This interaction is also evident in more common conditions. For example, certain genetic variations can increase a person’s risk of developing lung cancer. While these genes confer some increased risk on their own, their effect is amplified when combined with the environmental exposure of smoking. An individual with the genetic predisposition who also smokes faces a much greater risk than would be expected from either factor alone.