In nearly forty years of working with people, I've worked with hundreds of people who couldn't lose weight despite doing everything right. The diet was clean. The exercise was consistent. The calories were tracked. The willpower was iron. And yet: nothing. Or temporary loss, followed by rapid regain. Or loss in one area of the body and stubborn accumulation in another.
The standard response is to assume the person is wrong about their intake. That is demoralising to hear — and the uncomfortable truth is that it is sometimes right: in controlled studies most people under-report what they eat, without meaning to. So a good investigation checks intake honestly and looks for the physiology that makes the same intake harder to work with.
The reason the same approach works for some people and fails for others is that weight is regulated by multiple overlapping hormonal systems, not just by caloric arithmetic. Energy balance still applies: fat is only lost when intake is below expenditure. What hormones change is how hungry you are, how much energy you spend, where fat is stored and how hard a deficit is to sustain. The solution isn't trying harder. It's identifying what is making the deficit hard — and addressing that specifically.
The five patterns that block fat loss
Some of these are well established and testable (insulin resistance, overt thyroid disease); others are more hypothesis than proof. I say which is which below. In practice, more than one often overlaps.
The key: fasting glucose can appear completely normal for years while fasting insulin is already significantly elevated. By the time blood sugar rises on a standard test, insulin resistance has often been present for years. The correct test is fasting insulin, not fasting glucose — and it's almost never ordered on a standard panel.
The cruel irony: exercise, particularly high-intensity exercise, elevates cortisol. If your stress system is already dysregulated, intense exercise can reinforce the pattern rather than break it. I frequently prescribe less intense exercise — walking, resistance work, nothing that demands significant cortisol release — as the first intervention for this pattern, which is counterintuitive but clinically important.
The standard thyroid test checks only TSH — the pituitary signal to the thyroid, not what the thyroid is actually producing or whether that production is reaching cells as active hormone. A fuller picture comes from TSH with Free T4 and Free T3, plus antibodies if autoimmune thyroid disease is possible. Low Free T3 with a normal TSH is worth investigating — illness, undereating and stress all lower it — but it is not a diagnosis. Reverse T3 is rarely useful on its own.
Gut infections such as H. pylori or Giardia are worth confirming and treating through your GP where symptoms suggest them. Whether low-grade dysbiosis drives weight gain through inflammation is still a hypothesis, which brings us to Pattern 5.
The sources of chronic inflammation are varied: gut infections, food sensitivities creating ongoing mucosal inflammation, poor sleep, chronic psychological stress, environmental toxin burden, and excess body fat itself. Identifying the primary inflammatory driver — not just suppressing inflammation — is what breaks the cycle.
Why the same approach works for some and fails for others
Some people find a lower-carbohydrate diet easier to stick to when insulin resistance is present, because hunger is steadier. Others find very low carbohydrate intake leaves them tired and poorly recovered, especially under heavy stress or training. Some people do well with longer overnight fasts; people prone to energy crashes often do not. Exercise improves insulin sensitivity for almost everyone, but very high training volume on top of poor sleep and high stress can backfire. The point is that the best approach is individual, and knowing what is going on makes it easier to choose.
A client came to me having done two rounds of a very-low-calorie programme. She'd lost weight each time, regained it plus a little more each time. She was tracking 1,400 calories, exercising five days a week, and gaining weight. Her GP had run standard bloods twice. Normal. She'd been told she must be "eating back" her exercise calories without realising.
Testing revealed fasting insulin of 22 μIU/mL with completely normal fasting glucose — significant insulin resistance that no standard panel would flag. DUTCH showed elevated evening cortisol with low morning cortisol — an inverted pattern consistent with prolonged HPA stress. Free T3 was at the low end of its range with a normal TSH — worth watching, not a diagnosis. The insulin and cortisol findings gave us somewhere specific to start, which two rounds of “eat less, move more” had not. (Details changed to protect privacy.)
What investigation actually looks like
The TDG programme approaches weight loss resistance as a clinical investigation, not a diet plan. Five functional tests — advanced blood chemistry, GI-MAP stool analysis, DUTCH Plus hormone testing, Organic Acids Test, and food sensitivity panel — are run simultaneously and read together. The aim is to identify which patterns are active, in what order they should be addressed, and what specific interventions target each pattern in your specific biology.
This produces a very different kind of protocol. Not a generic diet. Not a supplement stack. A sequenced clinical programme that targets the specific physiological barriers to fat loss that testing has identified in your body. When the barriers are addressed, a sustainable deficit usually becomes easier to hold — which is what fat loss still depends on.
The starting point — a free screen
Before committing to the full investigation, the weight loss pattern finder identifies which of the five patterns is most likely dominant in your presentation. It takes three minutes, costs nothing, and gives you an immediate clinical framework for your situation — something more useful than another diet plan.