GLP-1 medications: what to monitor and potential side effects to test for

GLP-1 (glucagon-like peptide-1) receptor agonists mimic a natural hormone produced in the gut after eating. They increase insulin secretion in response to food, suppress glucagon (which would otherwise raise blood glucose), slow gastric emptying to promote prolonged fullness, and reduce appetite through direct effects on hunger signalling in the brain. The combination of reduced appetite and slowed gastric emptying typically produces calorie reductions of 16 to 39%, which is what drives the weight loss outcomes seen in clinical trials. Clinical trials for semaglutide 2.4mg weekly showed an average of 10 to 15% weight loss over 68 weeks. Tirzepatide (Mounjaro) has shown even higher average weight loss in trials.

These are genuinely significant clinical effects. The issue is that the same appetite suppression and slowed gastric emptying that produces weight loss also creates conditions in which nutrient intake and absorption are substantially reduced, with consequences that require monitoring.

Nutritional deficiencies

A 2025 retrospective study found that 12.7% of patients on GLP-1 receptor agonists developed a nutritional deficiency within 6 months, rising to 22.4% within 12 months. The most commonly affected nutrients are vitamin D, iron, vitamin B12, and folate. GLP-1 medications do not directly cause deficiencies, but the significant reduction in food volume they produce, combined with altered gastric emptying that affects nutrient absorption, creates conditions in which micronutrient intake frequently falls below what the body needs.

Vitamin D is the most commonly affected nutrient, with a 13.6% incidence of deficiency reported at 12 months in one large study. Iron deficiency is the next most common, with some research suggesting a possible link between GLP-1 use and reduced iron absorption beyond what reduced food intake alone would predict. B12 deficiency is a particular concern for people also taking metformin, as metformin independently impairs B12 absorption, and semaglutide may also interfere with B12 assay accuracy in people taking both drugs together.

Protein adequacy is a related concern that does not show up directly in standard blood tests but is critical. Calorie reductions of 16-39% frequently result in protein intakes well below optimal. The Endocrine Society reported in 2025 that older adults and women on semaglutide are at higher risk of muscle loss, and protein intakes of 1.2 to 1.6 grams per kilogram of body weight appear protective. Albumin on a blood panel provides one indirect marker of protein status.

Muscle mass loss

Rapid weight loss on GLP-1 medications is predominantly fat loss, but a proportion of the weight lost is lean mass including muscle. Studies evaluating semaglutide and tirzepatide found that approximately 1.4% and 2.6% of total weight loss respectively came from fat-free mass, primarily muscle. While small in percentage terms, this can represent a significant absolute loss of lean mass in people with higher starting body weight. Sustained muscle loss worsens resting metabolic rate, which contributes to weight regain when the medication is eventually stopped. Resistance training and adequate protein intake are the two interventions with the strongest evidence for preserving lean mass during GLP-1 therapy.

Kidney function

GLP-1 side effects including nausea, vomiting, and diarrhoea can cause dehydration, which has been linked to acute kidney injury in semaglutide users, particularly in the early months of treatment while doses are being titrated. Kidney function markers (creatinine, eGFR) provide a safety baseline and ongoing monitoring point during this period.

Liver markers

Liver enzymes (ALT, GGT) should be checked as part of a baseline panel before starting GLP-1 therapy. GLP-1 medications generally have a favourable effect on fatty liver disease (NAFLD/MASLD), but establishing a baseline is important for context. Elevated GGT and ALP can also indicate biliary obstruction, which matters because semaglutide increases the risk of gallstone formation (cholelithiasis).

Blood sugar control

For people using GLP-1 medications to manage type 2 diabetes, HbA1c monitoring is standard practice and typically managed by their prescriber. For those using GLP-1 for weight management without diabetes, HbA1c and fasting glucose at baseline and at 6-monthly intervals track the metabolic improvements being achieved and confirm that blood sugar regulation is improving rather than overcorrecting.

Thyroid monitoring

GLP-1 receptors are expressed in thyroid tissue, and in animal studies very high doses of GLP-1 agonists were associated with thyroid C-cell changes (the basis for the contraindication in people with personal or family history of medullary thyroid carcinoma or MEN2). In human studies to date, no causal link to thyroid cancer has been established. Nonetheless, annual TSH and Free T4 monitoring is recommended for people on long-term GLP-1 therapy, partly to capture any impact on thyroid function and partly because thyroid dysfunction can produce symptoms that overlap significantly with GLP-1 side effects.

GLP-1 medication monitoring should include both a pre-treatment baseline and ongoing monitoring at defined intervals. Private testing options in the UK mean that the comprehensive panels recommended by specialists are accessible without GP referral.

Before starting GLP-1 therapy: establish baseline kidney function (creatinine, eGFR), liver function (ALT, GGT, ALP), HbA1c, lipid panel, thyroid function (TSH, Free T4), and nutritional markers (Vitamin D, B12, ferritin, folate, albumin). Identify any pre-existing deficiencies that need addressing before calorie restriction makes them worse.

At 3 months: check kidney function, liver enzymes, HbA1c, and symptoms. This is the period of greatest dehydration risk and when GI side effects are most prominent.

At 6 months: comprehensive nutritional panel (Vitamin D, B12, ferritin, folate, albumin), thyroid function, HbA1c, lipid panel. The 6-month mark is when nutritional deficiency rates begin to climb significantly.

At 12 months and annually thereafter: full panel including nutritional markers, thyroid function, kidney and liver function, HbA1c, lipid panel, and CRP.

Protein prioritisation to protect muscle

The most important nutritional priority for anyone on GLP-1 therapy is adequate protein intake. When total food volume drops significantly, protein is often displaced by whatever volume of food is tolerated. Prioritising protein at each meal (targeting 1.2 to 1.6 grams per kilogram of body weight) is the single most evidence-supported strategy for preserving lean mass during rapid weight loss. Practical sources include eggs, fish, chicken, legumes, dairy, and protein supplements when whole food intake is limited by nausea or early satiety. Albumin on a blood panel provides one indirect indicator of protein status over time.

Resistance training throughout treatment

One study found that weight loss was maintained one year after stopping GLP-1 therapy only when a supervised exercise component was added to the medication. Resistance and combined resistance-endurance training preserve lean mass, improve insulin sensitivity, and support resting metabolic rate in ways that sustain weight management outcomes beyond the medication period. For people experiencing nausea or fatigue in the early months, lower-intensity resistance training that can be progressed as tolerance improves is preferable to no training.

Hydration and electrolyte management

GLP-1-induced nausea, vomiting, and diarrhoea increase the risk of dehydration, particularly in the titration phase. GLP-1 agonists also appear to suppress thirst (hypodipsia) in some users, reducing the natural drive to drink. Electrolyte-containing fluids support hydration when GI symptoms are prominent, and monitoring kidney function markers provides an objective check on whether dehydration is affecting renal function.

Nutrient-dense food choices within reduced volume

When appetite suppression limits total food volume, the quality of what is eaten becomes significantly more important than usual. Foods providing high nutrient density per calorie (fish, eggs, dairy, leafy greens, legumes, berries) protect against the deficiency trajectory that develops in people eating less but eating the same poor-quality dietary pattern. Tracking key markers at 6 months confirms whether food choices within the reduced intake are sufficient to maintain optimal nutrient status.