A friend of mine went keto about eighteen months ago. Strict keto, under 20 grams of carbs a day. He did it for weight loss and blood sugar management, and by both measures, it worked. He lost 14 kilograms. His fasting glucose dropped from borderline to solidly normal. His triglycerides halved.

Then he got his cholesterol checked. His LDL had gone from 3.2 to 5.8 mmol/L. His GP was alarmed. His keto community told him it was "normal on keto" and "LDL doesn't matter." His cardiologist said it absolutely does matter.

The truth was more nuanced than either camp acknowledged. His triglycerides had improved dramatically. His HDL had risen. His HbA1c was excellent. His inflammatory markers were low. But his LDL, the primary driver of atherosclerosis, had nearly doubled. And that needed to be addressed, even if every other marker looked better.

This article is for anyone following a ketogenic, low-carb, or intermittent fasting approach and wants to know what to monitor, what the blood work typically shows, where the genuine improvements are, and where the blind spots hide.

A note before we get into it

Why low-carb diets need blood testing more, not less

There's an assumption in some low-carb communities that because the diet feels good and produces visible results (weight loss, energy, blood sugar control), the internal picture must be uniformly positive. This isn't always the case.

Ketogenic and low-carb diets produce significant metabolic shifts: changes in how your body fuels itself, stores fat, processes cholesterol, and regulates hormones. Many of these shifts are beneficial. Some are neutral. And some, in some people, produce changes that need monitoring.

The argument for testing isn't that low-carb diets are dangerous. It's that they produce measurable metabolic changes, and any diet that changes your metabolism deserves the same monitoring you'd give a medication that does the same thing. Testing before you start, at three months, and periodically thereafter gives you the data to confirm the diet is working for you. Not just on the scales, but in your blood.

What keto and low-carb typically improve

The metabolic benefits of carbohydrate restriction are well-documented in clinical literature. These are the markers that most commonly improve.

Triglycerides. Often dramatically. Triglycerides are primarily driven by carbohydrate and alcohol intake. Reducing carbs reliably drops triglycerides, often by 30-50% or more. This is one of the most consistent and significant benefits of low-carb diets.

HDL cholesterol. Tends to rise on low-carb diets, particularly high-fat versions. Higher HDL is associated with lower cardiovascular risk.

Triglyceride/HDL ratio. Improves as triglycerides drop and HDL rises. This ratio is considered a surrogate marker for insulin resistance and small dense LDL particles, both cardiovascular risk factors.

HbA1c and fasting glucose. Carbohydrate restriction directly reduces blood sugar load. For people with pre-diabetes or type 2 diabetes, low-carb diets can produce significant improvements in glycaemic control, sometimes sufficient to reduce or eliminate blood sugar medications (under medical supervision). See the HbA1c article.

Fasting insulin. Drops as carbohydrate intake decreases and insulin resistance improves. This is arguably the most important metabolic marker to track, and one of the most consistently improved on low-carb approaches. See the weight gain article for detail on fasting insulin and HOMA-IR.

Liver enzymes (ALT/GGT). NAFLD often improves with carbohydrate restriction and weight loss. ALT and GGT may normalise as liver fat reduces. See the liver function article.

What they sometimes worsen, and the LDL question

This is the section that generates the most debate. I want to be honest about where the evidence stands.

LDL cholesterol: the controversy

Some people on ketogenic diets experience a significant rise in LDL cholesterol. Not everyone, but a meaningful minority. The phenomenon is most pronounced in "lean mass hyper-responders," typically lean, metabolically healthy individuals who show dramatic LDL increases (sometimes doubling or tripling) on high-fat, low-carb diets.

The keto community position: LDL rises because the body is using fat as fuel and transporting more cholesterol through the bloodstream. If triglycerides are low, HDL is high, and inflammatory markers are normal, elevated LDL may not carry the same risk as in someone with metabolic syndrome.

The cardiology position: LDL is the primary causal driver of atherosclerosis. The evidence linking cumulative LDL exposure to cardiovascular events is extensive and robust. A dramatically elevated LDL, regardless of the metabolic context, increases lifetime cardiovascular risk. See the cholesterol article and the heart health article.

Where I land (as someone who reads both sides): This is an unsettled area. There are no long-term randomised controlled trials tracking cardiovascular events specifically in lean mass hyper-responders on keto. The mechanistic argument that context modifies LDL risk has some theoretical support but limited direct evidence. Meanwhile, the population-level evidence linking LDL to cardiovascular events is among the strongest in medicine.

My practical recommendation: if your LDL rises significantly on keto, don't dismiss it. Discuss it with your GP or a cardiologist. Get your Lipoprotein(a) checked (once, as it modifies how aggressively LDL should be managed). Consider whether the dietary approach needs modification. Some people find they can maintain the metabolic benefits of low-carb without the extreme fat intake that drives LDL up.

Thyroid function (T3)

Some people on very low-carb diets experience a reduction in Free T3, the active thyroid hormone. The body may downregulate T3 as an energy-conservation mechanism when carbohydrate intake is very low. This can produce symptoms that mimic hypothyroidism: fatigue, cold sensitivity, hair changes, constipation.

If you're on keto and experiencing these symptoms, check your thyroid. A low Free T3 with normal TSH and Free T4 may indicate a dietary effect rather than primary thyroid disease. Slightly increasing carbohydrate intake (even to 50-75g/day) often resolves this. See the thyroid article.

Kidney function

High-protein versions of low-carb diets can increase the filtration load on kidneys. In people with healthy kidneys, this is generally well-tolerated. But in people with pre-existing kidney disease (even undiagnosed), high protein intake can accelerate decline. Monitoring eGFR is prudent if you have risk factors for CKD. See the kidney function article.

How fasting affects your blood work

Intermittent fasting (IF) adds another layer of complexity to blood test interpretation. The timing of your blood draw relative to your fasting window matters.

Fasting glucose: May be elevated during a prolonged fast (a phenomenon called "physiological insulin resistance" or "adaptive glucose sparing"). The body maintains blood glucose for the brain by reducing peripheral glucose uptake. This can produce a paradoxically elevated fasting glucose that doesn't indicate diabetes. It indicates adaptation. Context matters.

Fasting insulin: Typically drops with intermittent fasting, one of the primary metabolic benefits. Testing during your fasting window gives the clearest picture.

Cortisol: May be elevated during extended fasts, as cortisol is involved in gluconeogenesis (producing glucose from non-carbohydrate sources). This is physiological, not pathological, but it can confuse cortisol interpretation if you don't mention your fasting status.

Liver enzymes: Can be mildly elevated during fasting or rapid weight loss as the liver mobilises stored fat. Transient and typically benign, but worth noting.

Lipids: Acute fasting can affect triglycerides and LDL readings. For the most standardised lipid panel, test after a typical 10-12 hour overnight fast, not after a 24-hour or longer fast.

When you're fasting, tell the pathology staff and your clinician. The timing of your last meal, the duration of your fast, and whether you're in a regular fasting pattern all affect interpretation.

The full monitoring panel

If you're following a ketogenic, low-carb, or intermittent fasting approach, these are the markers worth tracking.

Metabolic improvement markers

Fasting insulin (the single best marker of metabolic improvement), HbA1c (three-month blood sugar average), fasting glucose (with context noted above), triglycerides (expect improvement), and HDL (expect improvement).

Potential concern markers

LDL cholesterol (may rise, needs monitoring), full lipid panel (the pattern matters more than LDL alone), thyroid function (TSH, Free T4, Free T3, watch for T3 suppression), and eGFR (if following a high-protein version of the diet).

Broad health context

Liver function (ALT, GGT) for NAFLD improvement or transition effects. Full blood count for baseline. Vitamin D (often low regardless of diet). Electrolytes (sodium, potassium, magnesium can shift on keto).

Once

Lipoprotein(a). Genetically determined, and it changes how you interpret LDL risk.

Testing protocol: before, during, and ongoing

Before starting (baseline): Full panel. This is your reference point. Without a baseline, you can't tell what the diet changed. Ideally done 1-2 weeks before starting.

At 3 months: Retest the full panel. This is where you see the initial metabolic response: triglyceride improvements, HbA1c changes, and any LDL movement. Three months gives enough time for lipid and metabolic markers to stabilise.

At 6-12 months: Retest key markers. Confirm that improvements are sustained and that any concerns (LDL, thyroid) are stable or addressed.

Annually thereafter: Standard monitoring. Compare against your baseline. Look for trends.

If you discontinue the diet: Retest at 3 months after transitioning back. Metabolic markers will shift again and a new baseline is useful.

How to prepare: timing matters more than usual

Tests to consider through Bloody Good

Keto/low-carb monitoring panel

Extended context

Comprehensive coverage

The Bloody Good Test covers 100 biomarkers including the full lipid panel, HbA1c, liver, kidney, thyroid, iron, vitamin D, inflammation, and more. For keto and IF practitioners, the comprehensive approach captures both the improvements and the potential concerns in a single draw. Pair with fasting insulin for complete metabolic assessment.

What to do with your results

If triglycerides dropped and HDL rose: The metabolic benefit is real. This is the pattern that low-carb diets do best, and it's clinically meaningful.

If HbA1c and fasting insulin improved: Even more significant. Improved insulin sensitivity is the strongest metabolic argument for carbohydrate restriction.

If LDL rose modestly (below 5.0 mmol/L): Monitor. If every other marker is improved, the net cardiovascular risk picture may still be favourable. Track LDL over time and discuss with your GP.

If LDL rose significantly (above 5.0 mmol/L): Take it seriously. Discuss with your GP or cardiologist. Options include modifying the diet (reducing saturated fat while maintaining carb restriction), adding more fibre, or considering medication if overall cardiovascular risk is elevated. The metabolic benefits of keto are not worth an LDL of 6.0+. The cumulative atherogenic exposure over years matters.

If Free T3 is low: Consider whether you're restricting carbs too aggressively. Adding 50-75g of carbs daily (targeted around training or evening) often resolves T3 suppression while maintaining most of the metabolic benefits.

If liver enzymes are transiently elevated: Common during the adaptation phase and rapid weight loss. Retest in 4-8 weeks. If persistently elevated, investigate further.

If everything looks good: You've confirmed the diet is working for your biology. Keep testing periodically. Metabolic responses can change over time, particularly if adherence varies or body composition shifts.

Explore more biomarkers

Browse the Bloody Good Biomarker Directory