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Episode
So Called "Normal Labs" are NOT Healthy
~19 min
Episode Brief·YouTube

So Called "Normal Labs" are NOT Healthy

Eric Berg
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TL;DR

The four things you'd lose by not watching

4 items

TL;DR

The four things you'd lose by not watching

4 items
1

So-called 'normal' lab ranges are statistical averages from an increasingly sick population, not a marker of health. Key example: in 1997, the fasting glucose threshold for diabetes was lowered from 140 to 126 mg/dL, instantly reclassifying 1.4 million people as diabetic; in 2003, the pre-diabetes threshold dropped from 110 to 100, adding 41 million pre-diabetics.

2

Fasting insulin is the most overlooked marker: it can be elevated 15–20 years before blood glucose rises, indicating pancreatic stress and insulin resistance. Target fasting insulin 2–6 μIU/mL, not the 'normal' range of up to 12 that many labs accept.

3

Standard cholesterol panels obscure risk. LDL comes in two forms: large buoyant Pattern A (non-pathogenic, common on low-carb diets) and small dense Pattern B (pathogenic, driven by high-carb intake). Only advanced lipid profiling reveals which type predominates.

4

Vitamin D blood tests only measure the inactive form and miss cellular vitamin D resistance. Use parathyroid hormone (PTH) as a proxy: if PTH is elevated despite 'normal' vitamin D, you are functionally deficient. Optimal levels are 50–70 ng/mL, far above the commonly accepted 20 ng/mL threshold.

Protocols

Concrete recipes — what, when, how much, and why

8 items

fasting-insulin-and-homa-ir-testing

WhatRequest a fasting insulin test and calculate HOMA-IR (using fasting glucose and insulin) to detect insulin resistance years before glucose abnormalities appear.
WhenAs part of routine blood work, especially if you have weight issues, fatigue, skin tags, or family history of diabetes, even when fasting glucose is normal.
DoseTarget fasting insulin: 2–6 μIU/mL. Be concerned at 8; 10–12 indicates high risk. HOMA-IR can be computed from fasting insulin (μIU/mL) × fasting glucose (mg/dL) / 405.
For whomAnyone concerned about metabolic health; especially those with normal glucose but signs of metabolic syndrome.
WhyInsulin resistance develops 15–20 years before fasting glucose rises; measuring only glucose misses the years when the pancreas is overworking. Early detection allows dietary intervention to prevent beta-cell burnout and diabetes.
CaveatsThere is no universally accepted normal range for fasting insulin; many labs report ≤12 as normal, which Berg argues is far too high and already indicative of significant insulin resistance.

Berg compares the situation to having a dam holding back a flood: glucose is the water level, insulin is the dam. As long as the dam holds, glucose looks fine, but the pressure on the dam (insulin) is immense. He notes that even when insulin is tested, doctors often accept values like 12 μIU/mL as normal. He bases his recommendations on research and his clinical experience. The HOMA-IR index adds prognostic power by modeling how well insulin is working relative to glucose. For someone with fasting glucose of 95 mg/dL and insulin of 10, HOMA-IR would be 2.35, indicating insulin resistance. A value below 1.0 is considered optimal. Early detection enables low-carb and intermittent fasting interventions that can reverse insulin resistance before permanent beta-cell damage occurs.

Mechanism

When carbohydrates are consumed, blood glucose rises. Insulin is secreted to move glucose into cells. If the diet is chronically high in sugar and refined carbs, cells become resistant to insulin's signal, forcing the pancreas to produce more insulin to keep glucose normal. Over time, this compensatory hyperinsulinemia becomes toxic and leads to further resistance, eventually exhausting beta-cells. At that point, glucose levels rise to pre-diabetic and diabetic thresholds. Fasting insulin thus provides a functional stress test for the pancreas, and HOMA-IR quantifies the degree of insulin resistance by combining fasting insulin and glucose in a mathematical model.

Personal experience

I've seen this in practice for a long time. These people coming in, they do not look healthy... but they come in with their blood values that are normal. ... The most missing test, or the test that is the most important that doctors should be doing, is a fasting insulin test.

This hormone right here will be elevated 15 to 20 years before your glucose starts to be elevated.

Also said
“What is the normal level of fasting insulin? There is no agreed-upon number, okay? So, I'm just going to give you my two cents on this, based on a lot of research that I've done on this. You want your fasting level of insulin to be between two and six.”— Provides the target range and notes the lack of consensus.
“HOMA-IR is basically telling you how glucose and insulin are working together.”— Explains the purpose of the HOMA-IR metric in simple terms.

dawn-phenomenon-management

WhatIf you have high fasting blood glucose in the morning (dawn phenomenon), adopt a low-carbohydrate diet combined with intermittent fasting and take a long morning walk to burn off the excess glucose; persist until morning readings normalize.
WhenUpon waking with elevated blood sugar, and continue as a daily practice until the pattern resolves (typically several months).
DoseLow-carb diet + intermittent fasting (e.g., 16:8) daily; morning walk for immediate glucose disposal. Continue until fasting glucose is normal upon waking.
For whomIndividuals with insulin resistance, pre-diabetes, or type 2 diabetes who experience high morning blood glucose despite not having eaten.
WhyDawn phenomenon is often driven by excessive liver glucose output due to insulin resistance and/or high morning cortisol. Reducing carbohydrate intake lowers insulin demand, reverses hepatic insulin resistance, and decreases endogenous glucose production.
CaveatsRequires patience and consistency; occasional higher readings early in the process are possible as the body adjusts. If cortisol is the primary driver, stress management may also be needed.

Berg explains that many people with insulin resistance see high morning blood sugar and wonder why, since they didn't eat carbohydrates the night before. He says that in severe insulin resistance, up to 80% of blood glucose can come from the liver's own production. The solution is to address the root cause: carbohydrate intake. By cutting carbs and implementing intermittent fasting, the liver's sensitivity to insulin improves, and the inappropriate gluconeogenesis subsides. He suggests monitoring morning blood sugar and staying the course until it normalizes. He also mentions that a morning walk is a practical tool to bring down the immediate high glucose while the dietary changes take effect.

Mechanism

In insulin resistance, the liver's insulin signaling is impaired, causing it to overproduce glucose through gluconeogenesis (making glucose from non-carbohydrate precursors) even when blood sugar is already high. Additionally, a morning cortisol surge normally raises blood glucose to provide energy for waking, but in dysregulated states this can be excessive. A low-carb diet reduces the liver's glycogen stores and lowers circulating insulin, gradually restoring insulin sensitivity in the liver. Intermittent fasting extends the fasting window, giving insulin levels time to fall and the liver time to reset. A morning walk uses circulating glucose for muscle fuel, acutely lowering blood sugar.

Even if you take a diabetic who has severe insulin resistance, 80% of their blood sugar is coming from their liver making a lot of glucose.

Also said
“I would recommend if you have this is you want to get rid of the thing that created in the first place, which is eating too many carbohydrates. If you start going on a low-carb diet, and you start reducing the need for this insulin, you are going to eventually correct this in relatively short period of time, several months.”— Causal intervention logic and timeline.
“You just want to stick with it, keep doing it until eventually you wake up in the morning, you check your blood sugar, and it's normal. Couple other things you could do, you can go for a long walk in the morning to walk off and burn off that sugar.”— Practical daily actions and encouragement.

crp-testing-and-anti-inflammatory-protocol

WhatTest C-reactive protein (CRP) as a marker of systemic inflammation. Aim for a level below 1 mg/L. If elevated, adopt an anti-inflammatory diet (avoid seed oils, sugar, refined carbs, junk food), lose visceral fat, prioritize sleep, and add omega-3 fats (such as cod liver oil).
WhenAs part of cardiovascular risk assessment or when concerned about chronic inflammation.
DoseCRP target: <1 mg/L (ideally close to zero). Dietary changes and lifestyle improvements are ongoing; omega-3 supplement per product guidelines.
For whomAnyone with visceral adiposity, poor diet, sleep issues, or known inflammatory conditions; particularly useful for those told their CRP is 'fine' at 2-3.
WhyA CRP level of 1.5–2 mg/L, often considered 'normal' by labs (cutoff 3), indicates low-grade inflammation that contributes to cardiometabolic disease. Reducing inflammation through diet and lifestyle lowers disease risk.
CaveatsSome doctors may dismiss intermediate CRP values as normal; optimal is much lower. CRP can also be transiently elevated by acute illness, so repeat testing may be needed.

Berg states that so many people are inflamed and that average CRP is not healthy. He disagrees with doctors who say below 3 is fine, arguing that even 1.8 is a low-grade inflammatory state that should be addressed. The interventions he recommends are broad lifestyle changes centered on removing inflammatory triggers and adding anti-inflammatory nutrients. He specifically mentions cod liver oil as a preferred omega-3 source. He frames this as part of a larger pattern where 'normal' does not mean 'healthy.'

Mechanism

CRP is an acute-phase protein produced by the liver in response to interleukin-6, reflecting systemic inflammation. Chronic low-grade inflammation is driven by factors like seed oils (high omega-6), refined carbohydrates, excess visceral fat (which secretes pro-inflammatory cytokines), and poor sleep. Omega-3 fatty acids (EPA/DHA) are precursors to anti-inflammatory resolvins and protectins, competing with pro-inflammatory mediators.

If your CRP is between like 1.5 or 2, like let's just say an average of 1.8, that's not good, okay? You don't want that. That is a low-grade inflammatory state.

Also said
“Avoid seed oils, avoid sugar, refined carbohydrates, junk food. Focus on getting rid of your visceral fat. Make sure you sleep better. These are all things that will greatly improve this in addition to omega-3 fats, which is a natural anti-inflammatory. I like cod liver oil.”— Specific actionable items and a supplement recommendation.

advanced-lipid-profile-for-ldl-particle-size

WhatObtain a specialized lipid profile that differentiates LDL particle size into Pattern A (large, buoyant) and Pattern B (small, dense) rather than relying solely on total LDL cholesterol.
WhenWhen evaluating cardiovascular risk, particularly if total cholesterol or LDL-C is elevated, if you follow a low-carb diet, or if there is a family history of heart disease.
DoseOne-time test to establish particle type; can be repeated to monitor response to dietary changes.
For whomIndividuals on low-carb or ketogenic diets who see elevated LDL; anyone with high LDL-C who wants a more nuanced risk assessment.
WhyLDL particle size determines pathogenicity: Pattern A is non-atherogenic and common on low-carb, while Pattern B is atherogenic and driven by high carbohydrate intake. Standard lipid panels cannot distinguish them, leading to misclassification of risk.
CaveatsNot all laboratories offer this test; it may need to be ordered as NMR lipoprofile or apolipoprotein B/LDL-P. A low-carb diet often raises total LDL but is typically Pattern A, which is not a cause for concern.

Berg emphasizes that the confusion around LDL arises because cholesterol is essential (the body makes it) and LDL is simply a delivery vehicle. The real issue is particle quality. He notes that people on a low-carb diet often see cholesterol levels rise because they are mobilizing fat for fuel, and the lipids in transit show up in blood work. A standard test may then alarm them or their doctor unnecessarily. The specialized test reveals whether the LDL is the benign Pattern A or the dangerous Pattern B. He also mentions that he has created a simplified video to help understand this topic, underscoring how muddled the public narrative is. His message: don't panic about high cholesterol; find out what kind of LDL you have.

Mechanism

LDL particles carry cholesterol to peripheral tissues. Large buoyant particles (Pattern A) are too big to penetrate the arterial intima and are efficiently cleared. Small dense particles (Pattern B) result from increased triglyceride content and are more susceptible to oxidation, can more easily enter the artery wall, and promote plaque formation. Carbohydrate intake, particularly fructose, stimulates hepatic de novo lipogenesis and increases production of small dense LDL. In contrast, low-carb diets decrease triglycerides and shift LDL to the larger, less harmful phenotype.

Pattern A is the large buoyant LDL. This is the one that is usually associated with people on a low-carb diet. This is usually the one that's non-pathogenic because the size of these particles are big and they're floating and they're not invading the arteries... On the other hand, the pattern B LDL is the small dense particle size, which can invade the arteries and is associated with more inflammation.

Also said
“Just because you have high cholesterol does not mean it's a problem, especially if you are on a low-carb diet because people that are on a low-carb diet, they eat more fat. They're mobilizing more fat. You're going to actually see more cholesterol in the body.”— Contextualizes why low-carb dieters see higher cholesterol without necessarily higher risk.
“The way that you get more of this [Pattern A] is you go low-carb. The way that you get more of this [Pattern B] is you eat more carbohydrates.”— Direct dietary determinant of particle type.

vitamin-d-status-via-parathyroid-hormone

WhatTest serum 25-hydroxyvitamin D together with parathyroid hormone (PTH). If vitamin D is in the 'normal' range but PTH is high, suspect vitamin D resistance and treat as functional deficiency. Aim for vitamin D levels of 50–70 ng/mL.
WhenWhen evaluating vitamin D status, especially if symptoms of deficiency (bone pain, frequent illness, fatigue) persist despite 'normal' vitamin D levels.
DoseTarget serum vitamin D: 50–70 ng/mL (higher for therapeutic goals). Adjust supplementation to bring PTH into normal range.
For whomAnyone with suspected vitamin D deficiency, autoimmune conditions, or those told their vitamin D is adequate but still symptomatic.
WhyStandard vitamin D tests measure the inactive form in blood and miss cellular Vitamin D resistance. Elevated PTH indicates that active vitamin D is insufficient to maintain calcium homeostasis, revealing a tissue-level deficiency.
CaveatsPTH can be influenced by other factors (calcium intake, kidney function). This is an indirect inference, not a direct measure of cellular vitamin D activity. Some doctors may be unfamiliar with the concept of vitamin D resistance.

Berg calls vitamin D resistance something that 'a lot of even doctors don't know.' He explains that if someone's vitamin D is, say, 30 ng/mL (often labeled sufficient) yet PTH is elevated, the body is essentially compensating for a lack of active vitamin D. He advises aiming for levels of 50–70 ng/mL and notes that the 20 ng/mL threshold is 'ridiculously too low,' based only on rickets prevention. He also brings up the RDA miscalculation where the actual requirement to hit 20 ng/mL is nearly 9,000 IU, not 600 IU, and that many doctors wrongly deem moderate doses toxic. He mentions having created 284 videos on vitamin D, signaling deep expertise on the subject.

Mechanism

Vitamin D from sun or supplements is first hydroxylated in the liver to 25-hydroxyvitamin D (the form measured in blood), then converted in the kidney to the active hormone 1,25-dihydroxyvitamin D. This active form binds to the vitamin D receptor (VDR) in cells to regulate calcium absorption and immune function. In vitamin D resistance, VDR signaling is impaired or conversion is inadequate, leading to functional deficiency despite normal 25-hydroxyvitamin D. Low active vitamin D reduces intestinal calcium absorption; the parathyroid glands sense this and increase PTH secretion to maintain serum calcium. Thus, a high PTH can be a surrogate marker for functional vitamin D insufficiency.

If you check your vitamin D levels and if it's normal, and then your parathyroid is high, you can kind of indirectly deduce that I'm probably not getting enough vitamin D, so this parathyroid hormone is compensating.

Also said
“A very high percentage of the population has what's called vitamin D resistance. Their blood levels look normal, but they're actually very deficient.”— Establishes the prevalence of the hidden problem.
“And this 20 ng per ml for vitamin D is ridiculously too low. I would recommend at least 50 to 70.”— Specific target range recommendation.

cortisol-assessment-via-saliva-or-hrv

WhatAssess cortisol dynamics either with a 4-point saliva cortisol test (morning, noon, evening, middle of night) or by tracking Heart Rate Variability (HRV) using a wearable device as a less invasive proxy for stress balance.
WhenWhen evaluating suspected HPA-axis dysfunction, chronic stress, fatigue, or sleep disorders, especially if a single morning blood cortisol was normal.
DoseSaliva test: collection at four specific times across 24 hours. HRV: daily or nightly readings from a watch, chest band, or ring; monitor trends over time.
For whomPeople with symptoms of adrenal fatigue, burnout, anxiety, poor sleep, or those who want to track stress objectively.
WhyCortisol follows a circadian wave; a single blood draw cannot capture a flattened curve, elevated nighttime levels, or other dysrhythmias. HRV offers a convenient ongoing measure of autonomic balance linked to stress.
CaveatsSaliva collection requires waking in the middle of the night, which can be disruptive. HRV is an indirect measure and influenced by factors like exercise, alcohol, and illness; it provides a trend, not a direct cortisol value.

Berg points out that the standard blood cortisol test is a snapshot that misses the full picture. The saliva test, though a bit of a hassle, gives the full curve and is the gold standard for non-invasive ambulatory cortisol assessment. He acknowledges the inconvenience of waking up in the middle of the night to collect saliva, but notes that HRV technology has advanced significantly and is now widely available in consumer wearables like watches, chest straps, and rings. This provides an accessible way to monitor stress and recovery indirectly, making it a practical alternative for many people. He presents this as another case where conventional single-point testing fails to detect dysfunction.

Mechanism

Cortisol is released in a diurnal rhythm, peaking 30–45 minutes after waking and declining throughout the day. Chronic stress flattens this curve or increases nighttime cortisol. Saliva free cortisol reflects the biologically active free fraction. HRV measures the variation in time intervals between heartbeats; higher HRV indicates a healthy balance between sympathetic (fight-or-flight) and parasympathetic (rest-and-digest) branches, while low HRV correlates with chronic stress and elevated nocturnal cortisol.

The problem with testing your cortisol is cortisol is on a wave, and if you just check your blood tests with cortisol at one time of the day, you're not going to pick up the whole picture.

Also said
“A better test would be a saliva cortisol where you're checking in the morning, noon, evening, and in middle of night so you can get a full picture what's going on, but of course it's a pain in the butt because you have to get up in the middle of the night.”— Explains the ideal method and its practical drawback.
“HRV technology has come a long way. That measures the autonomic nervous system through the heartbeat.”— Introduces the easier, tech-based alternative.

specialized-mineral-testing

WhatInstead of relying on standard blood tests for potassium, magnesium, selenium, or zinc, use specialized testing methods that better reflect tissue levels, as described in the video's description links.
WhenWhen suspecting mineral deficiencies despite normal serum electrolyte or mineral panels, particularly in cases of fatigue, cramps, or other deficiency symptoms.
DoseDepends on the specific test; see provided resources.
For whomIndividuals with symptoms suggestive of mineral deficiencies who have been told their bloodwork is normal.
WhyThese minerals are predominantly intracellular or stored in tissues; blood levels represent only 1–2% of body stores and can appear normal even when tissue levels are deficient.
CaveatsSpecialized tests may not be readily available and may require working with a functional medicine practitioner; links provided in the video description.
Mechanism

Potassium, magnesium, selenium, and zinc are primarily found inside cells or bound in bone and tissue. The body tightly regulates serum concentrations for critical functions like nerve conduction, so blood levels remain stable even when total body stores are depleted. For example, magnesium is mostly intracellular; serum magnesium can be maintained by drawing from bone and soft tissue reserves, masking deficiency.

These minerals are usually not hanging out in the blood. They're deep in the tissues. And so, when you're checking the blood, you're only checking a very tiny percentage of where that mineral is, maybe like 1 to 2%.

Also said
“Even magnesium, for example, which is super important, if you check the blood and it's normal, you could actually be deficient. Because in your cells, where the majority of magnesium is, it could be lowered, but allow a little bit of it to trickle in the blood, giving you the sense that you're normal, but you're really not.”— Illustrates the paradox with a concrete example.

b12-functional-testing

WhatWhen assessing vitamin B12 status, use an MMA (methylmalonic acid) test and/or homocysteine level instead of relying solely on a standard B12 blood test, which can include inactive B12 analogues.
WhenIf symptoms of B12 deficiency (fatigue, neuropathy, cognitive issues) are present, even if serum B12 is in the 'normal' range.
DoseOne-time testing as part of a comprehensive nutritional screen.
For whomAnyone with suspected B12 deficiency, especially older adults, vegans, or those on acid-suppressing medications.
WhyThe usual B12 test measures both active and inactive forms; MMA and homocysteine are metabolic markers that become elevated when B12 is functionally insufficient, providing a more accurate picture of cellular B12 status.
CaveatsHomocysteine can also be elevated due to folate or B6 deficiency, so it is not exclusively a B12 marker. MMA is more specific.
Mechanism

B12 is a cofactor for the conversion of methylmalonyl-CoA to succinyl-CoA; without adequate active B12, methylmalonic acid accumulates. Similarly, B12 is needed for homocysteine remethylation to methionine; deficiency leads to homocysteine elevation. Standard serum B12 may detect inactive forms and miss functional deficiency.

When you check B12 in the blood, you're not just checking the active form of B12, but you're also checking part of the inactive B12. There's another test called MMA test that will pick this up better. And another good one to test this out indirectly would be to check a homocysteine.

What's new

Personal practice updates, fresh positions, predictions

5 items

normal-lab-ranges-fallacy

Mainstream 'normal' reference ranges are based on a bell curve of the current population, which is increasingly metabolically sick; therefore 'normal' often means 'average,' not healthy. Numerous diagnostic thresholds (fasting glucose, pre-diabetes, cholesterol, vitamin D RDA) have been lowered over time, instantly creating millions of new patients without any change in the underlying health of the population.

Why this matters: Challenges the assumption that a 'normal' result equals the absence of disease. Reveals that many disease definitions have been tightened in ways that may mislead people about their true risk and mask early dysfunction.

Background

Before 1997, a fasting glucose of 140 mg/dL was required for a diabetes diagnosis; after 1997, it dropped to 126 mg/dL. Before 2003, pre-diabetes was defined at 110 mg/dL; after 2003, it dropped to 100 mg/dL. Similarly, cholesterol cutoffs were lowered in the early 1980s, and the vitamin D RDA was miscalculated (600 IU instead of the 8,895 IU actually needed to maintain 20 ng/mL, an error never corrected).

Berg argues that when you picture a bell curve of the population's lab values, the 'normal' range is created by chopping off the low and high ends. But as the population gets fatter and sicker, those ranges shift upward into pathology. He states that people are told their labs are normal when they are manifestly unwell—weight issues, hair loss, skin problems—and may even be told 'it's all in your head.' The 1997 glucose threshold change reclassified 1.4 million people as diabetic overnight, and the 2003 pre-diabetes change added 41 million. Berg suggests that trend watchers who see a diabetes explosion may attribute it solely to diet, ignoring that diagnostic criteria were artificially narrowed. The vitamin D RDA error is another example of systemic inaccuracy: the calculation set the requirement at 600 IU to prevent rickets when the true amount needed to maintain a minimal level of 20 ng/mL is nearly 9,000 IU, yet many doctors still deem that dose toxic. This pattern, Berg believes, leads to widespread underdiagnosis of metabolic and nutritional problems and a false sense of security.

Personal experience

I've seen this in practice for a long time. These people coming in, they do not look healthy. A lot of weight issues, they're losing hair, they have skin issues, but they come in with their blood values that are normal.

Your labs are normal. That is probably the most dangerous phrase in modern medicine. You know why? Do you actually know what normal means? It doesn't mean you are disease-free. You are just average.

Also said
“In 1997, they changed the normal fasting glucose level. It was 140, and then overnight, they changed it to a 126 mg per deciliter. So, before 1997, you would have to reach a blood sugar level of 140 before you're diagnosed with diabetes, and then of course right at this point if you just had 126 you're a diabetic. Overnight, 1.4 million people were diagnosed with diabetes.”— Shows the scale of definition-driven diagnosis changes.
“When they calculated the RDAs, they made an error, which they never corrected. Even now, they have never corrected this error. Because when they did this evaluation, they said it was 600. In reality, the true numbers that you need every day to keep your levels at 20 and prevent rickets is 8,895 international units.”— Highlights the persistent vitamin D RDA error as another example of flawed 'normal' standards.

fasting-insulin-blind-spot

Fasting insulin is rarely tested in routine blood work, yet it becomes elevated 15–20 years before blood glucose rises. Standard glucose testing creates a massive blind spot, labeling people as healthy while their pancreas is under extreme stress.

Why this matters: Exposes a critical gap in standard metabolic screening. Most doctors rely on fasting glucose and A1C, missing the long pre-diabetic window where insulin is chronically high and insulin resistance is developing.

Background

Conventionally, diabetes risk is assessed through fasting glucose and A1C. Insulin is not part of standard panels. Berg asserts that even when insulin is measured, many labs set the 'normal' upper limit at 12 μIU/mL, which he considers clearly pathological.

Berg explains that insulin's job is to clear glucose from the blood, and the body normally keeps only about one teaspoon of sugar in the entire bloodstream. The average person consumes 50–100 teaspoons of sugar per day, forcing the pancreas to work overtime. As long as insulin can push glucose into cells, fasting glucose stays normal, masking the underlying problem. Eventually cells become resistant to insulin's signal, the pancreas compensates by producing even more, and only after years or decades does the beta-cell burnout cause glucose to rise to pre-diabetic and diabetic levels. A fasting insulin test, along with the HOMA-IR calculation (which combines fasting insulin and glucose), can detect insulin resistance long before glucose becomes abnormal. Berg recommends a fasting insulin target of 2–6 μIU/mL, with concern starting at 8 and high risk at 10–12. He laments that many doctors label an insulin of 12 as 'normal,' missing the opportunity for early intervention.

Personal experience

I've seen this in practice for a long time. These people coming in, they do not look healthy. ... they come in with their blood values that are normal. ... The most missing test, or the test that is the most important that doctors should be doing, is a fasting insulin test.

This hormone right here will be elevated 15 to 20 years before your glucose starts to be elevated.

Also said
“You can have perfect blood glucose levels, but have such a major problem with insulin, which is actually made by your pancreas. And literally, your pancreas is screaming at you, but glucose is normal.”— Vivid imagery conveying the disconnect between glucose and insulin status.
“What is the normal level of fasting insulin? There is no agreed-upon number, okay? So, I'm just going to give you my two cents on this, based on a lot of research that I've done on this. You want your fasting level of insulin to be between two and six.”— Provides specific, contrarian target ranges.

vitamin-d-resistance

A high percentage of the population has vitamin D resistance: their blood levels of 25-hydroxyvitamin D appear normal, but they are functionally deficient because the vitamin is not entering cells or converting to its active form. This can be detected indirectly by a high parathyroid hormone (PTH) level.

Why this matters: Challenges the widespread 'normal vitamin D' dictum by introducing the concept of cellular resistance, analogous to insulin resistance. It also gives a practical diagnostic workaround using PTH.

Background

Standard medical practice checks serum 25-hydroxyvitamin D and considers 20–30 ng/mL sufficient. Berg argues that this only reflects the inactive circulating form and that 20 ng/mL represents severe deficiency.

Berg states that many people with symptoms of vitamin D deficiency—bone pain, immune dysfunction, fatigue—are told their levels are normal. This happens because the blood test does not capture what is happening inside cells, where the active form of vitamin D works. Vitamin D resistance means that despite adequate blood levels, cells do not respond adequately, possibly due to receptor dysfunction or insufficient conversion. The parathyroid gland is sensitive to calcium and vitamin D status; when active vitamin D is low, PTH rises to maintain calcium levels. Therefore, if a person's vitamin D blood test is normal but PTH is high, one can deduce that vitamin D is not working effectively at the tissue level. Berg recommends aiming for serum levels of 50–70 ng/mL, and even higher if using vitamin D therapeutically. He notes that the often-cited 'sufficient' level of 20 ng/mL was set only to prevent rickets, not to support optimal health, and that the RDA for intake is drastically underestimated.

Here's what a lot of even doctors don't know. A very high percentage of the population has what's called vitamin D resistance. Their blood levels look normal, but they're actually very deficient.

Also said
“If you check your vitamin D levels and if it's normal, and then your parathyroid is high, you can kind of indirectly deduce that I'm probably not getting enough vitamin D, so this parathyroid hormone is compensating.”— Provides the specific diagnostic clue.
“And this 20 ng per ml for vitamin D is ridiculously too low. I would recommend at least 50 to 70, but if you're trying to therapeutically fix something, you want it even higher than that.”— Gives the speaker's target range.

ldl-particle-size-distinction

LDL is not a single 'bad' cholesterol entity. It comes in two patterns: Pattern A (large, buoyant, non-pathogenic, typically increased on low-carb diets) and Pattern B (small, dense, atherogenic, associated with high-carb intake). Only advanced lipid profiles can differentiate them.

Why this matters: Corrects the common oversimplification that high LDL = high risk. This is especially relevant for individuals on low-carb diets who may see elevated LDL and be inappropriately advised to stop their diet.

Background

Most cholesterol panels report total LDL-C, which does not distinguish particle size. Conventional wisdom often labels all LDL as 'bad cholesterol.' Berg emphasizes that cholesterol is a vital substance the body produces and that its carrier, LDL, is not inherently harmful.

Berg explains that cholesterol does not float freely in blood; it is packaged in lipoproteins. LDL carries cholesterol to tissues. There are two main types of LDL particles: Pattern A are large, fluffy, and do not penetrate the arterial wall, so they are considered non-pathogenic. Pattern B particles are small and dense, can invade the endothelium, and are linked to inflammation and heart disease. He states that people on a low-carb diet tend to have more Pattern A because they mobilize fat and cholesterol for energy, and this is not a cause for alarm. People eating more carbohydrates are more likely to have Pattern B. Thus, a high LDL on a standard test may be harmless or dangerous depending on particle size. Berg recommends getting a specialized lipid profile that measures LDL particle size and number to make informed decisions, and he has created a dedicated video to simplify the topic.

Pattern A is the large buoyant LDL. This is the one that is usually associated with people on a low-carb diet. This is usually the one that's non-pathogenic because the size of these particles are big and they're floating and they're not invading the arteries... On the other hand, the pattern B LDL is the small dense particle size, which can invade the arteries and is associated with more inflammation and more problem with heart disease, and it's more pathogenic.

Also said
“LDL is the number one most confused part of this cholesterol story because there's actually two different types of LDL. And by the way, most people think LDL is bad cholesterol, but it's not. It's something your body makes to deliver cholesterol into the tissues.”— Sets up the foundational misconception before detailing particle types.
“Just because you have high cholesterol does not mean it's a problem, especially if you are on a low-carb diet because people that are on a low-carb diet, they eat more fat. They're mobilizing more fat. You're going to actually see more cholesterol in the body.”— Addresses the low-carb diet context directly.

cortisol-testing-inadequacy

A single blood draw for cortisol misses the hormone's circadian wave. Saliva cortisol testing four times per day (morning, noon, evening, middle of night) or heart rate variability (HRV) monitoring provides a truer picture of adrenal function and stress status.

Why this matters: Explains why many people with HPA-axis dysfunction are told their cortisol is normal when a snapshot test is used, and offers accessible alternatives like HRV wearables.

Background

Cortisol is typically measured in morning blood tests, but its secretion follows a diurnal rhythm. A one-point measurement cannot capture a flattened curve, elevated nighttime values, or other dysregulations.

Berg points out that cortisol is on a wave and that checking it at one time of day misses the full picture. He recommends a saliva test that captures the curve at four key time points, though he acknowledges the inconvenience of waking up in the middle of the night to collect a sample. As a more practical alternative, he highlights HRV technology, which measures the balance between sympathetic and parasympathetic activity through heartbeat intervals. HRV devices (watches, chest bands, rings) have become more accessible and can indirectly indicate chronic stress patterns. He suggests that this method can be a useful proxy for adrenal function without the hassle of nighttime saliva collection.

The problem with testing your cortisol is cortisol is on a wave, and if you just check your blood tests with cortisol at one time of the day, you're not going to pick up the whole picture.

Also said
“A better test would be a saliva cortisol where you're checking in the morning, noon, evening, and in middle of night so you can get a full picture what's going on, but of course it's a pain in the butt because you have to get up in the middle of the night.”— Shows practical trade-off of the gold-standard saliva test.
“HRV technology has come a long way. That measures the autonomic nervous system through the heartbeat.”— Introduces the easier alternative.

Recommendations

Products, supplements, and tools mentioned in the episode

1 item

Cod liver oil (omega-3 fatty acids)

Supplement

Referenced as a natural anti-inflammatory source of omega-3 fats to help lower CRP and improve inflammatory markers.

Personal experience

I like cod liver oil.

I like cod liver oil.

Find Cod
Disclosed sponsorships2speaker disclosed

Dr. Berg supplements (Amazon search)

Product Sponsored · disclosed

Berg briefly mentions his supplement line when asked about supplement recommendations, directing viewers to Amazon for more information.

DisclosureSpeaker states he has his own high-quality supplement line and suggests searching 'Dr. Berg supplements' on Amazon, asserting he is not biased.

Now, of course, I'm not biased with my own high-quality supplement line. But if you go to Amazon and type Dr. Berg supplements, you'll find more information.

Find Dr.

Eric Berg's LDL explanation video

Tool Sponsored · disclosed

After explaining pattern A vs pattern B LDL, Berg directs viewers to a dedicated video he made to fully clarify the complexity.

DisclosureSelf-promotion: speaker created the video to simplify the understanding of LDL particle size.

I've done 284 videos on this topic. Now that you know this basic information, I highly recommend you watch my video on this LDL to get all the details to really fully understand this because this is where so many people are confused... So I created a video to make it very, very simple right here. Check it out.

Find Eric

Notable quotes

Lines worth pulling out — contrarian, specific, or perfectly phrased

6 items
Your labs are normal. That is probably the most dangerous phrase in modern medicine.
Sets the contrarian tone and encapsulates the central thesis that 'normal' is a dangerous illusion.
You can have perfect blood glucose levels, but have such a major problem with insulin, which is actually made by your pancreas. And literally, your pancreas is screaming at you, but glucose is normal.
Vividly illustrates the silent progression of insulin resistance and the folly of relying on glucose alone.
If you have a vitamin D level of 20 ng/mL, that is a severe deficiency.
Starkly contradicts standard clinical guidelines that label 20 ng/mL as sufficient, advocating for much higher targets.
Just because you have high cholesterol does not mean it's a problem, especially if you are on a low-carb diet.
Challenges the widespread demonization of cholesterol, particularly relevant for those on low-carb or keto diets.
Even if you take a diabetic who has severe insulin resistance, 80% of their blood sugar is coming from their liver making a lot of glucose.
Reframes the source of high blood sugar in diabetes, emphasizing that the liver, not just dietary sugar, is a major contributor.
The most missing test, or the test that is the most important that doctors should be doing, is a fasting insulin test.
Directly identifies the biggest blind spot in routine medical screening, with a call to action.

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Topics covered

normal-lab-rangesfasting-insulininsulin-resistancehoma-ira1cdawn-phenomenonmineral-deficiency-testingb12-testingcrp-inflammationldl-particle-sizecortisol-testingvitamin-d-resistancelow-carb-dietintermittent-fastingcholesterol-mythsblood-sugar-monitoring
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Educational summary of the cited expert source — not medical advice. Open the source recording linked above and consult a qualified physician before acting on any protocol.