“Reaction to food” is not one thing. It is an umbrella term covering four fundamentally different mechanisms that produce overlapping symptoms but require different responses. Conflating them does not just lead to wrong conclusions — in some cases it leads to management strategies that actively make things worse. This is the first post in a series of three about allergies and intolerance.
Allergies and food intolerance are common topics among dog owners, but they are complex topics that are often discussed in simplified terms. I recently explored these topics out of curiosity, and thought that it is worth sharing what I learned in case it helps someone else – I certainly wish I’d known this stuff years ago!
Some of you will remember reading about Grace’s early history of food ambivalence on this blog (2021, 2022). For the first years of her life she was selective, inconsistent, and often indifferent to food in a way that made training and daily life genuinely complicated. In late 2022, I accidentally changed her diet while hosting another dog, removing chicken, beef and lamb and switching her to rabbit, boar, deer, duck and fish. Within weeks she was a completely different dog: waiting at the kitchen door before meals, working persistently for treats, finishing Kongs with gusto. I did not conclude she had a specific allergy to anything. I just observed that something had changed, and that it mattered.
That observation eventually led me to read more carefully about how food reactions in dogs actually work, and what I found was useful enough that I wanted to share it. I am not an authority on this topic. This is simply what I learned, in case it helps you think more clearly about your own dog.
The most important thing I learned is also the simplest: “reaction to food” is not one thing. It is an umbrella term covering at least four fundamentally different mechanisms, which produce overlapping symptoms but require different responses. Conflating them does not just lead to wrong conclusions — in some cases it leads to management strategies that actively make things worse.
The four mechanisms
1. True food allergy (immune-mediated reaction)
A true food allergy is an adaptive immune response against a specific protein fragment. What happens biologically is this: a protein is ingested, broken into fragments during digestion, and certain fragments are presented to immune cells. The immune system classifies them as a threat, produces IgE antibodies specific to that protein, and on every subsequent exposure, those antibodies trigger mast cells to release histamine and inflammatory mediators. This is sensitisation with immune memory, and it persists.
The key characteristics that distinguish true allergy from other mechanisms are:
- Protein-specific: the dog is reacting to a particular molecular structure, not to “chicken” as a category and not to kibble as a format
- Not dose-dependent: a small amount can trigger the same response as a large amount
- Reproducible: the same protein triggers the same response consistently
- Often non-seasonal: unlike environmental allergens, food proteins are present year-round
True food allergy is less common than most people assume, and it requires an elimination trial followed by a controlled re-challenge to confirm. Without that confirmation, the diagnosis is incomplete. More on that in Part 3.
2. Food intolerance (non-immune reaction)
Food intolerance does not involve the immune system at all. There is no sensitisation, no IgE, no immune memory. What it involves instead is a physiological difficulty processing or tolerating something, and the mechanisms include high fat load causing diarrhoea, poor digestibility of certain protein fractions causing gas or soft stool, too-rapid diet transitions causing temporary instability, or individual variation in digestive capacity.
The key characteristics that distinguish intolerance from true allergy are:
- Dose-dependent: larger amounts cause more pronounced symptoms
- Often inconsistent across brands and formulations: because the composition differs even when the named protein is the same
- Does not create immune memory: which means it does not escalate in the same way
This matters for management because intolerance does not require permanent elimination of a protein. It requires adjusting formulation, quantity, fat level, and transition speed. Treating intolerance as allergy and permanently eliminating proteins is an unnecessary restriction that often sends people down a path of progressive avoidance without resolution.
3. Inflammatory amplification
This is the mechanism most often overlooked, and probably the most frequently misread as a chicken allergy.
The key concept here is that the food does not need to be the antigen. Instead, the overall composition of the diet shifts the body’s baseline inflammatory tone, which makes existing sensitivities louder. Think of it as a volume knob: if background inflammatory noise is high, minor irritants become more disruptive, environmental allergens trigger stronger reactions, and the threshold for itching decreases.
What raises the volume knob? The main contributors are:
- A high ratio of omega-6 to omega-3 fatty acids, which shifts the body toward producing more pro-inflammatory mediators
- Oxidised fats, from poor storage or processing, which activate inflammatory signalling pathways
- Excess body weight, because adipose tissue produces inflammatory cytokines
- Chronic low-grade gut irritation
The result tends to look like food sensitivity but without the protein-specific reproducibility that true allergy produces. Symptoms often fluctuate with season, stress, or other environmental changes, and a dog may appear to react to a food without that reaction being reliably reproduced when the same protein is given in a simple, clean form.
This mechanism is why improving fat quality and omega-3 balance often helps dogs that appear to have food sensitivities, even when no single allergen is ever identified.
4. Gut barrier and microbiome instability
The gut is a significant immune organ, and so is the skin. When barrier integrity is compromised — by stress, infection, yeast overgrowth, antibiotics, sudden diet changes, or chronic inflammation — more antigen reaches immune tissue than would normally occur, which increases the probability of sensitisation. A disrupted microbiome compounds this by reducing the regulatory signals that normally support immune tolerance.
The pattern this produces is distinctive: symptoms that fluctuate without clear cause, what looks like sensitivity to multiple proteins at the same time, and symptoms that appear or worsen after a destabilising event such as a house move, a course of antibiotics, or a yeast flare.
The critical management implication is that stability helps more than novelty in this situation. Introducing multiple new proteins while the barrier is compromised increases antigen exposure during a period of higher sensitisation risk. This is precisely why repeated rapid protein switching — sometimes called protein roulette — can make things worse rather than better. The immune system is in a heightened state, and every new protein it encounters in that context is encountered in a danger context.
Why the distinction matters for management
The reason it is worth being precise about mechanism is that the correct response to each one is different, and in some cases opposite.
| Mechanism | What helps | What doesn’t help |
| True food allergy | Strict elimination trial, controlled re-challenge | Random supplementation, rotating proteins, ignoring trial rigour |
| Food intolerance | Slow transitions, adjusted fat/quantity, better digestibility | Declaring permanent allergy, restricting protein diversity |
| Inflammatory amplification | Omega-3 support, fat quality, lean body condition, environmental allergen management | Eliminating proteins unnecessarily, repeated brand switching |
| Barrier/microbiome instability | Stable diet, treating yeast/bacterial overgrowth, reducing stressors | Rapid protein rotation, multiple simultaneous diet changes |
The pattern that tends to produce the worst outcomes is treating every food reaction as true allergy, eliminating proteins one by one without confirmation, and introducing new proteins during periods of instability. Each of these steps is individually plausible as a response to symptoms, but the combination can turn a manageable situation into one where the dog appears to react to everything.
The threshold model: why it is never just one thing
The most useful single framework for understanding food-related symptoms is the threshold model, because it explains why the same dog can tolerate something for months and then suddenly not, why one sibling reacts and another doesn’t, and why symptoms can appear after a move or a vet visit with no obvious dietary change.
The model works like this:
Allergy risk ≈ Genetic predisposition × Barrier integrity × Inflammatory baseline × Allergen exposure
The reason this is multiplication rather than addition matters. If any one factor is very low, the total stays low even if other factors are elevated. But when multiple factors rise simultaneously, the combined effect can cross a threshold and produce symptoms, even though no single factor would have been sufficient on its own.
This is why the question “which ingredient caused this?” is often the wrong question. A more useful question is: “what shifted the threshold?” That framing opens up a much wider set of potential answers and a much wider set of interventions, most of which do not involve eliminating a protein.
Things that lower the threshold (reduce total risk):
- Strong gut and skin barrier
- Balanced omega-6 to omega-3 ratio
- Lean body condition
- Varied microbial exposure
- Stable, predictable diet changes
- Managed indoor allergen load when relevant
None of these prevents allergy in a dog that is highly genetically predisposed. What they do is reduce the probability of crossing the threshold, and that probability is often more modifiable than people realise.
In Part 2, I’ll look at what all of this means for commercial food specifically: what is and isn’t declared on labels, what mass-farming versus other production methods actually change (and what they don’t), and why “chicken kibble” is not a clean single-protein exposure.
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