Why A1C Isn't Enough: Insights from Dr. Ben Bikman with Dr. Ken Berry

Summary

The transcript discusses the importance of understanding insulin, particularly endogenous insulin produced by the pancreas, in managing type 2 diabetes. It challenges the misconception that beta cells fail in type 2 diabetes, emphasizing that insulin resistance and high insulin levels are often overlooked. The conversation also delves into the limitations of A1C as a diabetes indicator, the potential for diet-induced changes in red blood cell lifespan affecting A1C readings, and the role of fructose in glycation and uric acid production, highlighting the need for a more comprehensive approach to assessing metabolic health.

Takeaways

• 💉 The speaker emphasizes the importance of understanding endogenous insulin, which is produced by the pancreas, as opposed to exogenous insulin, which is administered to diabetic patients.
• 🔍 There's a misconception among many primary care practitioners that in type 2 diabetes, beta cells burn out and stop producing insulin as the disease progresses, which the speaker refutes.
• 📉 The speaker argues that even when insulin production decreases in type 2 diabetes, it remains higher than the initial levels before metabolic issues arose.
• ⚠️ The conventional focus on glucose levels in diabetes management overlooks the significance of insulin levels, which can be a more sensitive and early indicator of metabolic health.
• 🩺 The speaker advocates for measuring fasting insulin levels early in a patient's metabolic assessment and suggests that levels below 6 micro units per milliliter indicate insulin sensitivity.
• 🚫 There's criticism of the clinical norm that considers any fasting insulin level below 25 as normal, which the speaker believes represents severe hyperinsulinemia.
• 📚 The speaker promotes the use of the oral glucose tolerance test, which provides more detailed information than the A1C test, despite the latter being more commonly used.
• ⏳ The A1C test measures glycation, which is not solely a result of hyperglycemia but also influenced by the lifespan of red blood cells, potentially leading to false readings.
• 🍽️ A shift towards a carnivore diet may lead to longer-lived red blood cells, which could falsely elevate A1C levels, despite improved metabolic health.
• 📈 The speaker suggests using fructosamine tests or monitoring uric acid levels as alternative indicators of glycation in patients with potentially skewed A1C results due to diet changes.

Q & A

What is the main focus of the discussion in the transcript?

The main focus of the discussion is the importance of understanding endogenous insulin production by the pancreas, its role in type 2 diabetes, and the misconceptions in mainstream medical practice regarding insulin and glucose metabolism.

Why does the speaker believe that primary care practitioners are often oblivious to the insulin produced by the pancreas?

The speaker believes that primary care practitioners are often oblivious to the insulin produced by the pancreas because their training and focus are primarily on managing glucose levels and administering exogenous insulin, rather than understanding the intricacies of endogenous insulin production and its impact on health.

What is the speaker's bold statement regarding beta cells in type 2 diabetes?

The speaker's bold statement is that in type 2 diabetes, beta cells never completely disappear. Instead, insulin production may decrease due to insulin resistance, but it is still higher than before the onset of metabolic issues.

Why does the speaker argue against the common treatment approach of pushing insulin levels higher to lower glucose in type 2 diabetics?

The speaker argues against this approach because it can lead to increased insulin resistance and does not improve outcomes. The more insulin that is given, the higher the risk of mortality in type 2 diabetics.

What does the speaker suggest as a more effective clinical marker than fasting glucose for assessing insulin resistance?

The speaker suggests that fasting insulin levels are a more effective clinical marker than fasting glucose for assessing insulin resistance, as it provides an insulin-centric view of metabolic health.

What fasting insulin levels does the speaker consider to indicate insulin sensitivity or resistance?

The speaker considers fasting insulin levels of six micro units per milliliter or less to be a very good sign of insulin sensitivity, while levels in the high teens to 20s indicate compromised health due to insulin resistance.

Why does the speaker criticize the reliance on A1C as a primary marker for metabolic health?

The speaker criticizes the reliance on A1C because it can be falsely elevated or decreased due to factors affecting red blood cell lifespan, not just glucose levels. This can lead to misdiagnoses and an incomplete understanding of a patient's metabolic health.

What alternative test does the speaker recommend for patients who follow a carnivore diet and have slightly elevated A1C levels?

The speaker recommends a fructosamine test for patients on a carnivore diet with slightly elevated A1C levels, as it measures glucose glycation without being influenced by red blood cell lifespan.

Why is there no clinical test available to measure fructose glycation, according to the speaker?

The speaker indicates that there is no clinical test available to measure fructose glycation, which is a significant oversight since fructose is more reactive than glucose and can lead to increased glycation and inflammation.

What role do ketones play in mitigating the inflammation caused by uric acid, as discussed in the transcript?

Ketones are discussed as having anti-inflammatory properties that can counteract the pro-inflammatory effects of uric acid, potentially explaining why some individuals on a ketogenic diet may have elevated uric acid levels but improved metabolic and inflammatory markers.

Outlines

00:00

🧬 The Misunderstanding of Insulin in Medical Practice

The speaker begins by reflecting on the evolution of their understanding of insulin from primarily knowing about exogenous insulin to focusing on endogenous insulin produced by the pancreas. They express concern that primary care practitioners are largely ignorant about the role of endogenous insulin in type 2 diabetes, commonly but incorrectly believing that beta cells fail and stop producing insulin as the disease progresses. The speaker challenges this notion, asserting that beta cells are not typically depleted in type 2 diabetes and that insulin resistance and production levels are more complex than commonly taught.

05:00

📊 Rethinking Insulin Measurement in Diabetes Management

The speaker advocates for the measurement of fasting insulin levels as a critical yet overlooked aspect of diabetes management. They argue that conventional clinical practice often prioritizes glucose levels over insulin, leading to ineffective treatment strategies. The speaker provides a range for fasting insulin levels, suggesting that levels below 6 micro units per milliliter indicate insulin sensitivity, while levels in the high teens to 20s may indicate a problem. They also criticize the broad 'normal' range provided by major diagnostic labs, which they believe reflects a misunderstanding of insulin resistance.

10:00

🩸 The Complexities of Hemoglobin A1C Testing

The speaker discusses the Hemoglobin A1C (HbA1C) test, which measures the degree of glycation of hemoglobin in red blood cells, and its limitations. They explain that glycation is a chemical process that can affect various parts of the body, not just hemoglobin. The speaker points out that factors affecting red blood cell lifespan can lead to falsely high or low A1C readings, independent of actual glucose levels. They also lament the decline of the oral glucose tolerance test, which they believe provides more detailed information about an individual's metabolic health.

15:02

🍖 The Impact of Diet on Red Blood Cell Lifespan and A1C Levels

The speaker explores the impact of diet, specifically a carnivore diet, on red blood cell lifespan and A1C levels. They hypothesize that a diet focused on animal-sourced foods may lead to longer-lived red blood cells, potentially skewing A1C readings. They also discuss the role of iron, vitamin B12, and omega-3 fats in red blood cell health and how deficiencies can affect A1C levels. The speaker recommends the fructosamine test as a more accurate reflection of glycation for individuals following a carnivore diet.

20:04

🚫 The Overlooked Dangers of Fructose Glycation

The speaker raises concerns about the lack of clinical tests for fructose glycation, a process more reactive than glucose glycation and potentially more harmful. They discuss the ubiquity of fructose in modern diets and the potential for this to lead to widespread but undetected glycation damage. The speaker emphasizes the need for greater awareness among healthcare providers about the risks of fructose and the limitations of current testing methods.

25:05

📈 Uric Acid as a Surrogate Marker for Fructose Metabolism

The speaker discusses uric acid as a potential surrogate marker for fructose-induced glycation, given the absence of direct tests for fructosamine or fructose glycation. They explain the link between fructose metabolism and uric acid production and how this can impact inflammation and insulin resistance. The speaker also delves into the paradoxical effects of uric acid and ketones on inflammation, suggesting that ketones may counteract the pro-inflammatory effects of uric acid, leading to improved metabolic health despite elevated uric acid levels.

Keywords

💡Insulin

Insulin is a hormone produced by the pancreas that regulates blood sugar levels by allowing glucose to enter cells to be used for energy. In the video, the distinction is made between exogenous insulin, which is insulin administered as a treatment for diabetes, and endogenous insulin, which is naturally produced by the body. The speaker emphasizes the importance of understanding endogenous insulin and its role in type 2 diabetes, challenging the common misconception that beta cells 'burn out' in type 2 diabetes.

💡Beta Cells

Beta cells are a type of cell found in the islets of Langerhans in the pancreas, responsible for producing and secreting insulin. The script discusses the common misunderstanding that in type 2 diabetes, beta cells fail and stop producing insulin, which the speaker argues is not the case, and that beta cells are not 'gone' even in advanced stages of the disease.

💡Type 2 Diabetes

Type 2 diabetes is a chronic condition that affects the way the body processes blood sugar (glucose). The video script focuses on the misconceptions surrounding the progression of type 2 diabetes, particularly regarding insulin production and the role of beta cells. The speaker asserts that type 2 diabetes is often mismanaged by focusing on glucose levels rather than insulin resistance.

💡Insulin Resistance

Insulin resistance is a condition in which the body's cells do not respond properly to the hormone insulin, leading to high blood sugar levels. The script explains that insulin resistance is a critical factor in type 2 diabetes, and that the conventional focus on glucose levels can obscure the importance of addressing insulin resistance.

💡Fasting Insulin Levels

Fasting insulin levels refer to the amount of insulin in the blood after an overnight fast. The speaker in the video advocates for the measurement of fasting insulin levels as a key clinical marker for assessing insulin resistance and metabolic health, arguing that current standards for what is considered 'normal' may be too high.

💡Hemoglobin A1c (A1C)

Hemoglobin A1c, or A1C, is a blood test that measures the average blood sugar levels over the past 2 to 3 months. It reflects the degree of glycation, or binding of glucose to hemoglobin. The script discusses the limitations of A1C as a diagnostic tool, as it can be falsely elevated or decreased due to factors that affect red blood cell lifespan.

💡Glycation

Glycation is a chemical reaction between sugar molecules and proteins, lipids, or other sugars, resulting in the formation of new compounds known as advanced glycation end products (AGEs). The video explains that glycation is not limited to hemoglobin but can occur throughout the body, affecting various tissues and contributing to conditions like atherosclerosis and premature aging.

💡Oral Glucose Tolerance Test

The oral glucose tolerance test (OGTT) is a diagnostic test for diabetes that involves measuring blood sugar levels before and at intervals after consuming a glucose-rich beverage. The speaker in the video laments the decline in use of the OGTT, suggesting it provides more detailed information about glucose metabolism than the A1C test.

💡Fructosamine

Fructosamine is a blood test that measures the amount of glucose that has bound to proteins in the blood, reflecting short-term blood sugar control. The script mentions fructosamine as an alternative test to A1C for assessing glycation, especially in cases where red blood cell lifespan might skew A1C results.

💡Uric Acid

Uric acid is a waste product that results from the breakdown of purines, and its levels in the blood can be an indicator of various metabolic conditions. The video discusses uric acid as a surrogate marker for fructose metabolism and its potential role in insulin resistance and inflammation, particularly in the context of ketogenic diets.

💡Ketones

Ketones are molecules that the body produces as a byproduct of fat metabolism when glucose is not available. The script highlights the anti-inflammatory properties of ketones, suggesting they may counteract the pro-inflammatory effects of uric acid, which is particularly relevant for individuals following ketogenic diets.

Highlights

Insulin understanding has shifted from exogenous to a focus on endogenous insulin and its importance in type 2 diabetes.

Mainstream medicine often overlooks the role of endogenous insulin produced by the pancreas in type 2 diabetes management.

A common misconception is that beta cells burn out in type 2 diabetes, but in reality, they do not completely disappear.

Insulin resistance and production levels vary among individuals, and insulin levels remain high even when production starts to decline.

The conventional focus on glucose levels neglects the importance of insulin as a sensitive and early marker in diabetes.

Increasing insulin dosage in type 2 diabetics does not improve outcomes and can increase mortality.

The importance of measuring fasting insulin levels early in a patient's metabolic health assessment.

Fasting insulin levels can indicate insulin sensitivity, with levels below 6 µU/mL being very good.

High fasting insulin levels (high teens to 20s) can signal compromised metabolic health.

The need for clinicians to measure insulin levels as a clinical marker for better diabetes management.

LabCorp and Quest consider fasting insulin levels below 25 µU/mL as normal, which may not be accurate.

A1C test has limitations and can be falsely elevated or decreased due to factors affecting red blood cell lifespan.

The oral glucose tolerance test provides more detailed information than A1C but is less commonly used.

Glycation is a broader process affecting all cells in the body, not just hemoglobin in red blood cells.

Uric acid levels can serve as a proxy for fructose-induced glycation, which is not directly measurable.

Ketones have anti-inflammatory properties that can counteract the inflammation caused by uric acid.

The paradox of elevated uric acid levels alongside improved metabolic and inflammatory markers on a ketogenic diet.

Transcripts

e

I want to start talking first with you

about

insulin uh in the first few years of my

medical practice I definitely knew what

insulin was 99% of my understanding was

exogenous insulin and how to give that

to people with diabetes uh but

increasingly over the past few years all

I care about all I want to focus on and

study about is endogenous insulin the

that's produced by the beta cells in the

human pancreas and how important that is

and how under underestimated and and not

even underestimated by the mainstream uh

primary care practitioner but just com

they're completely oblivious to the

insulin that's produced by the pancreas

indeed I think if you lined up 100

practicing Primary Care Providers and

you ask them what happens to U the beta

cells in a person with type 2 diabetes I

think that the at least 70% of them

would say well as your type two diabetes

gets worse the the beta cells burn out

and they stop producing insulin and

that's why most people with type two

diabetes when the disease gets bad

enough they have to go on uh insulin

injections walk us through how this

is not true the vast majority of the

time yeah yeah in fact I would even be

more bold and bold enough indeed to say

that if it is if it is actually type two

diabetes and that's an important

distinction because there is the kind of

rare coincidence where someone with type

two actually develops true type one but

it's not a consequence of the type two

diabetes that is just a bizarre

Confluence of events that wherein this

person has had this later in life

autoimmune disease namely type one so my

bold statement is in type two diabetes

there will never be a situation in which

the beta cells are gone it is true that

in some instances insulin production has

been going up for years in this

individual and and then eventually the

body becomes so resistant to its own

insulin that the glucose starts to come

up and then in some people so that's a

reflection of the insulin resistance but

in some individuals the insulin

production will start to go down not all

some just have have a straight line and

the insulin is as high as ever sometimes

the insulin will come down a little

which further amplifies the glucose but

even when the insulin starts to come

down it is still much higher than it was

before they ever started on this descent

into metabolic derangement uh it's still

multiples higher than it was before but

all of this is just a reflection of how

the conventionally trained clinician has

been taught to focus on the glucose at

the expense of the much more sensitive

much earlier marker namely the insulin

if we had trained these clinicians to

have an insulin Centric view of type 2

diabetes in particular then we wouldn't

say let's lower that glucose at all

costs even if we have to push the

insulin up even higher which is a very

common course of treatment and yet it

doesn't work to help improve any outcome

the more you give the type two diabetic

more insulin the more they die

absolutely and do you believe that every

clinician should be trained by some

Society or organization to check fasting

insulin levels very very early in their

patients metabolic career so to speak

and if so what do you what would you

consider an insulin level that's too

high yeah in fact indeed Ken that is the

drum I beat louder than any other if I

can end my career um with having

realized one single outcome namely that

insulin becomes a more commonly measured

clinical marker than I will have

considered my career a success frankly

um so that is absolutely the drum I beat

the loudest and it's difficult to get a

firm cut off now I'm going to give them

anyway but I want people to know that

insulin like almost every hormone in the

body does have a little bit of Rhythm to

it and it has a little play and and so

while I'm going to give some hard cut

offs please everyone know that it's

possible to kind of be outside of this

and it be a bit of a false indicator now

having said that if someone has a fasted

insulin that is six micro units per Mill

or less that's a very very good sign

that they're insulin sensitive if

someone has uh fasting insulin that goes

from seven to about the mid teens let's

say seven to 17 just to kind of create a

nice range there that's a possible

problem now I emphasize possible because

it's it is possible that someone comes

in and gets a fasted insulin measurement

and it's at 11 but that just happened to

be the high point in their natural

little rhythm and in fact in most of the

time they're down around three or four

so that's why I say that's a bit of a

warning range but then if it's High

Teens into the 20s that's generally

going outside the natural oscillation of

insulin and then the score starts to get

a little compromised now please pardon

the Shameless plug in my newest book how

not to get sick that's this book right

here I actually give a bunch of clinical

tests and have people create a bit of a

an Al an amalgamation of all of these

numbers to really come to a firm

understanding of their own insulin

resistance but fasting insulin is the

first one I talk about because it is the

one that I think is the most overlooked

for the value that it provides oh I

totally agree and you know lab core and

Quest the two largest diagnostic labs in

the United States uh both have a any any

fasting insulin that's less than 25 they

consider that normal

isn't that remarkable and and to me

that's severe hyperinsulinemia if you're

that's just further evidence that the

average American because those those

blood those blood um C offs those ranges

are provided based on kind of national

averages yes that to me is just further

evidence of the problem that the average

American is so insulin resistant that we

think anything up to the mid-20s is

normal that's not normal I totally agree

let's let's talk about A1 C uh this is a

and again this if I ask that same 100

Physicians you've got a 40y old patient

who's slightly overweight their blood

pressure is a little high uh but their

fasting blood glucose is normal or just

a tiny bit elevated should you check an

A1C on that patient I think that at

least 40 if not 50% of those Primary

Care Providers would say no I don't

think it's worth the money uh let's talk

about the A1C test what it checks what

can falsely Elevate or falsely decrease

it and is there another test that we

should be considering if your A1C seems

to be falsely High yeah in fact let me

start with that last point because there

there are a group of there have been

several biomedic scientists that have

bemoaned the shift in clinical practice

um to focus on A1C given its its

challenges which which I'll elaborate on

in a moment but but boning it

particularly because with the rise of

A1C came the death of the oral glucose

tolerance test that used to be a more

commonly used clinical intervention but

you know it's a little timec consuming

which means it's more financially it's

more costly um there's a little more

Nuance into its interpretation but it

gives far more detail than the A1C gives

for reasons that I'll get into in just a

second but by way of brief background

it's helpful for people just to

appreciate that glycation is this

chemical process that is uh a function

of a reducing sugar irreversibly non

non-enzymatically so it doesn't need an

enzyme to do it it doesn't need

something to kind of mediate the two and

bring them together it's just this

reducing sugar glucose fructose

galactose even other molecules that you

wouldn't think of um can fit into this

where they will irreversibly bind to a

protein or DNA um or a lipid and create

this glycation end product now

importantly and this in fact is somewhat

driven from a conversation that Ken and

I have had just recently that term

glycation can even be invoked with other

reducing sugar so it's important for

people to know that that term is

sometimes used as an all-encompassing

term even though as we'll get into not

all tests will measure all of that but

it's important for people to realize

that as much as we focus on hba1c or

hemoglobin

A1c this is in fact itself a reflection

of

of glycation that can be happening

everywhere it's just not easy to measure

glycation in the kidney which is going

to be increasing the risk of kidney

failure or it's not easy to measure the

degree of glycation in the blood vessels

which is a very telling feature for

atherosclerosis or the the synthesis or

the beginning of an atherosclerotic

plaque so as much as we just want to

look at hba1c as some marker of glucose

in the blood we should also appreciate

that it can potentially be a sign of

glycation that's happening everywhere

even skin collagen causing wrinkles and

premature aging of the skin all of these

things can be impacted by glycation so

it helps us appreciate hba1c which if we

just drill right down to it is US

measuring the degree to which we've had

this irreversible glycation binding to

the functional part of the red blood

cell and very briefly within the red

blood cell we have this comp complicated

protein structure called hemoglobin

hemoglobin's most famous job is to carry

oxygen and at the same time to carry

some other gases even like carbon

dioxide albeit to lesser degrees one

immediate effect at the red blood cell

is that the more it is glycated the less

suitable it is now to carry oxygen so

one immediate consequence of this is the

person's reduced ability to move oxygen

potentially creating conditions of

hypoxia or compromised oxygen movement

through the body now this of course

becomes a particular problem in a

diabetic and someone who's chronically

hypoglycemic they not only have the the

the glycation of the blood vessels

damaging blood vessels but to compound

that they also have the blood itself not

carrying oxygen as well so no wonder

they develop such poor wounds and and

sort of Decay flesh because the blood

isn't flowing very well so it's

important for people to appreciate that

what glycation is and how the hb1c is a

reflection of a greater wholebody

phenomenon but then kenu

mentioned where it can be sort of

misdiagnosed or misunderstood it is so

important for people to realize the the

the problem with hba1c namely that while

we always focus on hba1c as a

consequence of hyperglycemia we need to

remember that there's another part of of

this formula that when we're measuring

hba1c as much as we say it's a marker of

gly of glucose and glycation we could

also say someone could equally make the

argument that no it's actually uh a

result of how long lived the red blood

cells are because a red blood cell that

lives longer that has gone beyond its

120 average days of life it just becomes

more likely that it will experience some

degree of glycation that's not the red

blood cell's fault it's not even

glucose's fault it's just the longer it

has lived the more likely it is to have

undergone some degree of glycation thus

you could have someone who has very

long-lived red blood cells has very

normal glucose and yet the their A1C is

high it's a false positive it's a false

sign of glucose and that's more a

function of the red blood cell living

long in contrast you could have someone

who has very short-lived red blood cells

perhaps because they're iron deficient

or they vit Vin B12 deficient alol yeah

yeah right yes so they a disease where

the red blood cells have a very short

life they turn over much more rapidly in

this case the red blood cells are never

around long enough to even undergo

glycation even if a person's fasting

glucose levels are high and they're

struggling with hypoglycemia so in this

case it's a false negative where the A1C

looks normal but in fact there is a

glucose problem it's just that the

fragility of that person's red blood

cells mask it you don't see it so people

we have to appreciate that while AWC has

value while it can be a sign of

glycation occurring elsewhere in the

body it also can't be taken as the

gospel Truth where it is the endall

marker of metabolic Health like you

started the conversation with we have

become so obsessed with A1C that we

refuse to acknowledge its flaws yeah and

any good doctors should know the list of

things that can shorten the life of a

red blood cell and give you a falsely

low A1C they should also know the list

of things that can cause your red blood

cells to live longer and thus give you a

falsely high A1C but I I can just tell

you from personal experience the vast

majority of Primary Health Care

Providers they might know about

alcoholism but that's that's literally

the extent of their knowledge about what

could give a falsely high or low A1c

uh so I have noticed a signal and that's

as a primary care doctor I look for

signal in patients right I i' change

something and then when they come back

in three or six months I'm like okay has

that made a noticeable difference in

enough people routinely enough

predictably enough that I can say okay I

need to adjust my practice based on that

uh I have seen a signal in the carnivore

Community very meat heavy meat Centric

diets where I'd say 5% five out of a 100

carnivores will notice that their a1c's

creeping back up not never to di to

diabetic levels but maybe 5.7 5.8

5.9 and many of we you and I have

discussed this before and I've discussed

this with Shawn Baker and many other

people in the carnivore Community How

likely is that that now that they're not

eating all the inflammatory hypoglycemic

Foods How likely is it that the red

blood cells are just living longer now

than 110 days which seems to be the

average it's living 120 130 140 days How

likely is that and how can we ever dig

into that and and maybe provide some

proof and some reassurance to the

carnivore Community oh yeah in fact my

whole um viewpoint on it that I just

elaborated with regards to the failure

to appreciate variables that influence

the longevity or the lifespan of a red

blood cell actually was born from this

very issue where I would hear from

carnivores where they would say hey I

don't know what's going on I reversed my

type two diabetes but yet my A1C is

creeping um it's exactly what you just

said and it was me wondering how could

the physiology fit into this that led me

to these conclusions all of which is

supported so just to kind of revisit

that I had mentioned two variables

namely iron which is a fundamental

component of hemoglobin in order to

carry the oxygen this is why someone

who's iron deficient will experience the

most common type of anemia on the planet

which is iron deficiency anemia the

number of red blood cells is fine but

the ability of the red blood cells to

carry oxygen is not because in the

absence of heem iron consumption you're

not going to have sufficient iron uh

oxygen binding capacity and then I'd

mentioned vitamin B12 once again this is

becomes relevant the further someone

gets from eating animal sourced Foods

because there is no plant version

there's no plant source of vitamin B12

and in this case it gives rise to

another one of the most common types of

anemia worldwide which is pernicious

anemia that's a fascinating physiology

to it or cell biology and I won't bore

everyone with the details that I share

when I teach this principle to my

students but basically in this scenario

the the bone marrow which is the origin

of the red blood cell it has enough

material to to prepare the the precursor

cells the cells that are going to

someday become red blood cells normally

the process is the cells will grow and

then divide grow and then then divide in

the absence of sufficient B12 because

for example the person isn't consuming

animal products or because they've had

gastric bypass and they don't have

enough of a stomach left to to absorb

the B12 so they need injections forever

but in that case the bone marrow is able

to grow the progenitor red blood cell

but not actually divide them so the

person has this kind of paradoxical

situation where the cells are big but

they're just not nearly enough and so in

this case once again the person has they

have the risk of having so few red blood

cells that it can give you know a sort

of mistaken um number here with A1C then

my last point would be the fluidity um

the ability of the red blood cell to be

as dynamic as it needs to be the red

blood cell is very unique among all

cells in the body in that while it

doesn't it has very little by way of

internal structure that enables it to

slip through incredibly tight spaces to

move in and out of sinuses and

capillaries and to do that it needs to

be very pliable and Squishy well the

more omega-3 fats you're eating the more

those fats get enriched in the membrane

of the cell allowing it to have a higher

fluidity to give it a little bit of

Squish and mean making it so that it can

fit through spaces without shattering as

opposed to other fats that start to get

enriched in that membrane which can make

it a little more rigid so for these

three reasons in addition to several

others the more a person is changing the

diet to be to quote you a proper human

diet focused on animal sourc Foods the

more those red blood cells are likely to

be more robust a little heer longer

lived and thus increasing the potential

of the individual having an artificially

inflated

A1C and in people like that in the five%

of carnivores that I'm seeing I don't

know if you're seeing a different

percentage but if they have an A1C

that's a little bit elevated and they're

like what's going on here the test I

recommend is a

fructosamine test I used to recommend a

glycated albumin but labor and Quest

both stop offering that test but the

fructosamine even though fructo is in

the name it checks only for glucose

glycation uh it looks for the the

glucose lysine Bond I think is what it

actually looks for and invariably every

time a carnivore gets a fructosamine

checked it's within normal limits uh

verifying verifying that they are not

overly glycating it's just that the red

blood cells almost certainly are living

longer because of their healthier diet

and I I want to dig into that a little

bit to my

knowledge there is no commercially

available test that a doctor can order

that checks for fructation or fructose

glycation and This concerns me because

there are many doctors out there who are

recommending to their patients eat lots

of fruits and vegetables and you know

what the patient's going to focus on the

one that taste better and the one that

they don't hate which is fruit and so

they wind up living on fruit juice

smoothies but but when you check an

A1C you don't you don't see reflected

you don't that fructose glycation and I

I want I want to reiterate a point you

said earlier which is super important

because a lot of people if you're not a

doctor or a PhD you just think oh well

glucose just glyc hates hemoglobin right

in the red blood cell that's that's what

it does that's the bad thing that it

does but Professor bman was very clear

it glyc hates every cell in your body

the cells in the nefron of the kidney

the cells in your heart your cardio

myocytes literally every cell in your

body is also being glycated we just use

the glycation of the hemoglobin molecule

the A1C as a proxy marker for all this

other dangerous glycation that's going

on in the human body do you know of a

test that a doctor can order because I

don't know of one that checks for

fructose gly or even when it comes to

drinking milk galactose gation because I

do not know of a test no no I don't

either um in fact I love in fact this

was something that as you and I have

communicated this you you opened my eyes

to this um so so we know that fructose

is much more reactive than glucose which

makes this part of the conversation all

the more relevant as much as we focus on

glucose and and rightly so fructose is

known to elicit the these reactive

reactions that's a little redundant

these glycation reactions again that

being a broad term to refer to any

reducing sugar binding irreversibly

these molecules it seven times more than

glucose so to make sayate that again

because it was a bit awkwardly delivered

fructose can induce glycation seven

times more readily than glucose can and

and thus I think it is uh much more

relevant but no no all the more tragic

this fact is made this is a this is a

non

enzymatic glycation this is does not

require an enzyme this is not a pathway

this is just a function of basically how

much fructose is in your bloodstream the

the higher the level the more the

glycation is going to be is that correct

there's no there's no clinical test to

answer the question no unfortunately

there's no way to do it so basically

people who are living on fruit juice

smoothies are eating hundreds of grams

of carbohydrates in fruit or fruit juice

per day there's currently all Healthcare

providers are blind to the fructose

glycation you cannot detect it yeah

that's right in fact I would say can at

the risk just to give some answer if

perhaps the closest a person could come

to understanding their fructation or the

degree of fructose induced glycation it

would probably be uric acid just as a

surrogate marker because uric acid just

runs so tightly with fructose metabolism

which itself of course is a product of

fructose consumption so yeah probably

the closest we can get is getting a uric

acid marker I I agree with you I think

uric acid is a a fairly good rough proxy

marker for the degree of fructation uh

what else do people need to know about

uric acid levels and how they how they

give us insight into our own metabolism

yeah yeah in fact what a timely question

because what if if what I was doing

literally one hour ago was working on a

manuscript that we are preparing to

publish this is something I've alluded

to over the past year or so it's finally

come to fruition and we're going to

submit it for publication the joys of

being a publishing scientist is the

frustration of trying to then get your

work published but I do it for the

students because these are all

student-led projects and I want them to

have that experience and then have that

help them get onto their next part of

their lives and career so what we found

was so so briefly uric acid um and and

my friend and even collabor on this

project Dr Rick Johnson has really been

the champion I was unaware I'll confess

of the effects of of FR of uric acid let

alone the involvement of fructose until

I read his work and became familiar with

him and it's been one of the great joys

of my life professionally to get to know

him better and now consider him a friend

he's a wonderful gentleman scientist

great guy he was really the one who

highlighted that every time your cell is

metabolizing a molecule of fructose it's

giving birth to a molecule of uric acid

which makes it far more relevant to uric

acid production than any amount of meat

or fish consumption which is an idea

that just continues to really fail you

see in the highest meat consuming

populations on the planet like Hong Kong

and Argentina their their uric acid

levels are are nothing they're

absolutely bottomed out and so let's we

just have to kind of drop this idea that

it's Meat and Fish that's contributing

to uric acid no it's fructose look at

those societies that are eating a lot of

fructose or a lot of sugar or drinking a

lot of fruit juice then you'll see the

uric acid then uric acid itself can have

Myriad consequences including what Rick

has outlined namely stimulating hunger

what I have focused on and back to the

paper we're publishing is looking at how

uric acid is a contributor to insulin

resistance however I consider a

secondary cause because it happens

through its increase in inflammation

uric acid is known to be an activator of

inflammation now what we're studying is

to try to reconcile the the Paradox that

some people notice on a ketogenic diet

which is twofold on one hand they may

notice that in some people the uric acid

levels stay high or even go up a little

second their inflammatory markers have

absolutely dropped so they much less

inflammation and indeed much greater

improvements in insulin sensitivity as

evidenced by their resolution of type

two diabetes this shouldn't be happening

given Uric acid's involvement however

what we are publishing so this is early

data here um so unpublished results at

the moment is that ketones are are

sufficient to wipe out the inflammation

caused by uric acid so ketones are known

to be anti-inflammatory molecules so

this is another instance whereby ketones

have gone beyond their simple caloric

value ketones have a caloric value

roughly compar able to glucose which is

good news for all the cells that want to

use the ketones as energy but at the

same time ketones act as a signaling

molecule and in this case controlling

literally inhibiting inflammation so

whereas uric acid levels are trying to

stimulate this kind of metabolic

inflammation ketones are inhibiting it

and that might help us reconcile how we

could have a situation where a person

has stubbornly elevated uric acid and

yet every metabolic and indeed

inflammatory marker has improved it's

because there's a lot else going on

including the contribution of the

ketones to directly antagonize the

pro-inflammatory effects of the uric

acid