I recently read an article asking whether we can truly “catch” a cold, and it prompted a deeper reflection on how we understand illness. The dominant narrative is still one of invasion, contagion and defence, yet anyone who has worked clinically for long enough knows that exposure alone does not determine outcome. Two people can sit side by side, breathe the same air, and only one becomes unwell. That discrepancy invites a more nuanced question, not simply about the microbe, but about the host response.

This is where genetics becomes clinically useful rather than abstract. One of the immune genes I frequently review in genetic reports is IFNG, the gene that encodes interferon gamma. Interferon gamma is a powerful immune signalling molecule. It plays an important role in coordinating the body’s response to viral triggers and other immune challenges. In a healthy, well regulated system, this response is proportionate and time limited. The immune system activates, deals with the threat, and then stands down.

However, some individuals carry genetic variants that predispose them to a stronger or more easily triggered interferon gamma response. In those cases, IFNG can become more readily upregulated. This does not mean the gene is “bad” or that the immune system is defective. It simply means that inflammatory signalling may be amplified or sustained for longer than necessary. When this happens, symptoms are often more intense, recovery may be slower, and the systemic effects of inflammation can extend beyond the respiratory tract.

Inflammation is not confined to the nose and throat. When interferon gamma rises, it influences whole body signalling. It can alter energy production, affect mood and cognition, and shift how the body processes key nutrients. Many people recognise that the early stages of a cold are accompanied by fatigue, low motivation or a sense of heaviness even before physical symptoms fully emerge. This is not weakness. It is inflammatory chemistry in action.

A heightened IFNG response can also influence metabolic pathways linked to tryptophan and neurotransmitter balance, contributing to the low mood or irritability that often accompanies inflammatory states. In someone whose inflammatory tone is already elevated because of chronic stress, environmental toxins, poor sleep, blood sugar instability or gut dysbiosis, an additional immune trigger may tip the system more dramatically. The visible illness may be the final straw rather than the original cause.

This is why the concept of terrain matters. The immune system does not operate in isolation. It is influenced by nutrient status, nervous system regulation, detoxification capacity and methylation efficiency. If these foundations are fragile, inflammatory genes such as IFNG are more likely to fire loudly and for longer.

From a practical perspective, I always return to fundamentals. Omega 3 fatty acids are essential for modulating inflammatory responses. They do not blunt immunity, but they help ensure that inflammatory signalling resolves appropriately. Adequate omega 3 status can soften excessive immune activation and support recovery.

Vitamin D plays an equally important role in immune regulation. It influences how immune cells differentiate and how cytokines are produced, including interferon related signalling. In the UK, suboptimal vitamin D levels are common, particularly during winter months, and this alone can skew immune responses towards dysregulation rather than balance.

Zinc is another cornerstone. It supports antiviral defence, maintains mucosal integrity in the respiratory tract, and helps regulate inflammatory output. Deficiency is not rare, particularly in individuals under chronic stress or with higher alcohol intake, and inadequate zinc can leave immune signalling less controlled.

Alongside these nutrients, methylation quietly shapes immune resilience. Efficient methylation supports detoxification, neurotransmitter synthesis and inflammatory resolution. If methylation pathways are compromised, whether genetically or nutritionally, inflammatory mediators can linger longer than they should. Supporting folate, B12, B6 and broader methylation capacity helps the immune system activate and then settle, rather than remain in a state of low grade reactivity.

So can you catch a cold. Yes, exposure matters, and viruses exist. But outcome is determined by far more than proximity. Your genetic wiring influences how intensely your immune system responds. Your nutrient status influences whether that response is proportionate. Your nervous system influences inflammatory tone. Your terrain determines whether a seasonal trigger becomes a minor inconvenience or a prolonged inflammatory episode.

Understanding IFNG within this broader context restores agency. It shifts the focus from fear of exposure to strengthening internal regulation. The aim is not to suppress immune responses, but to ensure they are intelligent, efficient and self limiting. When inflammatory genes are supported by adequate nutrition, balanced methylation and a regulated nervous system, recovery is smoother and resilience is greater.

Rather than asking only what we have caught, it may be more helpful and empowering to ask how well our immune system is calibrating. In that calibration lies the difference between panic and preparation, and between reactive inflammation and grounded resilience.

I make a wonderful immune boosting herbal blend packed full of delicious herbs btw!