Diagnostic criteria
The National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III; JAMA 2001, PMID 11368702) defined metabolic syndrome as the presence of three or more of the following five components:
The International Diabetes Federation (IDF) definition requires central
obesity as a mandatory criterion plus any two of the other four, using lower
waist thresholds for some populations. In practice the two definitions
identify largely overlapping groups.
Why the components cluster
The unifying pathophysiology is a combination of visceral adiposity and insulin resistance. Expanded visceral adipose tissue is not a passive energy store — it is a metabolically active organ that releases free fatty acids into the portal circulation and secretes pro-inflammatory adipokines (including TNF-α and IL-6). The free fatty acid flux to the liver drives hepatic triglyceride synthesis and VLDL overproduction, producing the atherogenic dyslipidaemia of raised triglycerides and low HDL. In skeletal muscle, intracellular lipid metabolites (diacylglycerols and ceramides) activate serine kinases that phosphorylate IRS-1 on inhibitory residues, impairing insulin-stimulated glucose uptake. The resulting compensatory hyperinsulinaemia increases renal sodium retention and sympathetic nervous system activity, contributing to the blood pressure component of the syndrome.Differential diagnosis
Several conditions can produce individual features of the syndrome. Primary hypertension must be distinguished from the blood pressure rise secondary to weight gain and hyperinsulinaemia. Familial combined hyperlipidaemia can mimic the lipid profile. Cushing’s syndrome causes central obesity, raised blood pressure and impaired glucose tolerance; clinical clues include proximal muscle wasting, thin skin and violaceous striae. Sleep apnoea can drive hypertension and insulin resistance and is often present alongside the syndrome rather than instead of it. The reviewing doctor distinguishes these possibilities from the history and, where available, laboratory data.Treatments a doctor considers
A licensed doctor decides case by case. Hi Doctor never prescribes without an evaluation.Semaglutide (Wegovy / Ozempic)
Weekly GLP-1 receptor agonist. A doctor may prescribe it if BMI and history match the indications. Requires follow-up.
Tirzepatide (Mounjaro)
Dual GLP-1/GIP agonist. Assessed by the doctor based on comorbidities and BMI.
Liraglutide (Saxenda)
Daily GLP-1 agonist. Indicated in selected patients with elevated BMI after medical evaluation.
Orlistat 120mg
Fat-absorption inhibitor. A non-GLP-1 alternative a doctor may consider based on history.
Rybelsus (oral semaglutide) — a once-daily semaglutide tablet authorised for type 2 diabetes. Any use in weight management is an individual medical decision and may be off-label.
Your path to treatment
1
Start the online visit
Answer a questionnaire about health and goal. No in-person appointment, no travel — an eligibility answer arrives within 24 hours.
2
A doctor reviews the case
A licensed doctor reviews the answers personally. If they need clarification, they message through the private chat in the account. If treatment is appropriate, they sign an electronic prescription.
3
Review and payment
If the doctor does not approve treatment, the consultation fee is refunded in full within 48 hours.
4
Ongoing support
Private chat with the doctor for questions, a 4-week check-in, and renewal before the prescription expires.
Related reading
- Semaglutide (Ozempic) — indication and dosing
- Liraglutide (Victoza) — trial evidence and side effects
- Safety and eligibility
Start a consultation
Weight-loss consultation
Answer the weight-loss questionnaire and a registered doctor reviews it.
They decide whether treatment is appropriate, which one, and at what dose —
and declining is a normal outcome. See what it costs
and how the review works.