#1 Absolute First Sign That Your Liver is Dying
It's not just going up; it is going up exponentially. This epidemic of fatty
liver disease is parallel to the epidemic of obesity and type 2 diabetes that is spreading
all around the world. If you remove those factors, especially if you remove most or
all of them at the same time for a period of time, the body starts to reverse the adaptation.
Hello, Health Champion. Today we're going to talk about the number one, absolute first sign
that your liver is dying. When we say dying, we're talking about the beginning stages where
the liver is moving toward some sort of stress, dysfunction, and degeneration. The reason we're
looking for the absolute first sign is that many of the traditional signs are actually quite late.
When we talk about things like jaundice, abdominal pain, and swelling of the feet,
legs, or ankles, when we talk about nausea and several other signs and symptoms as well,
we're talking about something that happens quite late. You have to have substantial
damage to the liver and significant reduction in liver function before any of those show up.
Instead of the traditional signs, we want to start understanding this a little bit
differently. We want to understand what is the absolute first sign.
To start understanding that, we need to know what the most common liver disease
is because there are many different things that can happen. You can have infections,
you can have cirrhosis, but the number one thing that happens is called nonalcoholic
fatty liver disease. The reason they call it that is that traditionally, historically,
only alcoholics—people who drank severe, high amounts of alcohol—would get a fatty
liver. Then they found that most people who got a fatty liver didn't drink alcohol
or didn't drink excessively. So now they call it nonalcoholic fatty liver disease,
but of course, it's not a great description to call something by what it isn't. Recently, they've
also started calling it MAFLD, which stands for metabolic-associated fatty liver disease.
My guess is that you probably have no idea how prevalent this is. I don't
think anyone takes this seriously enough because around 35%, more than
one-third of the entire adult population in the world, have fatty liver disease.
I have a question for you: do you think that number, that rate, is going up, going down,
or staying about the same? Unfortunately, the answer is it's not just going up;
it is going up exponentially. It's an epidemic of proportions that we have never,
ever seen and that we just can't quite grasp. In terms of healthcare costs, this is probably going
to account for the majority of healthcare or sick care expenses worldwide very shortly. Already,
there are about 1.9 billion people, more than a third of the adult population in the world,
who have this fatty liver disease. Even at that astronomical, unfathomable number, it may still
be a low estimate because this is something that's very rarely checked. There is a biopsy
you can do to check it, but that's very invasive and not entirely safe. There is an ultrasound,
which isn't very specific or exact. What we do know is that this epidemic of fatty
liver disease is parallel to the epidemic of obesity and type 2 diabetes spreading worldwide.
What we have to understand about type 2 diabetes is that it is a modern disease. It's not an
infection. It's not a purely genetic thing, even though there is a genetic predisposition
toward it. Type 2 diabetes virtually did not exist 200 years ago. There may have been a handful of
cases around the world, but nobody paid attention because it was so rare. As it started developing
and increasing, we thought of it for the longest time, in the last 50 years or so, as a primarily
Western problem, something that happened to Western industrialized nations such as the
US. The US was the first, in the 1970s and 80s, to have this exponential trend of obesity and type 2
diabetes. Typically, diabetes will run a few years behind obesity, but that differs a little between
cultures. Just to illustrate how global this problem is, the US might have been the first, but
they are no longer even in the top 10 of the large countries in the world. We have countries like
Pakistan at over 30% diabetes, Kuwait at about 25%, Egypt at over 20%, Malaysia at 19%, Sudan at
about the same, Saudi Arabia at 18.7%, and Mexico at 16.9%. This is not limited to one continent or
a few countries anymore; it is truly worldwide. On this list, I've only included some of the bigger
countries, those with at least 10 million or so in population. However, many other smaller countries
are also affected, with higher rates than some of these, especially among tropical islands.
I want to mention these separately because it's interesting that places like French Polynesia
have over 25% diabetes, Northern Mariana Islands at 23.4%, New Caledonia and Malaysia are about
the same, Marshall Islands at 23%, Mauritius and Kiribati over 22%, and American Samoa at 20.3%
type 2 diabetes. What these tropical islands have in common is a warm climate. Traditionally, they
would have had a good amount of tropical sweet fruit and would have lived off these islands,
doing a lot of fishing. They would have had some coconuts and other plants plus a good
amount of fruit. These people are probably genetically adapted to eating quite a bit of
sugar and high carbohydrate. Yet, just in the last 20-30 years, they have developed
extremely high rates of type 2 diabetes and obesity. What's the difference? Historically,
they ate real food, even if it included some fruit and other carbohydrates. Now, with the
addition of white sugar, processed sugar, white bread, cereals, and processed foods, these are
the insults that tip the scale. It's not that you can't eat a little bit of fruit if you're healthy,
or a good amount of fruit if you're healthy, but you can't eat it in addition to these processed,
high-carb foods. If you have developed type 2 diabetes, you have essentially broken the
body's carbohydrate-processing machine. You are carbohydrate intolerant, and now you have
to pull way, way back on all carbohydrates, all sugar, and all fruit to start reversing this.
The only direct way to measure a fatty liver is with a biopsy, where they cut out a little piece
and measure it. However, it's not a great idea because it's very invasive, and there are some
risks involved, so most people should not go that route. You could get an ultrasound,
which is an approximation and not all that expensive, so it's doable. There's one more good
approximation, a really good indication called the fatty liver index. All you do is take your BMI,
which is your body mass index—basically just how tall you are and how much you weigh—and put
that into a formula. Then you measure your waist circumference, how big your waist is. You plug
in a liver enzyme from your blood test, a very basic marker included in just about every blood
test called GGT. You also measure triglycerides, which are a strong marker of insulin resistance,
indicating how much fat is floating around in your blood at any given time. This is very easy to do;
there are calculators online that you can check out (after this video, of course, so you don't
miss any part of this understanding). You plug the numbers in, and you get a number back between
zero and 100. If it's less than 30, it's very unlikely that you have fatty liver disease;
you can basically rule it out. The lower your number,
the less likely you have fatty liver. If the number comes back between 30 and 60,
it's inconclusive. You'd probably want to follow up with an ultrasound or other
markers to help you understand if you have a fatty liver. You're kind of in the gray zone
here. If the number comes back over 60, it is very likely that you have fatty liver disease.
Now, we want to understand a little bit more about this. When we look at
the four variables you put in, we need to understand that insulin resistance is the
strongest driving factor for all of this. It's pretty much singularly responsible
for driving these. I've talked about this in many videos: obesity, type 2 diabetes,
high triglycerides—all have to do with insulin resistance. Type 2 diabetes is just the end stage,
the fully progressed version of insulin resistance. If you've watched some videos,
you understand that insulin resistance is merely an adaptation. We put the body under
a certain stress, have a certain lifestyle, provide conditions of high stress, high sugar,
white flour, seed oils, high carbohydrate, high processed foods. We overwhelm the metabolic
machinery of the body, and it starts adapting; it becomes insulin-resistant. If you remove those
factors, especially most or all of them at the same time for a period of time, the body starts
to reverse the adaptation. If you read some of the comments below this video, you'll find hundreds of
comments over time where people talk about how they did just that. They took out the sugar,
the carbs, and the processed foods, and started eating more real food—more meat, more leafy
greens, more eggs, more non-starchy vegetables. All these markers and indicators reversed.
If all these are markers of a fatty liver, and insulin resistance drives these markers, the next
step is to understand the early insulin resistance markers on a blood test. You'll find most of
these on almost any test. Unfortunately, the most important one is hardly ever on there, which we'll
talk about. The first thing to measure is blood glucose. I've never seen a blood test without
it. The problem is blood glucose fluctuates a lot, depending on the time of day or your stress level.
The better marker is called A1C (hemoglobin A1C), a 3 to 4-month average of what your blood glucose
is. It's an estimate but a fairly reliable one. Then we look at some inflammatory and metabolic
markers. If we take total cholesterol and divide by HDL cholesterol, if we have high insulin and
chronic low-grade inflammation, total cholesterol tends to go up, and HDL tends to go down. If
this ratio is high, it's an indicator of insulin resistance. The same holds true for triglycerides
divided by HDL. We have some liver enzymes you get on almost all blood tests. GGT might be something
you have to ask for, but ALT is on every other blood test I've seen. These are liver enzymes
inside metabolically functioning liver cells. These enzymes are not supposed to be in the
bloodstream. The amounts they measure come from liver cells that break and spill their enzymes
into the bloodstream. A small amount is normal because we always have a certain cell turnover.
When too many cells break simultaneously, these levels go up, indicating liver stress.
That being said, you could have a fatty liver where the cells are not sick enough or stressed
enough to start breaking yet, so you could have a fatty liver without these numbers being elevated.
Triglycerides are a strong indicator of insulin resistance because insulin resistance is when
your cells resist sugar and fat—they've had too much fuel already. Triglycerides are simply fat
in the blood, fuel trying to get to the cell. If the cell is resisting, the triglycerides stay in
the blood. The best marker for insulin resistance is insulin, unfortunately,
hardly ever measured. I've measured it on every blood test for the last 10 years on all my
patients because it's such a good basic marker to start understanding metabolic health. Yet,
I have patients who tell me they ask their doctor, and they flatly refuse; they laugh, they ridicule
it. This means nobody understands what it does, what it tells us, and I'll show you in a second.
Insulin and C-peptides are equivalent markers, two ways of measuring almost
the same thing. Insulin is the easier and usually slightly cheaper marker to measure.
C-peptide you can measure if you're trying to troubleshoot and get more information around
type 1 diabetes or another condition. There's one more thing called HOMA-IR,
not a marker but a calculation. It stands for homeostatic model assessment of insulin
resistance. You plug in glucose, multiplied by insulin, to see how much blood sugar rises and
how hard the body is working to keep it down. If you measure glucose in mg/dL, divide by
405. If you measure in mmol/L, divide by 22.5. An ideal number would be around 1, indicating
high insulin sensitivity. As it goes up, you're becoming more insulin resistant.
Here's how we understand this: if you have good metabolic health and this much blood glucose,
if your cells are not resisting the fuel, it should take a moderate amount of insulin to
keep that under control. If you start eating more sugar and processed foods, and 5 years later,
the glucose is still about the same, it's because it's a controlled variable. The body
compensates and works hard, but it takes more insulin to maintain the same blood glucose.
You're becoming more insulin resistant. If you continue for several years, the glucose
might go from 90 to 98, barely noticeable, but insulin has increased even more. This is why
it's useless to simply measure blood glucose or A1C because they're controlled variables,
not reflecting where you are on this spectrum. For example, an HOMA-IR of 1 could be 2.5 or 4,
indicating increasing insulin resistance. Even with slightly higher blood glucose, you might
still be called diabetic at 126, with very high insulin, and an HOMA-IR of 6 or 8.
Understanding this helps in avoiding sick care and practicing prevention. If you want to avoid
a fatty liver, you need to understand what causes it and recognize the early
signs. The earliest, most subtle sign is that your insulin and HOMA-IR are increasing.
Measuring the right markers early helps catch the process while it's still easy to reverse.
For more detail, I've created a blood work course for a bigger picture and better understanding of
what's happening in the body. My clinic can also provide blood work to ensure you get the right
markers. I'll put a link below where you can check that out. If you enjoyed this video, you'll love
that one. To master health by understanding how the body really works, subscribe,
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