Why Does a Cardiologist Recommend Body Recomposition to Many of His Patients?

Most cardiology consultations end with a conversation about lipids, blood pressure, or stents. This one starts somewhere different: with muscle.

Dr Edward Leatham, Consultant Cardiologist  |  Surrey Cardiovascular Clinic  |  April 2026

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I want to be clear from the outset: body recomposition is not a concept I apply to every patient, and it is not a weight loss programme. It is something more specific — and, in the right patient, considerably more powerful — than that.

Body recomposition means reducing fat mass while simultaneously preserving or building lean muscle mass. Not just losing weight. Not just shrinking the waistline. Changing the ratio of what the body is made of.

I find myself having this conversation increasingly often in cardiology clinic, particularly with patients in their 50s, 60s and 70s who have coronary disease, elevated visceral fat, glucose dysregulation, or all three. And the reason I have it is because the evidence supporting this approach has become, in recent years, genuinely compelling.

Why ‘just lose weight’ is the wrong target

The conventional framing in cardiometabolic medicine is straightforward: patients with excess weight should reduce it, and doing so will lower their cardiovascular risk. That is broadly true. But the framing is dangerously incomplete.

When patients lose weight — whether through caloric restriction, GLP-1 therapy, or lifestyle change — they do not lose fat alone. A significant proportion of the weight lost is lean mass: muscle, and sometimes bone. Studies of GLP-1 therapy have shown that between 25 and 40% of total weight loss can come from lean tissue when protein intake is not deliberately managed.¹

This matters enormously in cardiovascular medicine, for reasons that go well beyond aesthetics.

Skeletal muscle is not simply structural. It is the body’s largest metabolic organ.

Muscle accounts for 70–80% of insulin-mediated glucose disposal.² Lose muscle, and insulin resistance worsens. Lose muscle, and physical activity becomes harder. Reduce activity, and visceral fat accumulates further. The cycle is self-reinforcing, and it runs directly against everything we are trying to achieve.

Visceral fat: the specific problem in cardiac patients

Not all fat carries equal risk. Subcutaneous fat — the fat you can pinch — is largely metabolically inert. Visceral fat, which accumulates around the abdominal organs, is metabolically active in the worst possible sense: it secretes inflammatory cytokines, promotes insulin resistance, drives atherogenesis, and is independently associated with coronary artery disease, cardiac events, and mortality.³

What is increasingly clear from imaging studies is that patients with normal or near-normal BMI can carry substantial visceral fat loads — and patients with elevated BMI can have relatively low visceral fat. BMI is, in this context, a deeply imperfect tool.

Waist circumference and waist-to-height ratio perform better as screening measures, and CT or MRI visceral fat measurement — giving a VATI score — allows genuine personalisation of risk and targets.⁴ At SCVC we use VATI measurement to guide both the assessment of risk and the target we set for each patient.

Clinical note: VATI — visceral adipose tissue index — is measured in cm²/m² and represents the area of visceral fat at L3 on CT or MRI, normalised for height. Ethnicity-specific healthy thresholds exist, and proximity to the upper boundary of the normal range — particularly in patients with established coronary disease — still warrants active management.

What body recomposition actually means in clinical practice

Body recomposition, in the context of cardiometabolic disease, is not about gym aesthetics. It is about deliberately shifting the ratio of fat to lean mass — specifically reducing visceral fat while protecting the muscle that underpins metabolic health.

In practice, this involves three components working together:

• Protein targeting — ensuring sufficient protein intake, distributed across meals, to provide the substrate for muscle maintenance and synthesis. In older adults, this requires higher per-meal doses than most people currently achieve.
• Resistance exercise — structured strength training that signals muscle to adapt and grow, and which simultaneously improves insulin sensitivity and metabolic rate. Even modest programmes — 10 to 15 minutes a day, five days a week — have measurable effects.
• Visceral fat reduction — through a controlled caloric deficit, GLP-1 therapy where indicated, or both. The deficit must be managed carefully to avoid muscle loss.

These three are not separable. A caloric deficit without adequate protein and resistance training produces weight loss that is partly lean tissue. Protein intake without resistance training is less effective. Resistance training without adequate protein cannot deliver its full effect.

Which patients benefit most from this conversation?

Body recomposition is not a universal recommendation. In my practice, it tends to be most relevant for patients who share some combination of the following features:

• Established or suspected coronary artery disease with visceral adiposity — where reducing VAT load has direct cardiometabolic benefit
• Elevated VATI on CT scan, particularly when near or above the ethnicity-specific healthy threshold
• Glucose dysregulation, insulin resistance, or early T2DM — where improving muscle mass directly improves glucose disposal
• Starting GLP-1 therapy — where lean mass protection from day one is essential
• Adults over 60 with any of the above, where anabolic resistance means that protein and exercise targeting becomes increasingly important decade by decade
• Patients who have already lost weight but feel weaker, less functional, or have plateaued — the classic dynapenia pattern

Notably, this is not necessarily about BMI. I have had patients with BMI in the normal range who have elevated visceral fat and are insulin resistant, and who benefit significantly from this approach. And I have had patients with elevated BMI who have good muscle mass and relatively low visceral fat, for whom weight loss targeting is less of a priority.

The question is not ‘what does the scale say?’ It is ‘what is the body made of, and is the ratio working for or against the patient’s cardiovascular health?’

Why muscle matters in cardiology specifically

The cardiovascular evidence for muscle mass and function is now substantial. Low muscle mass is independently associated with increased all-cause mortality, cardiovascular events, and worse outcomes following cardiac procedures.⁵ Grip strength — a simple clinical measure of muscle function — predicts cardiovascular mortality more reliably than many established risk factors.

There is also a direct mechanistic link. Skeletal muscle is the primary site of glucose disposal after meals. When muscle mass and insulin sensitivity are adequate, glucose is efficiently cleared. When they are not, glucose remains in circulation longer, glycates proteins, drives vascular inflammation, and contributes to the atherosclerotic process.

Muscle is, in this sense, a buffer against the metabolic insults that drive cardiac disease.

And that buffer erodes with age — faster than most patients realise, and faster than most clinicians actively manage. From approximately age 60, the process of anabolic resistance means that muscle becomes progressively harder to maintain. Higher protein per meal, better distribution across the day, and structured resistance training are not optional additions for motivated patients: they are the clinical intervention.

The GLP-1 context: why this matters more than ever

The widespread adoption of GLP-1 receptor agonists — semaglutide, tirzepatide, and their successors — has transformed what is achievable in obesity and cardiometabolic medicine. These are genuinely effective agents with real cardiovascular outcome data.⁶ I prescribe them.

But they create a specific clinical challenge: GLP-1 therapy reduces appetite non-selectively. Without deliberate attention to protein intake and resistance training, a substantial fraction of the weight lost is muscle. The patient loses weight. They feel weaker. They exercise less. And the metabolic benefit of the weight loss is partly undermined by the muscle loss it causes.

Body recomposition thinking is therefore more important in the GLP-1 era, not less. These drugs are a powerful tool for visceral fat reduction. That tool works best when it is paired with the protein and exercise strategy that preserves what matters.

Practical guidance: Patients starting GLP-1 therapy should aim for protein at every meal from day one. The target on GLP-1 is the upper end of the age-appropriate range during active weight loss, and supplementation with whey or pea protein is appropriate when appetite suppression limits food intake. Resistance training should begin before or simultaneously with GLP-1 therapy, not after weight has been lost.

What I actually tell patients

In clinic, I try to make this as concrete as possible, because abstract advice about ‘body composition’ does not change behaviour.

The conversation usually goes something like this:

“The goal here isn’t to make the number on the scale go down. The goal is to reduce the fat around your organs, which is what’s driving your risk, and to keep the muscle that protects you. If we do it right, the scale might not move much at first — but what you’re made of will be healthier.”

I then explain the specific targets: the waist circumference or VATI goal, the protein target for their age and lean body mass, and the exercise programme. For patients on GLP-1, I explain why protein comes first at every meal, even when they are not hungry.

And I direct them to the VAT Trap Healthy Waist Calculator — a free tool that calculates their personalised waist target from their measurements or VATI score, along with their lean body mass estimate and age-adjusted protein target. It produces a downloadable PDF report they can bring back to the next appointment.

Use our free calculator to estimate your personalised waist target, LBM estimate and protein target. Free, no app needed.

What success looks like

Success in body recomposition does not always look like weight loss on a scale, at least not initially. It looks like:

• Waist circumference reducing — the most important anthropometric signal
• VATI tracking downward on repeat CT, when available
• Grip strength maintaining or improving
• Functional measures improving — the ability to rise from a chair, walk distance, carry shopping
• Glucose metrics improving — fasting glucose, HbA1c, post-meal glucose
• Energy and mood improving, which drives adherence

In patients who achieve genuine body recomposition — less visceral fat, maintained or improved muscle — the metabolic transformation can be striking. Insulin sensitivity improves. Inflammatory markers fall. Blood pressure often follows. The downstream cardiovascular benefit accrues not just from the fat lost but from the muscle preserved.

A final thought

Cardiology has become extraordinarily good at intervening in the consequences of cardiometabolic disease: stenting arteries, implanting devices, optimising pharmacology. We are considerably less systematic about addressing the upstream drivers.

Body recomposition — reducing visceral fat while preserving muscle — is one of the most effective upstream interventions available. It is not a quick fix. It requires attention to protein, exercise, and in many patients, pharmaceutical support. It requires a different conversation in clinic.

But for the right patient, it changes not just their risk profile but their lived experience: more strength, more energy, more functional reserve. That is a meaningful clinical outcome — and one that begins with asking a different question than the one most cardiology consultations start with.

Not what is your cholesterol, but what is your body made of, and is that ratio working for your heart?

References

¹ Barkoukis H. Nutrition in GLP-1 receptor agonist therapy: considerations for maintaining muscle mass during weight loss. J Acad Nutr Diet. 2022;122(5):867–869.

² Ferrannini E, Simonson DC, Katz LD et al. The disposal of an oral glucose load in patients with non-insulin-dependent diabetes. Metabolism. 1988;37(1):79–85.

³ Neeland IJ, Ross R, Després JP et al. Visceral and ectopic fat, atherosclerosis, and cardiometabolic disease: a position statement. Lancet Diabetes Endocrinol. 2019;7(9):715–725.

⁴ Shuster A, Patlas M, Pinthus JH, Mourtzakis M. The clinical importance of visceral adiposity: a critical review of methods for visceral adipose tissue analysis. Br J Radiol. 2012;85(1009):1–10.

⁵ Srikanthan P, Karlamangla AS. Relative muscle mass is inversely associated with insulin resistance and prediabetes: findings from the third National Health and Nutrition Examination Survey. J Clin Endocrinol Metab. 2011;96(9):2898–2903.

⁶ Lincoff AM, Brown-Frandsen K, Colhoun HM et al. Semaglutide and cardiovascular outcomes in obesity without diabetes (SELECT). N Engl J Med. 2023;389(24):2221–2232.

Further references: Leatham E. Consensus Statement on Healthy VATI Targets by Ethnicity. Internet Archive, 2026. Full bibliography: VAT_Trap_Complete_Bibliography.docx (77 refs).

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