Since COVID, obesity rates have risen sharply in the United Kingdom. What caught my attention was not that obesity is increasing — we already knew that. It was where the increase appears strongest.
The rise is most striking in younger adults. People in their 20s and 30s are showing a rapid jump in new obesity diagnoses compared with before the pandemic. The usual explanations are predictable. People ate worse during lockdown. They moved less. They were stressed. Food became more expensive, and cheaper food is often more processed. Working from home changed routines.
I do not dismiss any of that. It would be foolish to pretend food quality, stress, sleep, movement, and cost of living do not matter.
But I do not think it is enough.
I say that because I have spent months looking at post-pandemic health trajectories across many categories of disease. In isolation, obesity is easy to explain away as lifestyle. But when I place it beside the other changes I have been studying — cardiovascular inflammation, metabolic disturbance, neurological symptoms, gut dysfunction, fatigue, vascular instability — a different pattern emerges.
This looks less like a lifestyle shift and more like a phenotype.
Why I Think the Lifestyle Explanation Is Too Small
Obesity is usually discussed as though it is simply a problem of excess calories. Eat too much, move too little, gain weight. That is true at one level, but it is not the full biology.
Clinically, I have seen too many people who are genuinely trying. They are not eating wildly. They are cutting calories. They are exercising. They are doing what they have been told to do, and the weight does not shift.
When that happens, I do not assume the person is lying. I ask a different question.
What has changed in the body’s handling of energy?
That is where post-COVID inflammation becomes important. If the immune system has shifted into a chronic inflammatory state, the body may not process glucose the way it did before. The same food may produce a different metabolic response. The same activity may no longer be enough. The body may have become biased toward storage rather than use.
Fat Is Not Just Stored Energy
Most people think of fat as passive storage — excess energy sitting under the skin, waiting to be burned.
That is not how fat works.
Fat tissue is biologically active. It talks to the immune system. It produces hormones. It produces inflammatory signals. It can be infiltrated by immune cells. Once that happens, fat is no longer just stored energy. It becomes an inflammatory compartment.
This is where monocytes and macrophages matter. Monocytes are immune cells circulating in the blood. When they move into tissue, they can become macrophages, which are supposed to clear damage, coordinate repair, and resolve inflammation. But if they stay activated, they keep inflammation going.
One of the signals driving this is MCP-1, also known as CCL2. Its job is to attract monocytes. So if fat tissue starts producing MCP-1, it pulls more monocytes into the fat. Those monocytes become macrophages. Those macrophages produce more inflammatory signals. The cycle feeds itself.
This is what I mean by inflamed fat. Not fat that looks red or feels painful, but fat tissue behaving like an immune-active organ.
The Glucose Problem
To see why this could drive weight gain, look at what the body does with glucose.
When glucose is absorbed, the body has to put it somewhere. A small amount is stored in the liver as glycogen. But the major storage site is skeletal muscle — one of the most important glucose sinks in the body. If muscle is working properly, glucose moves into it and is stored as glycogen, ready for later activity.
If inflammation interferes with muscle glucose uptake, the glucose has to go elsewhere. It cannot stay in the bloodstream indefinitely, so the pancreas produces more insulin to force it into storage.
This is where the problem begins. If muscle is not taking up glucose efficiently, more of it is pushed toward fat. So weight gain is not always about eating more. It can be about the body losing its ability to direct glucose into the right compartment.
In simple terms, the body should be moving glucose into muscle. Inflammation may shift it toward fat instead.
Insulin Is Only Half the Story
Most people know about insulin. Far fewer know about amylin.
Amylin is produced by the pancreas alongside insulin. It helps regulate glucose handling, gastric emptying, appetite, and the balance between storing and releasing fuel. I think of it as part of the braking system.
When insulin rises, amylin usually rises with it. So if post-COVID inflammation causes insulin resistance, the pancreas produces more insulin — and more amylin.
This matters because a hyperinsulinaemic, hyperamylinaemic state is not neutral. It changes how the body partitions fuel and can make the system more prone to storing energy than using it.
The point is not that amylin is bad. It is a normal hormone with important functions. The issue is dysregulation. If the body is inflamed, if muscle glucose uptake is impaired, and if the pancreas is being pushed harder and harder, insulin and amylin may become part of a maladaptive loop.
That is why I believe the obesity conversation is missing something.
Where COVID Fits
COVID is not just a respiratory infection. Treating it as one was among the greatest mistakes of the pandemic. SARS-CoV-2 can affect the immune system, the vascular system, the gut, the nervous system, and metabolic regulation.
In my own work, I have increasingly focused on chronic macrophage activation as a central pathology in long COVID. Macrophages are not merely inflammatory cells. They are tissue decision-makers. They determine whether inflammation resolves or persists.
If spike protein, viral remnants, gut reservoirs, mucosal immune activation, or repeated immune stimulation keep macrophages activated, the consequences may surface in different tissues depending on the person’s predisposition.
In one person, the dominant phenotype may be vascular: chest pain, palpitations, endothelial dysfunction, exertional breathlessness.
In another, neurological: brain fog, dysautonomia, headaches, sleep disturbance.
In another, gut-driven: food intolerance, bloating, altered bowel function, histamine-type symptoms.
And in another, metabolic: central weight gain, insulin resistance, fatty liver tendency, fatigue after meals, difficulty losing weight.
That is why I do not see post-COVID obesity as a separate issue. I see it as potentially one branch of the broader phenotype.
The Immune-Metabolic Phenotype
The phrase I would use is immune-metabolic phenotype.
This is not ordinary weight gain. It is weight gain occurring alongside immune activation, impaired glucose handling, and inflammatory symptoms.
The pattern I look for is central weight gain after COVID or repeated infections, with fatigue, poor exercise tolerance, post-meal crashes, brain fog, gut symptoms, rising triglycerides, fatty liver markers, high fasting insulin, raised inflammatory markers, and possibly signs of monocyte or macrophage activation.
That pattern matters because it tells me the person may not need a standard weight-loss plan. They may need a phenotype-based approach.
This is where my research is heading. Hospital episode statistics and population data can show us what is rising, but the real task is to connect those rises into meaningful disease patterns. I am not interested in isolated statistics. I am interested in trajectories.
If obesity is rising alongside vascular inflammation, metabolic disease, mineral metabolism disorders, fatigue syndromes, gut inflammation, and cardiovascular complications, then the question is not simply, “Are people eating more?” The better question is, “Has the post-COVID immune environment changed the way the population handles energy?”
From Research to Practice: Mapping Long COVID Patterns
Over the past few years, research into Long COVID has expanded rapidly. We now have papers describing immune dysregulation, vascular injury, neuroinflammation, gut–immune signaling, and autonomic disturbance. None of this is particularly controversial anymore.
Why Exercise Advice Can Be Dangerous If It Is Too Crude
This is where standard advice can fail.
If someone is metabolically inflamed, movement matters. Muscle needs to become a glucose sink again. But in long COVID, exercise cannot be treated casually. Some people have post-exertional malaise. Some have dysautonomia. Some have vascular instability. Some get worse if they push too hard.
So I would not say, “Just exercise more.”
I would say the aim is to restore muscle glucose uptake carefully: short walks after meals, gentle resistance work, avoiding long sedentary periods after eating, rebuilding muscle gradually, tracking post-exertional symptoms, respecting the nervous system and vascular response.
Exercise becomes medicine. And like any medicine, the dose matters. Too little movement worsens insulin resistance. Too much, in the wrong phenotype, worsens symptoms. The answer is not intensity. The answer is precision.
Why the Gut Has to Be Included
I would also place the gut much more centrally.
If the gut is driving immune activation, food is not just calories. It becomes information for the immune system.
That is why generic dietary advice often fails. Some people need more fiber. Others cannot tolerate aggressive fiber early on. Some respond well to fermented foods. Others flare with histamine-type symptoms. Some tolerate carbohydrates poorly because their muscles are not taking up glucose efficiently. Others crash when they restrict too hard because their system is already unstable.
This is why phenotype matters. A gut-driven inflammatory phenotype needs gut repair and tolerance. A metabolic phenotype needs glucose stabilization and muscle restoration. A vascular phenotype needs careful attention to endothelial and autonomic stress. These may overlap, but they are not identical.
This is the mistake medicine keeps making. It treats long COVID as one disease, when it may be better understood as overlapping phenotypes built around a shared immune disturbance.
What I Would Actually Look For
If I suspected inflamed fat was part of the problem, I would not start by blaming the person. I would ask whether the body has shifted into an immune-metabolic state.
I would want to know whether there is new central weight gain, and what happens after meals. I would ask about fatigue, headaches, gut symptoms, brain fog, sleep, palpitations, breathlessness, and exercise tolerance.
Then I would look at the metabolic signal. Fasting insulin. C-peptide. Glucose. HbA1c. Triglycerides. HDL. ALT and GGT. Inflammatory markers such as hs-CRP and ferritin. Where possible, leptin, adiponectin, MCP-1, IL-6, CCL5, sCD40L, and monocyte subsets.
Not everyone needs every test. That is not the point. The point is that we need to stop treating all weight gain as though it has the same cause.
The Real Target Is Resolution
The goal is not simply to suppress inflammation. That is too crude.
The real goal is resolution.
Macrophages are supposed to move from inflammation into repair. They should clear debris, calm the immune response, restore tissue balance, and let the body return to normal function. If they stay stuck in an activated state, the system does not resolve.
That is why inflamed fat may matter so much. Fat tissue could become one of the places where the immune system remains activated — a reservoir of inflammatory signaling that keeps attracting monocytes, keeps producing MCP-1, keeps worsening insulin resistance. Once that loop is established, weight gain becomes more than weight gain. It becomes a sign of failed immune resolution.
The Bigger Implication
I am not saying post-COVID inflammation explains all obesity. That would be an overstatement.
But in a subset of people — particularly those with post-COVID symptoms, central weight gain, fatigue, poor glucose handling, and inflammatory features — obesity may be the expression of a deeper immune-metabolic phenotype.
That changes the conversation. The question is no longer, “How do we make people eat less?” It becomes, “How do we identify the phenotype, calm the inflammatory driver, restore muscle glucose uptake, repair the gut-immune axis, and help macrophages return to resolution?”
That is where I believe the research needs to go. If we keep treating the obesity surge as only a lifestyle problem, we will miss the biology. And if we miss the biology, we will keep blaming people for a system that may have been fundamentally altered by the post-COVID inflammatory landscape.
Once you see obesity through that lens, it stops being a story about willpower. It becomes another signal that the post-pandemic health trajectory has changed.
