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What is a high liver enzyme count number: Fatty Liver Disease, Cirrhosis & Symptoms


Top Causes of Elevated Liver Enzymes + How to Treat High AST and ALT

Elevated liver enzymes may act as a warning that something is damaging your liver and should never be ignored. 

Learn what causes elevated liver enzymes, what symptoms you may present with and more importantly how to treat this problem…


Liver Enzyme Made Easy (AST & ALT)

What are liver enzymes and what do they mean? 

In the most simple sense liver enzymes is used to represent a series of test that can help to determine if your liver is functioning appropriately. 

The standard “liver function tests” include: 

  • Alanine Transaminase (or ALT for short): ALT is produced in the liver cells known as hepatocytes and is a very specific marker of liver cell damage.
  • Aspartate Transaminase (or AST for short): AST is not quite as specific as ALT for liver damage as it is also found in skeletal muscle, heart muscle, and kidney tissue. AST tends to rise with ALT if liver damage is present. 
  • Alkaline Phosphatase (or ALP for short): ALP is produced by the cells lining the bile ducts or the “plumbing” of the liver. A rise in ALT is commonly seen in conditions that caused blocked “ducts” such as bile stones or direct damage to the bile ducts. 
  • Gamma-glutamyl transferase (or GGT for short): GGT is found in liver, kidney, pancreatic and intestinal tissues. If GGT is elevated along with ALP this is highly indicative of an obstruction in the plumbing of the liver or may indicate gallbladder disease. 

If you are dealing with “elevated liver enzymes” you most likely have an issue with AST and ALT. 

While ALP and GGT are still important to assess what is happening in the liver most physicians refer to AST and ALT as the “liver enzymes”. 

So what do liver enzymes tell us?

Liver enzymes help us determine if there is damage to the cells of the liver or direct damage to the liver tissue itself.  

If damage is present in the liver then it will react by releasing these special enzymes (AST and ALT) into the bloodstream as the cells become “leaky”. 

So if you are dealing with an elevation in liver enzymes that is an indication that there is some sort of damage occurring in your liver. 

And this is obviously less than ideal. 

Your liver is considered a vital organ (meaning you can’t live without it) and it helps to detoxify chemicals you come into contact with, break down supplements/medications, red blood cell production, hormone production and plays a critical role in protein synthesis and biochemical reactions. 

These reactions are critical to everyday life which is why you can’t live without your liver. 

In addition, we have no way to create “synthetic” livers in the event that you have permanently damaged your liver. 

So it’s in your best interest to keep yours healthy. 

For the purposes of this article, we want to focus on the most common causes of elevated liver enzymes so that you can determine what is causing the problem and then prevent long-term and permanent damage.  

When we talk about an “elevation” in AST and ALT we really need to define what we are talking about, what kind of numbers you should be worried about and how to address them. 

The “Rise” in Liver Enzymes

There are two basic types of elevated liver enzymes:

The first is a slight or subtle increase in AST and ALT which and the second is a massive increase in AST and ALT. 

We are going to focus on the slight or subtle increase in AST and ALT (levels less than 100-300 times normal)  because this usually indicates a chronic condition that results in low-grade inflammation and damage to the liver over time. 

Massively elevated AST and ALT (levels greater than 10x the normal reference range) usually indicates an acute life-threatening condition such as liver failure from medication overdose, physical trauma to the liver or massive organ failure. 

While massive elevations in liver enzymes are obviously important, the subtle increase is more relevant to most people because they can do something about it.  

So what does it mean to have elevated liver enzymes?

Most laboratory reference ranges include a “range” of values to indicate that you are “normal”. 

If you go outside (or too high) this range then you are considered to have elevated liver enzymes. 

The standard range largely depends on the laboratory but in general, is somewhere around 0-45 IU/l for ALT and 0-30 IU/l for AST. 

If your AST and ALT are higher than the 45 and 35 then they are said to be “elevated”.

And this is a big issue because by definition that means that you are experiencing some sort of liver damage. 

More important than just knowing that your liver function tests are elevated is figuring out why they are elevated, to begin with, and the picture behind their elevation. 

We will discuss the most common causes of elevated AST and ALT below (including treatment) but first, let’s talk a little bit about lab values. 

While the laboratory data shows there is a “range” for both AST and ALT you can picture the damage done to your liver on a spectrum.  

On this spectrum, the higher your AST and ALT values are the more damage that exists in the liver. 

This correlation exists to the point that you can almost define disease states based on the elevation of AST and ALT. 

For instance: 

Patients with chronic hepatitis tend to have AST and ALT levels in the 30-120 range, those with autoimmune hepatitis tend to have levels in the 100-600 range. 

Perhaps more important than these two causes is liver damage caused by a condition known as non-alcoholic fatty liver disease. 

If your liver enzymes are elevated then there is a VERY high chance the damage to your liver is actually caused by your diet and a condition known as insulin resistance. 

The elevation in AST and ALT observed in this condition tends to be mild (and may even be missed!). 

People with non-alcoholic fatty liver disease will often have a very “modest” elevation in AST and ALT, somewhere in the 30-70 range for both. 

What’s more interesting is that people with this condition tend to be completely asymptomatic, which means that this condition is really only picked up on routine screening.  

Patients with this condition often tend to also be overweight and have issues with glucose regulation. 

Once it is identified that you do indeed have elevated liver enzymes your Doctor should begin to do a workup to figure out the cause. 

Once the cause is determined then you can focus on the treatment. 

When thinking about what causes damage to the liver it’s important to focus on those conditions which are VERY common as opposed to rare conditions. 

Most Common Causes of High AST/ALT

There are MANY, MANY conditions and disease states that lead to high AST and ALT but the majority of them can be boiled down to just a few conditions. 

This list below is not all encompassing but should give you a good idea on how to get started. 

Emphasis should be put on #1 and #2 which will most likely account for the vast majority of slight elevations in AST and ALT in most people. 

The reason you should focus on these is that they are treatable and reversible.  

#1. Non-Alcoholic Fatty Liver Disease (AST and ALT levels in the 30-70 range)

This is by far the #1 cause of elevated AST and ALT in the United States with a prevalence of up to 30% (1) and it’s primarily caused by insulin resistance and almost entirely preventable!

How it happens:

As you consume sugary, especially refined sugar, your body rapidly metabolizes glucose into fats or lipids in the liver through a process known as de novo lipogenesis. 

As the influx of glucose becomes more than your body is able to handle this fat begins to get stored in the liver. 

As fat increases in the liver, it results in damage to the liver cells. 

This damage is seen in the serum (bloodstream) as an elevation in serum levels of AST and ALT. 

If the diet is not changed or if insulin resistance is not managed then this fat accumulation will eventually cause permanent and chronic damage to the liver. 

This may result in complete liver failure over time.  

It’s very important to find out if your elevated liver enzymes are caused by non-alcoholic fatty liver disease because it can be treated and damage can be prevented. 

Those with AST and ALT caused by fatty liver disease can be diagnosed by checking AST/ALT levels in conjunction with fasting glucose, Hgb A1c, serum cholesterol and by checking the BMI. 

People who have metabolic syndrome and high AST/ALT should be evaluated for diabetes and insulin resistance. 

Treating NAFLD and High AST/ALT

If you have liver damage from insulin resistance and obesity then you should be aggressive with your treatment. 

The following therapies have been shown to reduce (and even reverse) liver damage from NAFLD: 

  • Weight Loss: Losing weight has been shown to reduce AST and ALT levels and reverse liver damage. There’s a right way to lose weight and a wrong way, so focus on improving your diet and exercising more as opposed to simply restricting your calories.  
  • Medications: Certain medications such as metformin, GLP-1 agonists, SGLT-2 inhibitors and carb blockers have been shown to reverse insulin resistance help with weight loss and improve LFT’s. 
  • Dietary Intervention: Insulin resistance is often caused by over-consumption of refined sugars and carbohydrates. You can impact insulin levels by reducing the amount of sugar and refined carbohydrates you consume (2)(bread, pasta, bagels, pizza, sugary drinks, etc.). 
  • Supplements: Certain supplements have been shown to reduce inflammation and oxidative stress which is critical in the pathogenesis of NASH and NAFLD. These supplements have been shown in studies (3) to help: Vitamin E, Vitamin C, Berberine, Probiotics, Glutathione precursors (Betaine). 
  • Exercise: Exercise helps to increase insulin sensitivity and may assist with weight loss. If you have elevated liver function tests and you are overweight make sure you don’t forget the basics like exercise. 

Treatment should then be focused on managing blood sugar, dietary changes, and specific medications/supplements. 

#2. Alcoholic Liver disease (AST and ALT in the 70-700 range)

Alcoholic liver disease used to be the #1 cause of liver failure in the United States until it was taken out by non-alcoholic fatty liver disease and obesity. 

Having said that it is still an important cause of liver damage in many people. 

The liver damage caused by alcohol consumption occurs after prolonged and excessive drinking (usually years worth of damage to the liver). 

It can occur from daily drinking or episodes of binge drinking. 

Consuming 30 grams of undiluted alcohol for 10 years (4) may result in a condition known as cirrhosis (permanent liver damage). 

The mechanism of damage is similar to that of non-alcoholic fatty liver disease.  

Overconsumption of alcohol results in direct damage to liver cells and puts an increase in demand on your body. 

You can think of alcohol as a liquid carbohydrate source that must be metabolized by the liver. 

This produces chronic damage and fat accumulation in the liver much like non-alcoholic fatty liver disease.  

What’s interesting is that alcohol consumption, even in small amounts, can make existing liver conditions (such as non-alcoholic fatty liver disease) even worse. 

Because of this, it is recommended that you stop consuming alcohol if you have elevated liver enzymes – even if it is not primarily caused by alcohol consumption.

The primary treatment for alcoholic liver damage is to stop consuming alcohol, in some cases, this is enough to completely reverse the condition or at least stop further damage. 

#3. Prescription Medications (Low-grade elevation of AST/ALT)

Certain prescription medications can also cause liver damage. 


Medications must be metabolized by the body and that metabolism usually occurs in the liver.  

As your body breaks down certain medications it creates byproducts that can still remain active and some may even be toxic. 

If these metabolites are left in the body they can cause local injury to the liver or injury to other tissues. 

The perfect example is Tylenol (5).

In small doses, your liver can metabolize it without issues, but once doses become excessive Tylenol metabolites can cause serious damage to your body and even result in acute liver failure. 

In the case of Tylenol, even daily doses of 5 to 8 grams per day may lead to liver damage over time. 

This is very important to consider because Tylenol is available over the counter and commonly used for aches and pains. 

Other medications that may cause liver damage include: 

If you are taking a medication that is causing liver damage (and it isn’t necessary to take) then the treatment is to discontinue or reduce the dosage of medication. 

#4. Certain Supplements (Low-grade elevation of AST/ALT)

Even some supplements have been shown to cause acute liver damage and cause a rise in liver function tests.  

The supplements that tend to cause issues are hard to pinpoint exactly. 

Most of the information we have stems from case studies of patients who were taking very suspect types of “fat burners” and combining them with many different weight loss supplements. 

Some case studies (10) show that these type of supplements can cause acute liver damage in certain susceptible individuals. 

This shouldn’t be enough to cause alarm among most people, however. 

The people who experience these side effects tend to do so when they use poor quality supplements that likely contain actual hormones and medications in them. 

Not all supplements are regulated in the same way that the pharmaceutical industry is, which means that you can get more (or less) than what you are expecting. 

Some weight loss supplements have even been shown to contain toxic doses of actual thyroid hormone (11).

You can avoid all of these potentially dangerous side effects simply by purchasing high-quality supplements that ship from the United States (don’t purchase supplements overseas) from reputable companies and suppliers.  

Also, please avoid supplements with “too good to be true” advertising, especially in the weight loss area. 

You can read more about how to safely and correctly use supplements such as fish oil,
berberine, and CLA to augment weight loss therapies in my other guides. 

Using these types of non-gimmicky supplements can actually help with weight loss – provided they are used correctly. 

#5. Autoimmune Hepatitis (AST/ALT in the 100 to 600 range)

While autoimmune hepatitis is not as common as the other 4 listed above it’s still worth mentioning. 

Autoimmune disease is on the rise in the United States and is, therefore, a very important cause of diseases. 

The term autoimmune means exactly as it sounds – auto attack by the immune system on your body or tissues. 

In autoimmune hepatitis (12), your immune system creates antibodies that circulate in the body and target your liver as the “enemy”.  

This results in inflammation and chronic damage which can lead to irreversible damage in some cases. 

Who is at risk for developing this condition?

It turns out, like most autoimmune diseases, that women get this disease much more frequently than men. 

What causes it?

While the exact mechanism and trigger are unknown it is felt that the etiology of autoimmune hepatitis is multifactorial. 

What this means is that the disease can be “triggered” or “turned on” by certain environmental factors such as exposure to toxins or infection. 

Autoimmune diseases tend to occur in individuals with a genetic predisposition, meaning not everyone is at risk. 

#6. Viral Hepatitis & Other Viral Diseases (AST and ALT depend on the degree of the damage)

An elevation in liver function tests will prompt an immediate workup for basic viral hepatitis by your physician. 

A history of intravenous drug use, old tattoos or high-risk behavior may increase the risk that your liver damage is caused by a viral infection.  

Hepatitis B and Hepatitis C, both of which are viral infections, may lead to chronic and long-term damage to the liver. 

Hepatitis A (13) (spread via the fecal-oral route) on the other hand tends to be more acute in nature with an acute spike in AST and ALT in a short period.  

This should be compared to chronic Hepatitis B and C (14) which tend to cause a slower and more long-term elevation in liver function tests. 

But these aren’t the only viruses that cause liver damage. 

CMV and EBV (15) (both of which are very common) may also cause an acute spike in liver enzymes. 

The damage from CMV and EBV tends to be short-lived however and shouldn’t cause long-term damage. 

In addition, the rise in liver enzymes is almost always associated with other systemic symptoms such as fatigue, malaise, sore throat (in the case of EBV) and fever.   

It’s worth mentioning viral infections because they are an important cause of liver damage, but they are generally caught and treated appropriately in most patients.  

#7. Copper and Iron Overload Syndromes (AST and ALT depend on the degree of the damage)

Another sinister cause of liver damage and thus elevated liver enzymes is an overload of certain metals in the body. 

Overload syndromes such as Iron overload (also known as hemochromatosis (16)) and copper overload (also known as Wilson’s disease (17)) result in deposition of high levels of metals in specific tissues which results in damage to these tissues over time. 

While iron and copper deposit in more than just the liver, they definitely can and do cause liver damage if they are deposited there. 

The prevalence of Hemochromatosis is estimated to be around 1 in every 200 to 500 people which are fairly high. 

Generally, those people who have Hemochromatosis are often asymptomatic and the diagnosis is made by finding a slight elevation in liver function tests with abnormal serum iron levels. 

As long as it is caught early the damage can be mitigated.  

Wilson’s disease is much less common and more difficult to diagnose but still worth mentioning as it is an overload disease that can cause liver damage. 

Tips to Naturally Treat and Improve Liver Function

Regardless of the cause of liver damage in your body, there are several steps that you can take to improve liver function and perhaps impact your liver enzyme levels. 

If you aren’t sure where to start then you can consider following these guidelines. 

And remember:

The #1 cause of elevated liver enzymes in the United States is non-alcoholic fatty liver disease which is caused by obesity and insulin resistance.  

It’s also one of the most treatable causes of liver damage. 

Find the Root Cause

Whenever possible your main goal should be to find the source and cause of your elevated liver enzymes. 

Once you know the source you can direct your treatment to that specific problem. 

For example:

The root cause of non-alcoholic fatty liver disease = insulin resistance and obesity (which should be your target treatment).  

The root cause of alcoholic fatty liver disease = alcohol intake.

The root cause of iron overload syndrome = inability to get rid of iron adequate (treatment should focus on reducing oral iron intake and phlebotomy (18)). 

You should never “ignore” elevated liver enzymes because they indicate something wrong in your body!

I also recommend keeping an eye on your AST and ALT levels with a goal to try and get both to less than 20 IU/l. 

Take inventory of Supplements and Medications

Make sure you are only taking those medications and supplements that are absolutely necessary for your body. 

Supplements AND medications must be processed through the liver which can increase demand on your body. 

Some medications you may need to continue even if they are potentially causing increase demand but the same may not be true with all supplements. 

You should also try to avoid sketchy weight loss supplements or supplements that come from overseas.  

Taking supplements such as B12, a multivitamin, fish oil, etc. should not be an issue. 

Clean Up Your Diet

That means eating more fruits and vegetables!

Even if your liver issues are not caused by insulin resistance you can bet that eating excess sugar or refined carbs will definitely NOT be helping your issue. 


Once the liver is slightly damaged it becomes susceptible to other potential causes of damage. 

If you have non-alcoholic fatty liver disease you can be sure that excess alcohol consumption is NOT going to help your liver out. 

Stick to these tips:

  • Consume plenty of fresh and whole fruits and vegetables (19) (a rich source of antioxidative vitamins like B carotene and Vitamins C & E)
  • Avoid refined carbohydrates (bread, pasta, bagels, etc.)
  • Avoid refined sugars (especially sugary drinks such as flavored coffee, and sodas)
  • Avoid alcohol 100%
  • Avoid fast food
  • Consume walnuts (a rich source of a-linoleic fatty acid)

Certain Supplements

While some supplements may potentially be damaging to the liver, others may offer considerable help.  

One such supplement is Milk Thistle. 

In various studies, milk thistle has been shown to work as an antioxidant in the liver, protect the liver against genomic injury, increase hepatocyte protein synthesis and decrease the activity of tumor promoters (20).

In animal studies (21), silymarin (the active ingredient in milk thistle) has been shown to reduce liver injury caused by Tylenol, iron overload, alcohol, and other causes. 

With this in mind, milk thistle may be considered in many individuals with elevated liver enzymes. 


Abnormalities in liver function tests should never be ignored. 

If you have been identified as having an elevation in liver enzymes then you should go to work to find the root cause. 

Whenever possible address and treat this condition and try to lower your AST and ALT levels as much as possible with treatment. 

Now I want to hear from you:

Are you suffering from an elevation of AST and ALT?

Do you know why?

Leave your comments below! 

References (Click to Expand)

#1. https://www.ncbi.nlm.nih.gov/pubmed/21875310

#2. https://www.ncbi.nlm.nih.gov/pubmed/25527677

#3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2387293/

#4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321494/

#5. https://www.ncbi.nlm.nih.gov/pubmed/900673

#6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3983981/

#7. https://www.ncbi.nlm.nih.gov/pubmed/900673

#8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3897047/

#9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3940315/

#10. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076034/

#11. http://online.liebertpub.com/doi/abs/10.1089/thy.2013.0101?journalCode=thy&

#12. https://emedicine.medscape.com/article/172356-overview

#13. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC88961/

#14. https://www.ncbi.nlm.nih.gov/pubmed/21108341

#15. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2932915/

#16. https://www.ncbi.nlm.nih.gov/pubmed/23418762

#17. https://www. ncbi.nlm.nih.gov/pubmed/10470603

#18. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3149125/

#19. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4027841/

#20. https://www.ncbi.nlm.nih.gov/pubmed/9468229

#21. https://www.ncbi.nlm.nih.gov/pubmed/20564545

Canine Liver Disease: Diagnosis and Care

Canine liver disease is among the top five leading causes of
non-accidental death in dogs, and should be taken seriously. The liver is
responsible for a number of essential bodily functions. If compromised in any
way, it puts your dog’s overall health in jeopardy. Luckily, liver disease
and death can be avoided just by educating yourself about the disease and
learning what you can do to help prevent it.

Liver disease
is just a general medical term used to describe any kind of disorder or
condition affecting the liver, causing elevated blood levels of liver
enzymes. There are many different forms of liver disease. This should not be
surprising when you consider the importance and metabolic activity of the
liver. Just like the human liver, a dog’s liver removes toxins and
other hazardous things from its bloodstream. A dog’s liver is able to
function even when 80% is consumed by the disease, which is amazing. Unfortunately,
the fact that the liver can function when it’s this diseased leads to
other well developed diseases before diagnostics are eventually made, which
makes it even more important to prevent or treat as soon as possible.

Want to learn how to save on liver disease treatments? Click here

Possible Causes of Liver Disease

Some things that may cause your dog to suffer from liver
disease are:

  • Exposure to toxins such as
    lead, iron, and phosphorus
  • Skin infections throughout
    the dog’s body
  • Viral and bacterial
  • Altered blood flow to the
    liver due to heart disease or other congenital abnormality
  • Hepatitis
  • Dental cavities and other
    various dental diseases
  • Genetics – common in West
    Highland Terriers and Cocker Spaniels
  • Inbreeding
  • Drugs – even drugs prescribed
    by a veterinarian can cause liver disease if used for a prolonged period
    of time

Signs and Symptoms

Some changes that you may notice if your dog has liver
disease are:

  • Yellowing of the gums, skin,
    and eyes
  • Loss of appetite
  • increased thirst
  • Lethargy
  • Prolonged vomiting
  • Severe diarrhea
  • Orange urine and an increased
    frequency of urination
  • Behavioral change such as pacing
    and/or severe depression
  • Swollen stomach
  • Seizures – in severe cases

Want to learn how to save on liver disease treatments? Click here

Different Types of Liver Disease

1. Infectious Canine
– an acute liver infection in dogs caused by the
canine adenovirus type-1 (CAV-1). This disease is spread in the feces, urine,
blood, saliva and nasal discharge of infected dogs. It’s contracted
through the mouth or nose, where it replicates in the tonsils. The virus then
infects the liver and kidneys. The incubation period is 4 to 7 days.

Symptoms: fever, depression, loss of appetite, coughing and
a tender abdomen. Severe cases will develop bleeding disorders which can
cause hematomas to form in the mouth.

2. Leptospirosis
– an infectious disease which is passed to dogs through contact with urine
from other animals infected with leptospirosis.
Carriers of leptospirosis may be rodents, skunks,
raccoons and other infected animals, including both dogs and people.

Symptoms: weight loss, fever, loss of appetite, nausea,
vomiting, muscle or joint pain, bloody urine and uveitis
(changes in the eye).

3. Idiopathic
– not a single disease, but a group of liver
diseases causing cirrhosis. Idiopathic chronic hepatitis is an autoimmune
disorder. There is no known cause, but the immune system of the dog produces
antibodies that attack the liver, which then becomes inflamed and
progressively leads to liver failure.

Symptoms: anorexia, depression, weakness. More severe cases
may include lesions.

Diagnosing Liver Disease

Liver disease is diagnosed by various blood and urine tests,
abdominal radiographs (x-rays), and abdominal ultrasounds. In some cases a
biopsy of the liver is needed to determine the cause of the liver disease.

1. Blood Tests
– will show elevated levels of various enzymes. In addition high levels of bilirubin, an orange-yellow pigment formed in the liver
by the breakdown of hemoglobin, which is then excreted in bile will also be
present. A bile acids test will frequently appear elevated, as well as the
blood ammonia level.

2. Radiography
(x-rays) – will show if the liver is enlarged. Weight loss may also be more
apparent on the radiograph, even though abdominal fat stores might appear

3. Ultrasound
– reveals any changes in the internal anatomy of the liver, including
abnormal growths, if any. This test also helps to reveal any inflammation of
the pancreas, which could be an underlying cause of liver disease or

4. Exploratory
– usually performed when extreme symptoms appear or
diagnosis by any of the previous tests is inconclusive. This allows a biopsy
of the liver, as well as visualization of the surrounding abdominal organs
for any disorders that might be contributing to the liver disease.


Supportive care is crucial, and may even require temporary
hospitalization until all primary medications have been given, and blood
parameters return to the normal range or show continuous significant improvement.
Correction of any developed dehydration, as the result of poor appetite, will
be performed intravenously (IV), along with B-complex vitamin supplementation
to correct any nutritional deficiencies caused by the disease.

As with many medical disorders, dietary therapy is important
in the treatment of a dog with liver disease. High quality and highly
digestible carbohydrates are recommended to supply energy for your dog.
Inferior types of carbohydrates that are undigested are fermented by
intestinal bacteria, which increase the bacteria in the colon. These bacteria
then break down dietary proteins and produce extra ammonia, which is absorbed
into the body and contributes to toxicity in dogs with liver disease.
Frequent meals of high quality simple carbohydrates, such as white rice and
potatoes, are recommended. Vegetables act as a source of complex carbohydrates
and provide fiber. The fiber helps bind intestinal toxins, and promotes bowel
movements to remove these toxins from the body.

Your veterinarian will schedule regular visits during
treatment to monitor the improvement of your dog, as well as any new or
reoccurring symptoms that may have appeared. It is very important that you do
not skip any appointments with your veterinarian or fail to follow the
prescribed regimen. It may cause your dog to relapse, causing further damage
and more serious consequences.

Elevated Liver Enzymes In Your Dog? Now What?

Have you ever been confused by your dog’s blood work results?

The numbers you get from your dog’s blood tests can be baffling, and sometimes veterinarians don’t do a good job of explaining them.

A liver enzyme test can be especially difficult to understand. The letters that appear on your dog’s test results will probably include AST, ALT, ALP and GGT … but what is this alphabet soup?

If your dog’s had his labs checked recently and those tests show elevated liver enzymes, you need to understand what this means. What to do about it is another topic, but let’s take a look at the information we get from those elevated liver enzyme results.

First, what’s this vital organ’s role in your dog’s body?

What The Liver Does

The liver is one of the largest and most important organs in your dog’s body, performing about 500 daily tasks (in combination with other organs).

Here are just a few of the liver’s key activities:

1. Detox

First, the liver clears potentially toxic chemicals from both inside and outside the body, including drugs, vaccines, environmental toxins and even intestinal microbes. In order to detox, the liver needs critical antioxidant nutrients and enzymes such as glutathione (an important antioxidant molecule that helps prevent aging and chronic disease). The liver detoxifies harmful substances by a complex series of chemical reactions. The role of these various enzyme activities in the liver is to convert fat-soluble toxins to water-soluble substances. Once these substances are bio-transformed and no longer toxic, they then exit the body via urine or bile.

2. Storage

The liver is a storage unit, storing sugar as glycogen and regulating blood sugar levels. The liver also stores nutrients like iron, copper, vitamins B-12, A, D, E and K.

3. Production And Regulation

The liver is all about production, including:

  • Production of bile, which aids the digestion of fats.
  • Production of blood proteins, clotting factors and substances important to the making of red blood cells. Red blood cells, which carry oxygen around the body, are also recycled in the liver.

The liver also regulates a number of hormones and neutralizes free radicals produced during oxidation with antioxidants like vitamins C and E, as well as glutathione.

4. Nutrient Breakdown and Absorption

The liver not only breaks down nutrients from the diet, it also helps the body use those nutrients in the buildup of tissues. There is hardly a more important organ in the body and so when the AST, ALT, ALP and GGT all start to elevate, what does this mean?

Liver Enzymes

There are other liver measurements you’ll see in your dog’s blood panel, but I want to focus on the liver enzymes and what they mean.

  • AST – Aspartate transaminase (formerly SGOT or serum glutamic oxaloacetic transaminase). If your dog’s AST is elevated, it may come from the liver but this enzyme is also found in red blood cells, heart, muscle, pancreas and bile. So if your dog’s AST isn’t normal, your vet should find out what’s causing the elevation. AST is normally low in serum so should be measured along with ALT as part of a liver panel to see what’s going on.
  • ALT – Alanine aminotransferase (previously called SGPT or serum glutamic pyruvic transaminase). If it’s elevated, ALT can signify liver or hepatic alert as to liver cell death … but this enzyme also comes from the kidney as well as the intestines, so liver problems aren’t necessarily the only cause of elevated ALT, and further analysis is warranted.
  • ALP – Alkaline phosphatase is found in bone, kidney, bowel (intestines) and the placenta (if pregnant), as well as the liver. The levels of this enzyme are highest in the bone and the liver. Basic phosphatase is a homodimeric enzyme that is high in young fast growing animals, so it’s not unusual to see elevated ALP in young dogs. But whatever your dog’s age, if ALP is elevated, ask your vet to investigate the reason.
  • GGT – Gamma glutamyl transferase. This enzyme is useful for diagnosing and monitoring hepatobiliary (liver and bile) disease. GGT is the most sensitive enzymatic indicator of liver disease. If you’re concerned about your dog’s liver health make sure that your veterinarian includes GGT as a part of the panel.

I really want to emphasize the need for a GGT test. Not all veterinarians measure this enzyme but it’s a really important one, so make sure you ask for it.

Why GGT Is Important

GGT can help confirm or rule out liver problems, as well as other diseases. Liver And Bile (Hepatobiliary) Disease

  • GGT is the key liver enzyme linking lab reports to liver disease. This enzyme increases in post-hepatic biliary obstruction and can reach 5 to 30 times normal.
  • If ALP is elevated but not GGT then skeletal disease is more likely the problem, and not hepatobiliary disease.
  • Increased GGT and increased ALP often indicates hepatobiliary disease … but in rare cases there can be gammopathies (abnormal gamma gobulin levels) present that could lead to unreliable GGT results.
  • In diagnosing infectious hepatitis, GGT is less useful than the transaminase enzymes, as it rises only modestly (2 to 5 times normal).

Other Liver Problems

  • GGT is highly effective in detecting jaundice, cholangitis and cholecystitis. The rise of GGT happens earlier than other measurements and it stays high longer.


RELATED: Top Foods For Preventing Cancer In Dogs.  Fight back by reading this post.

Environmental Toxins

  • GGT is elevated with exposure to chemicals and persistent organic pollutants (POPs) so it’s a sensitive marker for environmental toxicity.
  • Elevated GGT can also indicate exposure to fungus and molds. These may be environmental or in your dog’s kibble, where mold found in corn and other grains comes in the form of dangerous mycotoxins in the food. These mycotoxins can cause liver failure and can precede cancer of the liver so it’s important to know if your dog’s been exposed.

GGT Can Help Rule Out Other Diseases

  • Patients with renal failure and skeletal or muscular diseases can actually have normal GGT levels so GGT testing can also help exclude those diagnoses.

Here’s an example of a healthy dog’s liver enzyme results, showing all enzymes including GGT well within normal ranges.

Keep in mind some of the things that might affect your dog’s liver.

What Affects The Liver

These are some of the many outside influences that can impact your dog’s liver enzyme levels.


Drugs like phenytoin and phenobarbital prescribed for seizures, as well as any other drug, including heartworm medication, can result in abnormal liver enzymes, so if your dog is on any medication your vet should always consider whether that may be the cause.

Vaccine Adjuvants

Viral infections can affect liver enzyme tests and so can the vaccines for viral diseases. In humans, the Hepatitis B vaccine induces liver damage primarily when it contains the toxic vaccine adjuvant aluminum hydroxide, the common aluminum salt adjuvant in vaccines – and found in all veterinary vaccines. The aluminum hydroxide adjuvant also triggers the motor neuron autoimmunity issues seen in Gulf War Syndrome sufferers. This syndrome has been found to be indistinguishable from the autoimmune disease ALS or Amyotrophic Lateral Sclerosis (Lou Gehrig’s disease).   This is essentially what happens in MS or multiple sclerosis, another neurodegenerative disease, and I have seen cases of this type of disease in dogs following vaccination.

Aluminum hydroxide also caused a loss of mitochondria and cell death in mouse livers exposed to low doses of the Hepatitis B vaccine. 144 genes in the mouse livers were altered in their expression only a day following vaccination. In 2002, Hepatogastroenterology reported that the Hepatitis B vaccine was associated with high risk for hepatitis, gastrointestinal disease and other liver function tests.

Endocrine Disrupting Chemicals

Other important things that can affect the liver are the EDCs or endocrine disrupting chemicals so pervasive in the environment. Hormones, pesticides and herbicides are also rampant in our water and food supply. The liver is the most important internal organ and is open 24/7/365. It’s involved in every bodily process so protecting liver health is essential. Following a natural lifestyle can help your dog avoid compromise to this vital organ that helps detoxify the body from our increasingly toxic world.

Liver Function Tests (LFTs) | HealthEngine Blog

The liver carries out numerous synthetic, excretion and detoxification functions, however only a minority of these can be measured by levels of products in the blood. Liver function tests (LFTs) measure the concentrations of various different proteins and enzymes in the blood that are either produced by liver cells or released when liver cells are damaged. Liver function tests are very common investigations carried out in people with suspected liver disease. Specific patterns of results can tell your doctor the likely type of liver disease so they can decide whether any further tests are required. Liver function tests can also help tell how severely the liver is damaged and help monitor your response to drugs and other treatments.

The procedure

The term “liver function tests” is actually a misnomer as several of the tests do not measure total liver function at all. Levels of enzymes known as aminotransferases and alkaline phosphatase are used to detect damage to liver cells and obstruction by bile (a substance produced by liver cells to help digest fats) respectively. Thus, liver tests can be divided into measures of liver function, cell injury and biliary obstruction. No single test is able to provide an overall measure of liver function. Instead the group of values measured is interpreted collectively to determine the likelihood of liver disease, possible causes and the severity of disease. Laboratory tests of liver function can also be used to monitor the progress of disease and the response to treatments. LFTs are performed after a simple blood test. The requirements for preparation differ between laboratories. Some require the patient to have fasted overnight but often no specific preparations are required. Collection of samples for LFTs follows a simple, safe and quick procedure. After checking your name and identification, a physician or trained phlebotomist (person who takes blood samples) will place a tourniquet (a tight strap) around your arm to help them identify a suitable vein, usually in front of your elbow. You may have to pump your hand a number of times to increase the blood flow to this area. After disinfecting the site with an alcohol wipe, they will insert a needle into the vein to withdraw blood. Sometimes a special butterfly apparatus is used, especially if multiple blood samples are to be collected at once. Once blood has been drawn into the required number of tubes, the needle and tourniquet will be removed. Pressure is then applied to the area to stop bleeding. Usually the whole procedure is completed in a short space of time with minimal pain or discomfort for the patient. Blood tubes are sent to the appropriate laboratory where the following values are measured. Note that different laboratories may have different cut-off values for each test as they may use different methods.

  • Total protein: Total protein should be between 63-80g/L and reflects the synthetic functions of the liver.
  • Albumin: This protein is produced only by liver cells, thus its concentration reflects liver synthetic function. Albumin stays in the blood for a long period of time so changes in its level occur only in chronic (long-standing) liver disease. Normal values for albumin are between 35-50 g/L. Other conditions can produce low levels of albumin. Malnutrition may decrease albumin as not enough protein is absorbed into the body. Kidney damage can result in loss of albumin into the urine. Low levels of albumin cause peripheral oedema, which is swelling (typically of the ankles) due to low levels of salts and proteins in the blood.
  • Bilirubin: Bilirubin is produced in the breakdown of red blood cells in the body. The liver is usually responsible for the detoxification of bilirubin and its excretion into bile. An increase in the total level of bilirubin produces the symptom known as jaundice. Jaundiced patients have yellow discolouration of their skin and the sclera (whites) of their eyes. Bilirubin is not only increased in liver disease but other conditions that cause an increased breakdown of red blood cells. Normal values for total plasma bilirubin are quoted as less than 20 umol/L.
  • Alkaline Phosphatase (ALP): This enzyme is mainly implicated in the diagnosis of biliary obstruction and is normally found in small bile tracts in the liver. There are many different types of this enzyme found in the body in the liver, bone and placenta so elevated levels may be due to a problem outside the liver such as a malignancy (cancer). A normal ALP is between 35-50 g/L.
  • Gamma Glutamyl Transpeptidase (GGT): GGT enzyme is found in certain liver cells and bile duct cells. It is also elevated in diseases that decrease or obstruct the flow of bile. Alcohol abuse, warfarin (a blood-thinner) and drugs used for epilepsy can increase GGT levels. GGT has been used to detect chronic alcohol abuse but it is increased in a range of conditions so it is not always correct. GGT should be less than 60U/L in a normal individual.
  • Alanine Amino Transferase (ALT) & Aspartate Amino Transferase (AST): Both aminotransferase enzymes are good markers of damage to liver cells that occurs in disorders such as viral hepatitis. AST is found in the liver, cardiac muscle, skeletal muscle, kidneys, brain, pancreas, lungs, leukocytes (white blood cells) and erythrocytes (red blood cells) whilst ALT is found primarily in the liver. Both enzymes are normally present at low levels in the blood so if liver cells are damaged we would expect some of the enzymes to leak into the blood and increase levels. Virtually any injury to liver cells can raise aminotransferase levels. However, the level of enzymes does not necessarily reflect how severely the liver is damaged. Reference values for ALT are less than 36U/L and for AST are less than 42U/L.
  • Ammonia: Ammonia is a by-product of protein metabolism and is produced by bacteria in the large intestine. The liver is responsible for the detoxification of ammonia by converting it to urea (a product found in urine). Sometimes ammonia levels will be measured in the blood to gain further information about liver function and the presence of encephalopathy (a condition where ammonia toxins impair brain function leading to confusion and tremors). However, ammonia blood levels correlate poorly with the above situations so measurements have their limitations. Reference values for ammonia vary widely between laboratories.

Results usually come back from the laboratory promptly (often the same day in hospital). Once the tests come back from the laboratory, any abnormalities and their meanings will be discussed with the patient.

Benefits and Risks

The benefits of liver function tests have already been alluded to. In summary these include:

  1. Detection of liver disease
  2. Determining the likely type of disease and possible causes
  3. Determining the severity or stage of disease
  4. Monitoring the response to treatment

Risks of the actual procedure are minimal. Some patients may experience bleeding or haematomas (large bruises) at the venepuncture site (where blood was taken). These are in fact more common in patients with severe liver disease as the liver is unable to produce sufficient clotting factors to stop bleeding. Fainting, dizziness and lightheadedness may also occur.


Liver function tests have various limitations and are only a small part of overall patient evaluation. Doctors will interpret the results after considering the patient as a whole, including medical history and signs and symptoms at presentation. Like many other investigations, LFTs do not always produce reliable results. They may be normal in patients with serious liver disease and abnormal in patients without liver disease or other diseases that may interfere with results. Liver tests don’t usually tell the doctor the exact type of disease but give them clues of the likely type of disease so they can do more definitive tests and investigations. For example, results suggesting damage to liver cells may trigger the physician to do tests looking for viruses in the blood that cause hepatitis. In addition, several drugs and other medical conditions can interfere with results so they may not necessarily provide the needed information. Patients may need to have the tests repeated or have different investigations performed.

Results of the Tests

Discussed below are some common patterns of liver function tests and their interpretations that may be discussed with patients. It should be noted that liver function tests can have various different values even in the same condition. They often add only small amounts of information to the final diagnosis. Large elevations of AST or ALT occur in conditions with marked damage to liver cells including viral hepatitis or drug-induced injury. In alcoholic liver disease, AST is often much more elevated than ALT. To contrast, in viral hepatitis or non-alcoholic fatty liver disease ALT is often much higher than AST. Elevated levels of both ALP and GGT are highly suggestive of obstructive disease. However, these values often aren’t able to tell the site of obstruction. ALP can also come from form bone, placenta or prostate cancer. Increased levels of GGT alone, may suggest alcohol or other drug use. Elevated bilirubin without any other abnormal LFTs occurs in conditions that break down red blood cells and in Gilbert’s syndrome. Low levels of albumin occur in chronic conditions such as cirrhosis. Sometimes results may be a mixed picture of liver damage and bile obstruction that can occur in various liver diseases. Liver function tests are only a small part of the diagnostic workup. Following interpretation of results several special tests for other markers and liver imaging may be performed to gain further information about the aetiology of liver disease. If the cause of the symptoms can be determined, treatment may be started. This may include antiviral medications to treat viruses, advice and medications to help reduce alcohol consumption, medications to protect the liver and other drugs to treat some of the symptoms of liver disease.


  1. Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison’s Principles of Internal Medicine. 15th Edition. McGraw-Hill. 2001.
  2. Longmore, Wilkinson, Rajagopalan. Oxford Handbook of Clinical Medicine. 6th Edition. Oxford University Press. 2004.

Elevated liver enzymes in senior dogs- what does it really mean?

It happens quite often that I’ll run a blood panel on a seemingly healthy senior dog, and I discover one or two liver enzymes are higher than normal. How worried should we be? Well, it depends, but here’s some general patterns.

The usual culprit is an enzyme called Alkaline Phosphatase, or Alk-Phos, or Alk-P. I commonly see this enzyme rise in older dogs that have no symptoms. The other liver enzymes always seem to be behaving – it’s just this one that’s wonky. The normal range depends on the lab your veterinarian uses, but most consider anything up to 130 or so as normal. It’s not a shock at all to see a dog have an Alk-P of 200, even 400. My old dachshund mix has had an Alk-P over 300 for the last 3 years. He’s doing great.

This enzyme drives a lot of veterinarians crazy. We need to look at the whole dog, and the severity of the increase. For starters, if the other liver enzymes are normal, the dog has not lost weight, bloodwork is otherwise perfect, many veterinarians will simply recheck the blood in a couple months. If everything else stays in line, and the Alk-P is not rapidly rising, maybe even dropping, we’ll be happy, shrug our shoulders, and say we’ll keep tabs on it.

We get worried about Alk-P when it becomes drastically high, like 800, or 1,500. Then there’s probably something going on. One possibility is a disease of the adrenal gland called cushings disease. With this disease, the adrenal glands produce too much adrenaline, making the dog start drinking lots of water (think of a dog on prednisone), possibly have hair loss, and can even develop a pot belly. (Here’s my in-depth article on cushings disease). The excess adrenaline causes an increase in Alk-P, with other liver enzymes staying the same. I can’t tell you how many second opinions I get where the veterinarian did routine blood work on a healthy dog (senior screen, pre-anesthetic for a dental, etc), found a mild-moderate increase in Alk-P, and wants to diagnose cushings. That’s not how we diagnose cushings. Again, we have to look at the whole dog. If your dog isn’t drinking a lot, or showing any other symptoms, that high Alk-P is most likely not cushings.

What else can cause an Alk-P to elevate while the other liver enzymes stay the same? Liver tumors. I’ve seen both benign and cancerous masses on the liver causes this change in the bloodwork. One patient had a tumor the size of a volleyball on her liver. She had it removed at the specialist, her Alk-P went back to normal, and she went on with life.

Guess what else can cause an increase in this liver enzyme – severe dental disease! The liver is trying to filter all that infection, and it’s not pleased. I had an older dog that we drew pre-anesthetic bloodwork on for a dental cleaning. Her Alk-P was over 800, so we took notice! We had her abdomen ultrasounded, worried about putting a dog under anesthesia with a questionable liver. The ultrasound specialist said “how soon can you do the dental and get this liver happy?” So do not let an increase in liver enzymes prevent your dog from having a dental if he has significant disease! In this case, we ended up pulling many teeth (this dog had SEVERE dental disease) and when we rechecked the blood 2 months later, all had gone back down to normal!

My Sam has had an Alk-P over 300 for a couple years now. He’s cool with it.

So if we get a really high Alk-P, an ultrasound of the abdomen (the liver) is a very good idea. What if it’s normal? Well, this is where it gets tricky. I have many dogs with elevated Alk-P on their bloodwork and very normal livers on ultrasound. Good news…but now what? The only way to get a 100% diagnosis of liver disease is with a biopsy. Yep, we have to cut a piece out of the liver and send it off to the lab. If your dog is acting sick, losing weight, or we know something ain’t right, this can be a great step! If your dog is healthy, happy, not losing weight, just had routine bloodwork done and has one elevated liver enzyme…do you want to go cutting into your dog? I’m not sure I would on my dog!

This is the point where I tell owners they are not terrible people if they choose to do nothing. Of course, if your dog decides to start showing any symptoms, we have a different story. But I can’t tell you how many healthy older dogs have mild-moderate increases in Alk-P and it never amounts to anything. There is a syndrome called vacuolar hepatopathy that can only be diagnosed on liver biopsy, but is common in older dogs…and doesn’t really do anything except cause these changes on the bloodwork. So for owners who want a name for the probable underlying cause that really isn’t much of a thing, we can say we suspect vacuolar hepatopathy….sure, why not.

What about other liver enzymes? If your dog has an increase in ALT (alanine transferase) then this could be different. I commonly see Alk-P rise in older dogs, but I not-so-commonly see ALT rise. If BOTH of these enzymes are high, then I would do some looking into it….literally….with an ultrasound. Again, if that shows no cancer or craziness, it doesn’t mean the liver is normal, just that it looks superficially normal. In healthy dogs, we’ll routinely recheck the blood in a couple months and see what direction these enzymes are going. I’ve had cases where I recheck and they are normal. Can’t explain what was going on, but we’ll take it! Other times, if they are on the rise, there’s something up. Sometimes I’ll add a medication I call the “happy liver pill.” Denamarin is the brand I use. It contains the tools the liver needs to repair itself, if it feels the urge. If the liver is not in a self-healing kind of mood, this supplement will not help. But if the liver IS in the mood, all the tools it needs are right there! This medication is well-tolerated in most dogs, so many owners take the “it can’t hurt!” attitude and try it.

The main two liver enzymes we look at on routine screens are Alk-P and ALT. There are a couple other players that tend to behave – GGT and total bilirubin. I rarely see an elevation in either of these without the main two first getting involved. These enzymes both loosely correlate to the gallbladder and bile ducts. If they are high, I take notice. Especially if they are part of a theme of all liver enzymes being high.

I of course can’t go into every possible liver disease here. This was more to help calm the nerves of the typical dog owner whose dog has some slight changes on the senior blood test. Sometimes there’s an underlying disease process, but many times there isn’t! I also do not let a little high Alk-P prevent a painful dog from getting arthritis medication. Again, we have to look at the whole dog here, and maintaining a good quality of life.

Bottom line – if your veterinarian tells you your otherwise healthy dog has a single liver enzyme that’s high and she’s not too worried about it, you shouldn’t be either. Rechecking blood in a month or two can tell us if we caught something early, or if this is our new normal. And if you want to make sure, an ultrasound of the liver is not invasive, doesn’t require anesthesia, and may rule out some scary things.

Body weight, alcohol consumption and liver enzyme activity—a 4-year follow-up study | International Journal of Epidemiology


Background This prospective study was performed in order to investigate the effect of baseline body mass index (BMI), BMI changes, baseline alcohol consumption, and changes in alcohol consumption on liver enzyme activity.

Methods This study population consisted of 6846 male workers in a steel manufacturing company who had undergone health examinations in 1994 and 1998.

Results The risk for elevated both aspartate aminotransferase (AST) and alanine aminotransferase (ALT) values over the four years increased with the baseline BMI and BMI changes, but not with alcohol consumption. Compared with the subject BMI <20, the adjusted odds ratios (OR) for those with baseline BMI 20–21.9, 22–24.9, 25– were 1.2, 1.6, 1.7 in AST and 1.4, 2.4, 2.8 in ALT, respectively. Compared with subjects who either lost or maintained their weight, the adjusted OR for men with slight, moderate, and heavy weight gain were 1.7, 2.6, 6.8 in AST and 2.4, 3.9, 11.3 in ALT, respectively. However gamma-glutamyl transferase (GGT) was associated with BMI changes and baseline alcohol consumption, not with baseline BMI and changes in alcohol consumption. Compared with subjects who lost or maintained weight, the adjusted OR for men with slight, moderate, and heavy weight gain were 2.4, 4.4 and 8.5, respectively. In comparison with non-drinkers, the adjusted OR for light, moderate and heavy drinkers were 1.8, 2.1 and 5.8, respectively.

Conclusion These data suggest that body weight, rather than alcohol consumption, may be the major factor in determining the serum level of liver enzymes. Even when body weight was not generally considered to be overweight, slight to moderate gains in weight were associated with increases in serum liver enzymes.

Alcohol is one of the factors most frequently associated with increased liver enzyme and the association between alcohol intake and alcohol-induced liver disease is well known. The Italian Dionysos study showed that alcohol was suspected to be the cause in 23% of all cases of liver disease, with a dose-dependent increase in the risk of developing liver disease.1,2 Conversely, two studies from Japan did not show a strong relationship between alcohol consumption and serum liver enzymes; specifically, aspartate aminotransferase (AST) and alanine aminotransferase (ALT).3,4

Obesity has also been identified as an important factor known to contribute to raised levels of serum liver enzyme in several cross-sectional studies.58 In the Dionysos study,9 it appeared that obesity rather than alcohol abuse was the main cause of raised values of ALT and the presence of fatty liver.

There have been a few studies evaluating the effects of the changes of alcohol consumption or the changes of body mass index (BMI) on the level of liver enzymes in a prospectively systematic way among apparently healthy people.1013 In these studies, the effect of the changes of alcohol consumption was very weak on liver enzyme, in comparison to that of the BMI change. This is an apparently surprising result given the strong association between alcohol consumption and serum liver enzymes consistently reported in many cross-sectional studies from western countries.1,2 Some clinical-based studies1416 have also showed that the effect of weight loss seemed to be more crucial in normalizing the liver enzyme than reduced alcohol consumption.

However, one study which analysed liver enzymes separately showed that the effect of body weight or alcohol consumption could be different depending upon which liver enzyme is assessed.10 In addition, most studies1013 published to date have usually focused on moderate or severe obesity, defined as a BMI >25. The aim of this prospective study was to investigate the association of baseline BMI, BMI changes, baseline alcohol consumption, and changes in alcohol consumption on serum liver enzyme activity in male workers, most of whom were in a normal range of BMI at baseline, at a large steel company in the Republic of Korea.


Study population

All workers in this company are required to have an annual health check-up consisting of clinical and laboratory measurements. Throughout 1994, health check-ups were performed between 9:00 a.m. and noon after an overnight fast, in a health care centre at the factory. Male workers between 25 and 50 years old without definite liver disease or hepatitis B antigen were eligible for follow-up for this study. Of the 11 867 men who met these criteria, 8553 men (72.1% follow-up rate) were re-examined in 1998. Among these subjects, 8445 men without diseases requiring continuous medication became the base population for a cross-sectional analysis. For the incidence analysis, subjects with abnormal levels of liver enzyme activity at baseline defined as an AST over 33 U/L, ALT over 35 U/L, or gamma glutamyl transferase (GGT) over 50 U/L, were excluded. After all exclusions, 6846 men were included in the incidence analyses.


Information on lifestyle factors including cigarette smoking, alcohol consumption, exercise, and medical history were obtained by self-reported questionnaires. Each year, all workers were asked to complete the same, or slightly modified, questionnaire. For each questionnaire, changes spotted by a computerized data system (which contained information from previous years) were confirmed by a nurse in a direct interview.

The workers were asked how many times per week or per month they consumed alcohol and the typical quantities consumed. They were asked to estimate the amount in terms of soju, a popular Korean liquor. Based on this information the amount of alcohol consumed per week was calculated. All subjects were divided into four groups by the baseline amount of alcohol consumption (non-drinker; light drinker, 1–180 g/week; moderate drinker, 181–360 g/week; heavy drinker, 361+ g/week). The population was stratified into four groups by changes in alcohol consumption (decreased, no change, increased 1–90 g/week, increased 91+ g/week). The BMI value, defined as weight (kg)/height (m2), was used as a weight index; and during weighing, almost all subjects wore the standard company uniform. Subjects were classified into four groups according to baseline BMI or BMI change, respectively. The criteria for the former were: <20 kg/m2; 20–21.9 kg/m2; 22–24.9 kg/m2; and ≥25 kg/m2. Criteria for the latter were: weight loser or maintainer, ≤0 kg/m2 or 0 kg/m2; slight weight gainer, 0.1–1.0 kg/m2; moderate weight gainer, 1.1–2.0 kg/m2; heavy weight gainer, >2.0 kg/m2.

Venous blood samples were obtained from a cubital vein after overnight 12 hours fasting. The serum samples were kept at 4°C and analysed within 48 hours. Laboratory tests were performed with an automatic analyser (Hitachi 7170, Japan) by optimized methods based on the recommendations of the Korean Society for Clinical Chemistry, at 37°C. Our normal ranges (U/L) for men were as follows: AST ≤33; ALT ≤35; GGT ≤50.

Statistical analyses

The relationship between alcohol consumption and BMI, and the prevalence and incidence of elevated liver enzyme were analysed by multiple logistic regression, using the SAS statistical program, version 6.12. In the incidence analyses, we included four main variables (baseline BMI, baseline alcohol consumption, BMI change, change in alcohol consumption), covariates (age, cigarette smoking [pack-years], exercise [frequency/week], baseline AST or ALT or GGT [baseline for the dependent variable]), and interaction terms between main factors. There were no interaction terms that reached statistical significance; therefore, these terms were dropped from the final model. We included baseline AST or ALT or GGT as covariates because amounts of changes of these enzymes during 4 years were dependent upon the baseline value of these enzymes. Those with relatively high values of serum liver enzymes at baseline, although in normal range, tended to increase more than those with low values. In the prevalence analyses, two main variables (baseline BMI, baseline alcohol consumption) and covariates (age, cigarette smoking [pack-years], exercise [frequency/week]) were included in the final model. The P-values used are two-sided, and values <0.05 were regarded as statistically significant.


Baseline characteristics (Table 1)

Table 1 shows the baseline characteristics of the subjects. The mean age of the subjects was 38.3 years and 84.2% of subjects were within the normal range of BMI. The prevalence of elevated liver enzyme at baseline was 7.8% in AST, 15.6% in ALT, and 4.4% in GGT.

Cross-sectional analyses (Table 2)

The prevalence of elevated liver enzyme showed clear dose-response relationships with BMI in 1994 for all three liver enzymes. Compared with those with BMI <20, the adjusted odds ratios for BMI 20–21.9, 22–24.9, 25 or more were as follows: 1.7 (95% confidence interval [CI] : 1.1–2.5), 2.9 (95% CI : 2.0–4.1), 7.1 (95% CI : 4.9–10.4) in AST, respectively; 1.8 (95% CI : 1.3–2.4), 5.0 (95% CI : 3.7–6.8), 14.2 (95% CI : 10.4–19.4) in ALT, respectively; and 1.7 (95% CI : 0.8–3.5), 4.5 (95% CI : 2.3–8.5), 12.6 (95% CI : 6.6–24.1) in GGT, respectively. GGT also showed a dose-response relationship with the amount of alcohol consumption, however, AST and ALT showed little or no statistically significant relationship. In comparison with non-drinkers, the adjusted odds ratios in GGT were as follows: 2.1 (95% CI : 1.4–3.1) for light drinkers, 3.1 (95% CI : 2.0–4.9) for moderate drinkers, 5.9 (95% CI : 3.5–10.0) for heavy drinkers.

Incidence analyses (Table 3)

During the follow-up periods 4.3%, 14.1% and 2.6% of the subjects developed abnormal liver enzyme levels of AST, ALT and GGT, respectively. The risk of developing both abnormal AST and abnormal ALT values increased with baseline BMI and the increase BMI. The magnitude of the effect of the change in body weight was much larger than that of baseline body weight. Compared with subjects with BMI <20, the adjusted odds ratios for men with baseline BMI 20–21.9, 22–24.9, 25– were as follows: 1.2 (95% CI : 0.8–1.8), 1.6 (95% CI : 1.1–2.4), 1.7 (95% CI : 1.0–2.8) in AST, respectively; 1.4 (95% CI : 1.0–1.9), 2.4 (95% CI : 1.8–3.2), 2.8 (95% CI : 2.0–4.0) in ALT, respectively. Compared with the weight losers or maintainers, the adjusted odds ratios for slight weight gainers, moderate weight gainers, and heavy weight gainers were as follows: 1.7 (95% CI : 1.2–2.5), 2.6 (95% CI : 1.9–3.7), 6.8 (95% CI : 4.6–10.0) in AST, respectively; 2.4 (95% CI : 2.0–2.9), 3.9 (95% CI : 3.2–4.9), 11.3 (95% CI : 8.6–14.8) in ALT, respectively. However, baseline alcohol consumption and the change of alcohol consumption did not show any notable relationship with either AST or ALT, even though there was a slight relationship with baseline alcohol consumption.

GGT showed a marked difference from both AST and ALT with regard to alcohol consumption and/or BMI. There were clear dose-response relationships with BMI changes and baseline alcohol consumption, but not baseline BMI and the changes of alcohol consumption, even though the changes of alcohol consumption affected slightly the incidence of abnormal GGT. Compared with weight losers or maintainers, the adjusted odds ratios for slight weight gainers, moderate weight gainers, and heavy weight gainers were 2.4 (95% CI : 1.5–3.9), 4.4 (95% CI : 2.7–7.1) and 8.5 (95% CI : 4.6–15.7), respectively. In comparison with non-drinkers, the adjusted odds ratios were 1.8 (95% CI : 0.9–3.7) for light drinkers, 2.1 (95% CI : 0.9–4.8) for moderate drinkers, and 5.8 (95% CI : 2.3–14.7) for heavy drinkers.


We explored the relationships between BMI and alcohol consumption, and the prevalence and/or incidence of abnormal serum liver enzyme activity in both cross-sectional and prospective designs. First, serum activity of both AST and ALT showed strong dose-response relationships with body weight rather than with alcohol consumption. In particular, the association of enzymes with BMI changes was much stronger than that with baseline BMI. Regarding alcohol consumption, there was only a weak relationship with baseline alcohol consumption and no relationship with the changes of alcohol consumption. A second major finding was that serum GGT activity was related to both the baseline amount of alcohol consumed and the changes of body weight, while there were only weak or no relationships with the changes of alcohol consumption and the baseline BMI.

Several cross-sectional and clinical studies58 have shown consistently that the increased serum activity of various liver enzymes is related to overweight or obesity. The results of a few prospective studies10,12,1416 also confirmed this association. However, earlier studies usually focused on moderate or severe obesity with BMI >25. In this prospective study, higher levels of adiposity as assessed by baseline BMI and BMI change were monotonically related to an increase in the incidence of elevated serum liver enzymes, especially AST and ALT, even though most of our subjects had a BMI within the normal range. Our study allows a more precise quantification of the dose-response relationship than has been possible previously due to the large sample size. Also, we explored the association of baseline BMI and BMI change simultaneously and showed that the effect of BMI change was a more important factor in developing abnormal liver enzymes than was baseline BMI. To our knowledge, this is the first study to report these findings. Among our subjects, those with higher baseline BMI tended to experience an increase in body weight less than those with lower baseline BMI. Hence, one of these factors should be considered as a confounder when interpreting associations with the other. Although Bruns et al.10 assessed the effect of body weight change, they did not consider these two covariates concurrently as possible confounders.

Among liver enzymes, the serum activities of ALT were more clearly related to BMI than were the other enzymes. These findings were similar to those observed in other studies.7,9,10 On the basis of such observations, Wejstal et al.17 suggested that ALT values should be corrected for body weight, especially when ALT measurements are used as a surrogate test in screening for non-A, non-B hepatitis. According to another study,18 AST values also should be corrected for body weight because in various animal species, ranging from mice to cattle, the expected enzymatic activity can be expressed as a function of a power of the weight.

AST and ALT had a surprisingly weak or non-existent relationship with alcohol consumption in both the cross-sectional and longitudinal analyses in our study; although the relationship between alcohol consumption and GGT was clear, as expected. The studies9,10,19 from western countries reported that the magnitude of the effect of alcohol consumption was similar to, or slightly smaller than, that of obesity. This could be because the total alcohol consumption in our subjects might have been lower than in other studies. Alternatively, Asians may be less sensitive to alcohol than Caucasians. Studies3,4 from Japan also reported that alcohol consumption was not significantly related to ALT or AST.

The Serum GGT level showed a strong relationship only with BMI change, but not baseline BMI. The importance of BMI change means that the effects of adiposity might be temporary. A 7-year longitudinal population study from Norway also showed that the change in BMI was the single strongest determinant of change in GGT.12 Our study suggested that liver enzymes could be influenced by a slight weight change even within normal range.

One of the most interesting findings of this study was that GGT showed a relationship only with baseline alcohol consumption, not change in alcohol consumption, the opposite finding to the relationship observed for BMI. As far as we know, though, there has been no previous study exploring the relationships between both baseline and the changes of alcohol consumption, and liver enzyme concurrently, the results of some studies support our finding. As a screening test for alcoholism and alcohol abuse, the sensitivity of GGT has been considered to be acceptable, but its specificity is poor.20 In contrast to this, GGT has been found to have reasonable specificity but low sensitivity to changes in alcohol consumption.21 The Tromsø study12 in Norway also reported a strong relationship between alcohol consumption and GGT in a cross-sectional setting, but a surprisingly weak association between the changes of alcohol consumption and the changes of GGT in longitudinal analyses. They interpreted this as reflecting the imprecision of their alcohol questions, which may have introduced random measurement errors that obscured the true changes in alcohol consumption. However, our result suggested that it could be a real association. Some investigators22,23 have suggested that elevated GGT activity in drinkers is probably related more closely to the biological effects of alcohol than to the amount of alcohol consumption.

In conclusion, these data indicate that body weight rather than alcohol consumption may be the major factor in determining the level of liver enzyme, though some ethnic differences may need to be taken into consideration. In particular, even slight or moderate gains in weight, and levels of body weight not generally considered to be overweight, were associated with increases of liver enzyme. With regard to the alcohol consumption, further study is needed to clarify the reason for the small effect of changes in alcohol consumption on GGT.

  • The risk for elevated both aspartate aminotransferase (AST) and alanine aminotransferase (ALT) values increased with the baseline BMI and BMI changes, but not with alcohol consumption.

  • Gamma-glutamyl transferase (GGT) was associated with BMI changes and baseline alcohol consumption, not with baseline BMI and changes in alcohol consumption.

  • Body weight, rather than alcohol consumption, may be the major factor in determining the serum level of liver enzymes.

Table 1

Baseline characteristics of the cohort (n = 8436)

Mean (range)
aAbbreviations: BMI, body mass index; AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase. 
Age (years)  38.3 (25–50) 
BMIa (kg/m2)  22.6 (13.3–32.3) 
% overweight (≥25)  15.8 
Alcohol (g/week)  131.7 (0–900) 
Smoking (pack-years)  13.7 (0–50) 
Physical activity(frequency/week)  0.9 (0–7) 
ASTa (U/L)  23.5 (9–150) 
Geometric mean  22.2 
% elevated AST  7.8 
ALTa (U/L)  24.2 (2–331) 
Geometric mean  20.1 
% elevated ALT  15.6 
GGTa (U/L)  16.8 (1–271) 
Geometric mean  12.2 
% elevated GGT  4.4 
Mean (range)
aAbbreviations: BMI, body mass index; AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase. 
Age (years)  38.3 (25–50) 
BMIa (kg/m2)  22.6 (13.3–32.3) 
% overweight (≥25)  15.8 
Alcohol (g/week)  131.7 (0–900) 
Smoking (pack-years)  13.7 (0–50) 
Physical activity(frequency/week)  0.9 (0–7) 
ASTa (U/L)  23.5 (9–150) 
Geometric mean  22.2 
% elevated AST  7.8 
ALTa (U/L)  24.2 (2–331) 
Geometric mean  20.1 
% elevated ALT  15.6 
GGTa (U/L)  16.8 (1–271) 
Geometric mean  12.2 
% elevated GGT  4.4 

Table 1

Baseline characteristics of the cohort (n = 8436)

Mean (range)
aAbbreviations: BMI, body mass index; AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase. 
Age (years)  38.3 (25–50) 
BMIa (kg/m2)  22.6 (13.3–32.3) 
% overweight (≥25)  15.8 
Alcohol (g/week)  131.7 (0–900) 
Smoking (pack-years)  13.7 (0–50) 
Physical activity(frequency/week)  0.9 (0–7) 
ASTa (U/L)  23.5 (9–150) 
Geometric mean  22.2 
% elevated AST  7.8 
ALTa (U/L)  24.2 (2–331) 
Geometric mean  20.1 
% elevated ALT  15.6 
GGTa (U/L)  16.8 (1–271) 
Geometric mean  12.2 
% elevated GGT  4.4 
Mean (range)
aAbbreviations: BMI, body mass index; AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase. 
Age (years)  38.3 (25–50) 
BMIa (kg/m2)  22.6 (13.3–32.3) 
% overweight (≥25)  15.8 
Alcohol (g/week)  131.7 (0–900) 
Smoking (pack-years)  13.7 (0–50) 
Physical activity(frequency/week)  0.9 (0–7) 
ASTa (U/L)  23.5 (9–150) 
Geometric mean  22.2 
% elevated AST  7.8 
ALTa (U/L)  24.2 (2–331) 
Geometric mean  20.1 
% elevated ALT  15.6 
GGTa (U/L)  16.8 (1–271) 
Geometric mean  12.2 
% elevated GGT  4.4 

Table 2

Adjusteda odds ratio (aOR) of prevalence of elevated liver enzyme by body mass index (BMI) and alcohol consumption at baseline (n = 8436)

95% CI
95% CI
95% CI
aAdjusted for baseline age, cigarette smoking, exercise. 
bAbbreviations: AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase. 
BMIb  –19.9  1168  1.0    1.0    1.0   
  20–21.9  2333  1.7  (1.1–2.5)  1.8  (1.3–2.4)  1.7  (0.8–3.5) 
  22–24.9  3598  2.9  (2.0–4.1)  5.0  (3.7–6.8)  4.5  (2.3–8.5) 
  25–  1337  7.2  (4.9–10.4)  14.2  (10.4–19.4)  12.6  (6.6–24.1) 
Alcohol (g/week)  1507  1.0    1.0    1.0   
  1–180  5590  1.1  (0.9–1.4)  0.9  (0.8–1.1)  2.1  (1.4–3.1) 
  181–360  1087  1.1  (0.8–1.5)  0.7  (0.6–0.9)  3.1  (2.0–4.9) 
  361–  252  1.3  (0.8–2.1)  0.8  (0.5–1.1)  5.9  (3.5–10.0) 

95% CI
95% CI
95% CI
aAdjusted for baseline age, cigarette smoking, exercise. 
bAbbreviations: AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase. 
BMIb  –19.9  1168  1.0    1.0    1.0   
  20–21.9  2333  1.7  (1.1–2.5)  1.8  (1.3–2.4)  1.7  (0.8–3.5) 
  22–24.9  3598  2.9  (2.0–4.1)  5.0  (3.7–6.8)  4.5  (2.3–8.5) 
  25–  1337  7.2  (4.9–10.4)  14.2  (10.4–19.4)  12.6  (6.6–24.1) 
Alcohol (g/week)  1507  1.0    1.0    1.0   
  1–180  5590  1.1  (0.9–1.4)  0.9  (0.8–1.1)  2.1  (1.4–3.1) 
  181–360  1087  1.1  (0.8–1.5)  0.7  (0.6–0.9)  3.1  (2.0–4.9) 
  361–  252  1.3  (0.8–2.1)  0.8  (0.5–1.1)  5.9  (3.5–10.0) 

Table 2

Adjusteda odds ratio (aOR) of prevalence of elevated liver enzyme by body mass index (BMI) and alcohol consumption at baseline (n = 8436)

95% CI
95% CI
95% CI
aAdjusted for baseline age, cigarette smoking, exercise. 
bAbbreviations: AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase. 
BMIb  –19.9  1168  1.0    1.0    1.0   
  20–21.9  2333  1.7  (1.1–2.5)  1.8  (1.3–2.4)  1.7  (0.8–3.5) 
  22–24.9  3598  2.9  (2.0–4.1)  5.0  (3.7–6.8)  4.5  (2.3–8.5) 
  25–  1337  7.2  (4.9–10.4)  14.2  (10.4–19.4)  12.6  (6.6–24.1) 
Alcohol (g/week)  1507  1.0    1.0    1.0   
  1–180  5590  1.1  (0.9–1.4)  0.9  (0.8–1.1)  2.1  (1.4–3.1) 
  181–360  1087  1.1  (0.8–1.5)  0.7  (0.6–0.9)  3.1  (2.0–4.9) 
  361–  252  1.3  (0.8–2.1)  0.8  (0.5–1.1)  5.9  (3.5–10.0) 

95% CI
95% CI
95% CI
aAdjusted for baseline age, cigarette smoking, exercise. 
bAbbreviations: AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase. 
BMIb  –19.9  1168  1.0    1.0    1.0   
  20–21.9  2333  1.7  (1.1–2.5)  1.8  (1.3–2.4)  1.7  (0.8–3.5) 
  22–24.9  3598  2.9  (2.0–4.1)  5.0  (3.7–6.8)  4.5  (2.3–8.5) 
  25–  1337  7.2  (4.9–10.4)  14.2  (10.4–19.4)  12.6  (6.6–24.1) 
Alcohol (g/week)  1507  1.0    1.0    1.0   
  1–180  5590  1.1  (0.9–1.4)  0.9  (0.8–1.1)  2.1  (1.4–3.1) 
  181–360  1087  1.1  (0.8–1.5)  0.7  (0.6–0.9)  3.1  (2.0–4.9) 
  361–  252  1.3  (0.8–2.1)  0.8  (0.5–1.1)  5.9  (3.5–10.0) 

Table 3

Adjusteda odds ratios (aOR) of incidence of elevated liver enzyme by baseline body mass index (BMI), BMI change, baseline alcohol consumption, and change in alcohol consumption (n = 6846)

95% CI
95% CI
95% CI
aAdjusted for baseline age, cigarette smoking, exercise, AST or ALT or GGT (baseline for the dependent variable). 
bAbbreviations: AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase. 
Baseline BMI  –19.9  1067  1.0    1.0    1.0   
  20–21.9  2083  1.2  (0.8–1.8)  1.4  (1.0–1.9)  0.8  (0.4–1.7) 
  22–24.9  2882  1.6  (1.1–2.4)  2.4  (1.8–3.2)  1.2  (0.6–2.4) 
  25–  814  1.7  (1.0–2.8)  2.8  (2.0–4.0)  0.8  (0.4–1.8) 
BMI change  ≤0  2518  1.0    1.0    1.0   
  0.1–1.0  2194  1.7  (1.2–2.5)  2.4  (2.0–2.9)  2.4  (1.5–3.9) 
  1.1–2.0  1597  2.6  (1.9–3.7)  3.9  (3.2–4.9)  4.4  (2.7–7.1) 
  2.1–  537  6.8  (4.6–10.0)  11.3  (8.6–14.8)  8.5  (4.6–15.7) 
Baseline alcohol (g/week)  1258  1.0    1.0    1.0   
  1–180  4544  1.1  (0.8–1.6)  1.0  (0.8–1.3)  1.8  (0.9–3.7) 
  181–360  852  1.5  (0.9–2.4)  1.2  (0.8–1.6)  2.1  (0.9–4.8) 
  361–  192  1.7  (0.8–3.4)  1.3  (0.8–2.1)  5.8  (2.3–14.7) 
Alcohol change (g/week)  2204  1.0    1.0    1.0   
  <0  2772  0.8  (0.6–1.1)  1.1  (0.9–1.3)  0.6  (0.4–1.0) 
  1–90  1213  0.8  (0.6–1.2)  1.0  (0.8–1.2)  1.2  (0.7–2.0) 
  91–  657  1.2  (0.8–1.8)  0.9  (0.7–1.1)  1.5  (0.9–2.5) 

95% CI
95% CI
95% CI
aAdjusted for baseline age, cigarette smoking, exercise, AST or ALT or GGT (baseline for the dependent variable). 
bAbbreviations: AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase. 
Baseline BMI  –19.9  1067  1.0    1.0    1.0   
  20–21.9  2083  1.2  (0.8–1.8)  1.4  (1.0–1.9)  0.8  (0.4–1.7) 
  22–24.9  2882  1.6  (1.1–2.4)  2.4  (1.8–3.2)  1.2  (0.6–2.4) 
  25–  814  1.7  (1.0–2.8)  2.8  (2.0–4.0)  0.8  (0.4–1.8) 
BMI change  ≤0  2518  1.0    1.0    1.0   
  0.1–1.0  2194  1.7  (1.2–2.5)  2.4  (2.0–2.9)  2.4  (1.5–3.9) 
  1.1–2.0  1597  2.6  (1.9–3.7)  3.9  (3.2–4.9)  4.4  (2.7–7.1) 
  2.1–  537  6.8  (4.6–10.0)  11.3  (8.6–14.8)  8.5  (4.6–15.7) 
Baseline alcohol (g/week)  1258  1.0    1.0    1.0   
  1–180  4544  1.1  (0.8–1.6)  1.0  (0.8–1.3)  1.8  (0.9–3.7) 
  181–360  852  1.5  (0.9–2.4)  1.2  (0.8–1.6)  2.1  (0.9–4.8) 
  361–  192  1.7  (0.8–3.4)  1.3  (0.8–2.1)  5.8  (2.3–14.7) 
Alcohol change (g/week)  2204  1.0    1.0    1.0   
  <0  2772  0.8  (0.6–1.1)  1.1  (0.9–1.3)  0.6  (0.4–1.0) 
  1–90  1213  0.8  (0.6–1.2)  1.0  (0.8–1.2)  1.2  (0.7–2.0) 
  91–  657  1.2  (0.8–1.8)  0.9  (0.7–1.1)  1.5  (0.9–2.5) 

Table 3

Adjusteda odds ratios (aOR) of incidence of elevated liver enzyme by baseline body mass index (BMI), BMI change, baseline alcohol consumption, and change in alcohol consumption (n = 6846)

95% CI
95% CI
95% CI
aAdjusted for baseline age, cigarette smoking, exercise, AST or ALT or GGT (baseline for the dependent variable). 
bAbbreviations: AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase. 
Baseline BMI  –19.9  1067  1.0    1.0    1.0   
  20–21.9  2083  1.2  (0.8–1.8)  1.4  (1.0–1.9)  0.8  (0.4–1.7) 
  22–24.9  2882  1.6  (1.1–2.4)  2.4  (1.8–3.2)  1.2  (0.6–2.4) 
  25–  814  1.7  (1.0–2.8)  2.8  (2.0–4.0)  0.8  (0.4–1.8) 
BMI change  ≤0  2518  1.0    1.0    1.0   
  0.1–1.0  2194  1.7  (1.2–2.5)  2.4  (2.0–2.9)  2.4  (1.5–3.9) 
  1.1–2.0  1597  2.6  (1.9–3.7)  3.9  (3.2–4.9)  4.4  (2.7–7.1) 
  2.1–  537  6.8  (4.6–10.0)  11.3  (8.6–14.8)  8.5  (4.6–15.7) 
Baseline alcohol (g/week)  1258  1.0    1.0    1.0   
  1–180  4544  1.1  (0.8–1.6)  1.0  (0.8–1.3)  1.8  (0.9–3.7) 
  181–360  852  1.5  (0.9–2.4)  1.2  (0.8–1.6)  2.1  (0.9–4.8) 
  361–  192  1.7  (0.8–3.4)  1.3  (0.8–2.1)  5.8  (2.3–14.7) 
Alcohol change (g/week)  2204  1.0    1.0    1.0   
  <0  2772  0.8  (0.6–1.1)  1.1  (0.9–1.3)  0.6  (0.4–1.0) 
  1–90  1213  0.8  (0.6–1.2)  1.0  (0.8–1.2)  1.2  (0.7–2.0) 
  91–  657  1.2  (0.8–1.8)  0.9  (0.7–1.1)  1.5  (0.9–2.5) 

95% CI
95% CI
95% CI
aAdjusted for baseline age, cigarette smoking, exercise, AST or ALT or GGT (baseline for the dependent variable). 
bAbbreviations: AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase. 
Baseline BMI  –19.9  1067  1.0    1.0    1.0   
  20–21.9  2083  1.2  (0.8–1.8)  1.4  (1.0–1.9)  0.8  (0.4–1.7) 
  22–24.9  2882  1.6  (1.1–2.4)  2.4  (1.8–3.2)  1.2  (0.6–2.4) 
  25–  814  1.7  (1.0–2.8)  2.8  (2.0–4.0)  0.8  (0.4–1.8) 
BMI change  ≤0  2518  1.0    1.0    1.0   
  0.1–1.0  2194  1.7  (1.2–2.5)  2.4  (2.0–2.9)  2.4  (1.5–3.9) 
  1.1–2.0  1597  2.6  (1.9–3.7)  3.9  (3.2–4.9)  4.4  (2.7–7.1) 
  2.1–  537  6.8  (4.6–10.0)  11.3  (8.6–14.8)  8.5  (4.6–15.7) 
Baseline alcohol (g/week)  1258  1.0    1.0    1.0   
  1–180  4544  1.1  (0.8–1.6)  1.0  (0.8–1.3)  1.8  (0.9–3.7) 
  181–360  852  1.5  (0.9–2.4)  1.2  (0.8–1.6)  2.1  (0.9–4.8) 
  361–  192  1.7  (0.8–3.4)  1.3  (0.8–2.1)  5.8  (2.3–14.7) 
Alcohol change (g/week)  2204  1.0    1.0    1.0   
  <0  2772  0.8  (0.6–1.1)  1.1  (0.9–1.3)  0.6  (0.4–1.0) 
  1–90  1213  0.8  (0.6–1.2)  1.0  (0.8–1.2)  1.2  (0.7–2.0) 
  91–  657  1.2  (0.8–1.8)  0.9  (0.7–1.1)  1.5  (0.9–2.5) 



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Wejstal R, Hansson G, Lindholm A, Norkrans G. Persistent alanine aminotransferase elevation in healthy Swedish blood donors mainly caused by obesity.

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Pappas NJ Jr, Quereshi AR. Liver aspartate aminotransferase activity as a power function of body weight.

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Steffensen FH, Sørensen HT, Brock A, Vilstrup H, Lauritzen T. Alcohol consumption and serum liver-derived enzymes in a Danish population aged 30–50 years.

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© International Epidemiological Association 2001

Causes of High Liver Enzyme Levels

Causes of High Liver Enzyme Levels

Image Credit: Moussa81/iStock/GettyImages

Your liver performs hundreds of metabolic tasks. Numerous specialized proteins called enzymes propel these biochemical processes. Although the liver contains many different enzymes, high liver enzyme levels typically refers to a group of 2 to 5 enzymes present in particularly high concentrations. Elevated liver enzymes often indicate liver cell damage, which can occur with a wide array of conditions of varying severity. Transient, mild increases are relatively common and rarely cause lasting health effects. Persistent or marked increases in liver enzyme levels, however, may indicate a potentially serious medical disorder.

Liver Enzymes and Evaluation

Elevated liver enzymes generally refers to increased levels of one or more of the following enzymes:

  • Alanine transaminase (ALT)
  • Aspartate transaminase (AST)
  • Alkaline phosphatase (ALP)
  • Gamma-glutamyl transferase (GGT)
  • Lactate dehydrogenase (LDH)

When liver cell injury occurs, these enzymes leak from the damaged cells causing elevated blood levels. Healthcare providers evaluate the levels of these enzymes relative to one another, blood levels other substances related to liver health, as well as a physical examination and possibly additional diagnostic tests to determine the cause of elevated liver enzymes.


Hepatitis — inflammation of the liver — is the leading cause of elevated liver enzymes. Many disorders and conditions cause of hepatitis, including:

  • Excess alcohol use
  • Hepatitis virus infection (A, B, C, D and E)
  • Other viral infections, such as infectious mononucleosis
  • Fatty liver disease
  • Autoimmune hepatitis
  • Medications, toxins and poisons

Hepatitis can be acute (occurs suddenly and lasts less than 6 months) or chronic (persists for longer than 6 months). Acute hepatitis sometimes leads to severe liver injury and failure, a condition called fulminant hepatitis. Chronic hepatitis can scar the liver over time, which may eventually result in cirrhosis.

Other Liver, Digestive and Systemic Disorders

Conditions that block bile flow from the liver to the gallbladder or intestine — collectively known as bililary disorders — often cause elevated liver enzymes. Examples of these disorders include:

  • Gallstones
  • Chronic pancreatitis (inflammation of the pancreas)
  • Tumor or cyst of the gallbladder or bile ducts
  • Sclerosing cholangitis (inflammatory scarring of the bile ducts)

Whereas hepatitis refers to generalized liver inflammation, liver granulomas are localized areas of inflammation, which may cause elevated liver enzymes. These can occur for a variety of reasons including: certain infections (tuberculosis, syphilis, cat-scratch fever, etc.), medications (allopurinol, quinidine, etc.) and connective tissue disorders (sarcoidosis, etc.)

Other liver, digestive and systemic disorders that might cause elevated liver enzymes include:

  • Hemochromatosis: iron overload, usually an inherited disorder
  • Wilson disease: inherited condition that leads to copper overload
  • Inflammatory bowel disease: ulcerative colitis and Crohn disease
  • Thyroid disease: hypothyroidism and hyperthyroidism
  • Cancer that arises or spreads to the liver
  • Hodgkin lymphoma
  • Systemic lupus erythematosus
  • Anorexia nervosa
  • Alpha-1-antitrypsin deficiency

Other Considerations

While so-called liver enzymes are present in high concentrations in the liver, large amounts also exist in other body tissues. Therefore, elevations of certain liver enzymes might be due to non-liver-related causes. For example, strenuous physical exercise can cause a temporary increase in ALT, AST and LDH levels. Bone, small bowel and kidney diseases often cause elevated ALP levels.

Many commonly used over-the-counter and prescription medications can potentially cause elevated liver enzyme levels, including:

  • Acetaminophen (Tylenol)
  • Nonsteroidal anti-inflammatory drugs, such as diclofenac (Voltaren)
  • Cholesterol-lowering statin drugs, such as atorvastatin (Lipitor), rosuvastatin (Crestor) and simvastatin (Zocor)
  • Estrogens and oral contraceptives
  • Antibiotics, such amoxicillin-clavulanate (Augmentin) and tetracycline
  • Antiepileptics, such as phenytoin (Dilantin), carbamazepine (Tegretol) and valproic acid (Depakote)

Some herbs can also cause liver enzyme elevations and potentially serious liver injury, including germander, chaparral, valerian, skullcap, amanita, pennyroyal, greater celandine, kava, black cohosh, ma huang and jin bu huan.

The best course of action with a finding of elevated liver enzymes differs based in individual circumstances. Talk with your doctor if you have any questions or concerns.

Reviewed and revised by: Tina M. St. John, M.D.

Increased ALT in blood – CMD

ALT (glutamatpyruvate transaminase; GPT, L-alanine: 2 oxoglutarate aminotransaminase, EC Belongs to the enzymes of the class of transaminases that play a key role in the synthesis and catabolism of amino acids (transamination or transamination reaction) and providing cells with energy. ALT catalyzes the transamination reaction between alanine and a-ketoglutarate, which leads to the formation of pyruvate and glutamate. The reaction coenzyme is pyridoxine, vitamin B6.

ALT is an intracellular enzyme, its content in the blood serum of healthy people is significantly lower than in many organs and tissues, its greatest activity is detected in the liver, skeletal muscles, myocardium. An increase in ALT activity in the blood indicates damage or destruction of the enzyme-rich cells.

The most significant increase in ALT activity (exceeding the upper limit of the norm by more than 15 times) is noted with necrosis of liver cells (acute viral hepatitis, toxic hepatitis).In acute viral hepatitis, a multiple increase in the activity of ALT in the blood occurs much earlier than the development of jaundice. A slightly smaller increase in ALT activity (exceeding the upper limit of the norm by 5-10 times) is found in various liver diseases (chronic hepatitis, cholangitis, liver tumors), acute pancreatitis, burns, taking hepatotoxic drugs, acute myocardial infarction, etc.

An important indicator is the ratio of the activity of AST / ALT enzymes (de Ritis coefficient); it is advisable to calculate its values ​​only with increased activity of one or both enzymes.An increase in the coefficient of more than 1.4 is noted in cirrhosis, severe alcoholic and toxic liver damage, which is evidence of deep necrosis of hepatocytes with damage to the mitochondrial cell apparatus and the release of the mitochondrial AST fraction. With uncomplicated viral hepatitis or non-alcoholic liver damage, the coefficient value is less than 1.0.

Indications for research

  • Liver diseases;
  • donor screening;
  • examination of persons in contact with patients with viral hepatitis in the focus of infection.

Research methods. Spectrophotometric (kinetic) methods based on the recommendations of the International and National Federations of Clinical Chemistry. The addition of pyridoxal-5-phosphate to the reaction mixture provides the maximum catalytic activity of ALT. The enzyme activity depends on the temperature and the presence or absence of pyridoxal-5-phosphate in the reaction mixture.

Increased values ​​

  • Acute and chronic liver diseases;
  • taking hepatotoxic drugs;
  • acute and chronic pancreatitis;
  • acute myocardial infarction, acute myocarditis;
  • trauma, skeletal muscle necrosis, myopathy, myositis;
  • heatstroke;
  • erythrocyte hemolysis, hemolytic diseases;
  • renal failure.

Reduced values ​​

  • Vitamin B6 deficiency;
  • obstructive jaundice;
  • terminal stage of liver failure.
  • 90,021 90,000 Statins and Liver. what’s new?

    A diagnosis of metabolic syndrome requires central obesity and two of the following four additional criteria: elevated triglycerides, low HDL cholesterol, high blood pressure, or high fasting glucose (or previously diagnosed type 2 diabetes).A fairly common manifestation of metabolic syndrome from the liver is NAFLD. Treatment of hyperlipidemia leads to an improvement in the biochemical and histological picture of the liver in patients with NAFLD. Several studies have shown that statins significantly lower cholesterol levels as well as liver fat.

    According to the WHO, currently more than 1 billion people are overweight. Among them, about 300 million are obese 1.

    Obesity plays an important role in the pathogenesis of many diseases, such as diabetes mellitus (DM), insulin resistance, arterial hypertension, dyslipidemia, endocrine disorders, kidney stones, tumors, cardiovascular diseases, atrial fibrillation , myocardial infarction, thrombosis, etc.5 A combination of several of the above diseases occurring simultaneously is known as metabolic syndrome (MS).

    The concept of MS was first formulated by M. Reaven in 1988. Summarizing the data of numerous studies, M. Reaven concluded that hyperinsulinemia, impaired glucose tolerance, increased triglyceride levels and a decrease in high-density lipoprotein (HDL) plasma levels, as well as arterial hypertension can develop as a result of a decrease in the sensitivity of tissue cells to insulin.He suggested that insulin resistance with compensatory hyperinsulinemia underlies all the manifestations of “syndrome X”.

    N. Kaplan expanded the definition, drawing attention to central obesity, which is present in the majority of patients with this syndrome, and in 1989 proposed the term “lethal quartet”, which included obesity, arterial hypertension, diabetes mellitus and hypertriglyceridemia 2. Finally, in 90s M. Henefeld and W. Leonhardt proposed the term “metabolic syndrome”, which is currently the most widely used among clinicians.

    Until now, there have been two different definitions of MS: the first was proposed by the World Health Organization (WHO) (Alberti and Zimmet 1998), the second was proposed by the US National Cholesterol Education Program (NCEP) in 2001. Both definitions include glucose intolerance in the concept of MS. , obesity, arterial hypertension and dyslipidemia, however, differ somewhat in the quantitative values ​​of these criteria. In April 2005, the International Diabetes Federation, based on the previously given definitions of MS, proposed a new one, according to which the main criterion for it is abdominal obesity as the most significant in MS.

    The new definition requires central obesity and two of the following four additional criteria: elevated triglycerides, low HDL, high blood pressure, or high fasting glucose (or previously diagnosed type 2 diabetes) to make a diagnosis of MS. For the first time, to assess central obesity in MS, it was proposed to consider such criteria as gender and race 2.

    Currently, there is no unified theory explaining the development of MS and its complications.It is proposed to consider insulin resistance, chronic inflammation, accumulation of ectopic fat and further saturation of adipose tissue as the primary reasons for the development of MS. One theory is primary insulin resistance and concomitant systemic hyperinsulinemia. Hyperinsulinemia, on the one hand, is compensatory, that is, it is necessary to overcome insulin resistance and maintain normal glucose transport into cells; on the other hand, it is pathological, contributing to the emergence and development of metabolic, hemodynamic and organ disorders, which ultimately lead to the development of type 2 diabetes, ischemic heart disease and other manifestations of atherosclerosis.

    According to another theory, central obesity may be the primary cause of MS. According to one of the theories (portal / visceral theory), it is an increase in obesity, especially abdominal (accumulation of fat in the intraperitoneal space around organs), that leads to an increase in the content of free fatty acids (FFA) in the blood of the portal vein and liver and inhibition of the action of insulin 11. B in turn, an increase in the content of FFA contributes to a decrease in glucose utilization, stimulates the production of LDL and glucose in the liver, which leads to hyperglycemia and lipoproteinemia.

    Increased FFA content, insulin resistance and cytokine imbalance are the three main mechanisms that lead to dyslipidemia (decreased HDL cholesterol, increased LDL cholesterol and triglycerides), increased blood pressure, endothelial dysfunction, inflammatory response caused by cytokine imbalance, glucose intolerance and diabetes.

    The development of hyperglycemia causes an increase in the synthesis and secretion of insulin by the B-cells of the islet apparatus of the pancreas to compensate for impaired insulin sensitivity and maintain normal glucose tolerance.Hyperinsvlinemia develops, which is able to maintain normoglycemia for a long time, for many years. With the depletion of b-cells of the pancreas, insulin resistance develops, and then diabetes. A stable increase in blood glucose levels is accompanied by glycosylation of proteins, which leads to damage to their structures and functions. Damage to proteins in arterial vessels contributes to the progression of atherosclerotic changes, and brain proteins to neurological disorders. As a result, symptoms of micro- and macroangiopathies, polyneuropathies are formed.

    Insulin is known to regulate the rate of very low density lipoprotein (VLDL) synthesis by the liver. With an increase in its concentration, an increase in the synthesis of these lipoproteins occurs. VLDL elimination is regulated by the enzyme lipoprotein lipase, the activity of which is also controlled by insulin. In the presence of insulin resistance, this enzyme, like other tissues, is resistant to the effects of insulin. Therefore, the elimination of VLDL is slowed down. An increase in synthesis and a slowdown in elimination lead to an increase in the concentration of VLDL (triglycerides) in the blood plasma.A decrease in the activity of lipoprotein lipase is accompanied by a decrease in the content of HDL, since they are formed in the body during the hydrolysis of VLDL. Moreover, hyperinsulinemia has been shown to directly contribute to HDL catabolism. Thus, the development of insulin resistance and hyperinsulinemia leads to dyslipidemia, characterized by an increase in the concentration of VLDL (triglycerides) and a decrease in the concentration of HDL in the blood plasma. This dyslipidemia is atherogenic.

    FFAs present in high concentrations, on the one hand, become a substrate for the formation of atherogenic lipoproteins, and on the other hand, they prevent the binding of insulin to hepatocytes, which leads to hyperinsulinemia and potentiates further insulin resistance.

    The previously proposed theories of the pathophysiology of the development of MS (IR, chronic inflammation, accumulation of ectopic fat and further saturation of adipose tissue) create some paradoxes, for example, the absence of a pronounced decrease in the risk of developing cardiovascular diseases with intensive control of blood glucose levels in diabetics, treatment, leading to weight loss. In this regard, an alternative point of view was proposed 6, 7. As a model for interpreting the manifestations of MS and reconciling obvious paradoxes, Martin Laclaustra et al.proposed a theory of the functional incompetence of adipose tissue. The basis of this theory is the functional inability of adipose tissue to assimilate postprandial lipids. The turnover of fat is determined by a complex equilibrium in which insulin is the main factor, but not the only one. With functional failure of adipose tissue, the main factor that negatively affects the entire system is the growing chronic energy imbalance. The developing insolvency of adipose tissue, in turn, leads to changes in systemic energy supply, impaired glucose consumption and activation of autoregulatory processes (changes in adipokine secretion, vascular effects), which affect the entire homeostasis system in the body.

    Thus, systemic insulin resistance is a factor linking visceral obesity and adverse metabolic consequences. However, it is not clear how adipose tissue causes impairments in insulin glucose sensitivity. It should be noted that insulin resistance is often associated with infection and inflammation, and visceral obesity is also associated with chronic inflammatory status, suggesting that inflammation may be a potential mechanism through which obesity leads to insulin resistance 15.

    A fairly common manifestation of MS from the liver is non-alcoholic fatty liver disease (NAFLD) 8. It can be regarded as an early manifestation of metabolic disorders, especially in people with normal weight.

    NAFLD is described as a condition characterized by significant lipid deposition in hepatocytes or liver parenchyma in patients with no history of excessive alcohol consumption. The spectrum of this disease is quite wide: from simple steatosis, necrotic-inflammatory disorders of non-alcoholic steatohepatitis to fibrosis, cirrhosis and liver cancer 9.NAFLD occurs in one third of the population and in most patients with metabolic risk factors such as obesity and diabetes.

    The relationship of NAFLD with the components of MS, for example, obesity, hyperglycemia, dyslipidemia, hypertension, is widely known. Hamaguchi et al. define MS as a predictor of the development of NAFLD 10. The authors observed men and women with MS for 414 days and showed that 10% of patients developed NAFLD during this time. In addition, it was shown that in people with a history of MS, NAFLD underwent less regression.

    It is believed that the pathogenesis of NAFLD is a complex multifactorial process. It is most closely associated with visceral obesity, type 2 diabetes, MS. The pathogenetic concept of the development of NAFLD includes overnutrition, lack of activity, genetic factor and insulin resistance, which is one of the main links in the pathogenesis of NAFLD 4. In hepatocytes, insulin resistance is associated with hyperglycemia and hyperinsulinemia, increased FFA levels and their metabolites, and oxidative stress. adipocytokines, which may further contribute to the progression of liver damage and inflammation12,13.

    The prognosis of uncomplicated hepatic steatosis is quite favorable, but non-alcoholic steatohepatitis may further progress to cirrhosis or even hepatocellular carcinoma (in 10-15% of patients). Currently, there is no single approach to the treatment of NAFLD, with the exception of weight loss and treatment of each of the components of MS separately. The most important is increasing insulin sensitivity, lifestyle changes, and weight loss. It has also been proven that the treatment of hyperlipidemia leads to an improvement in the biochemical and histological picture of the liver in patients with NAFLD.Several studies have shown that statins significantly reduce cholesterol and liver fat 14.

    Both MS and type 2 diabetes are usually accompanied by an abnormal lipoprotein phenotype, which manifests itself in elevated triglyceride levels, low HDL cholesterol, and accumulation of VLDL (so-called atherogenic lipoproteins). It is now recognized that low HDL levels (less than 1.04 mmol / L) and increased triglycerides (above 1.7 mmol / L) are markers of an increased risk of cardiovascular disease.

    Thus, dyslipidemia associated with MS is a leading risk factor for the development of cardiovascular diseases, leading to early atherosclerosis of the arteries and heart diseases such as coronary artery disease, myocardial infarction, etc. Wall thickness of the carotid arteries (intima and media), measured by ultrasonography, is an important criterion for assessing the presence of atherosclerosis of the arteries and the degree of its severity. A relationship has been established between the thickness of the intima and media of the carotid arteries and MS and diabetes in elderly men and women without manifestations of subclinical atherosclerosis 16.

    So, based on all of the above, we can distinguish two main approaches to the treatment of MS: the first – leveling the causes underlying it through lifestyle changes, weight loss and increased physical activity; the second is the use of pharmacological therapy. At the same time, therapy aimed at correcting the atherogenic dyslipidemic profile plays the most important role in preventing the premature manifestation of cardiovascular diseases.


    Currently, 4 groups of drugs are known to correct the lipid profile.These include bile acid sequestrants, nicotinic acid, fibrates, and 3-hydroxy-3-methylglutaryl CoA reductase inhibitors – statins. Statins are the most widely used.

    Statins reversibly inhibit HMG-CoA reductase, a key microsomal enzyme on the pathway of cholesterol synthesis in the liver, by which HMK-CoA is converted into mevalonate, which serves as a source of cholesterol synthesis. As a result, the concentration of cholesterol in hepatocytes decreases, which further stimulates the expression of LDL receptors on the cell surface and leads to an increase in the clearance and catabolism of apo-B containing particles, such as LDL and VLDL.Statins can also lower LP levels by decreasing the rate at which the liver synthesizes VLDL. Fluvastatin, lovastatin, pravastatin and simvastatin have similar pharmacodynamic properties – lowering LDL cholesterol by 20–35%. This reduction in LDL cholesterol leads to a 30–35% reduction in adverse cardiovascular outcomes. At the same time, it has been proven that when using simvastatin, the desired effect is achieved in doses that are half that of other statins 17.

    Over the past 15 years, large-scale clinical studies have been carried out to determine the antihyperlipidemic activity of inhibitors of 3-hydroxy-3-methylglutaryl CoA reductase statins: Scandinavian Simvastatin Survival Study (4S), West of Scotland Coronary Prevention Study (WOSCOPS), Expanded Clinical Evaluation of Lovastatin – EXCEL …It has been proven that the use of lipid-lowering pharmacotherapy is indicated for patients with hypercholesterolemia who are at increased risk of coronary artery disease.

    Clinical studies have shown that statins reduce mortality from coronary heart disease, the risk of myocardial infarction, stroke and peripheral vascular disease, and the need for revascularization. It was found that they differ in a rather safe profile, although, like all drugs, they are not devoid of side effects, among them rhabdomyolysis, hepatotoxicity, nephrotoxicity, peripheral neuropathy, and allergic reactions.

    The question of the safety of statins was especially acute in 2001, when Cerivastatin was withdrawn from production due to the high risk of rhabdomyolysis in patients. Subsequent studies, however, have demonstrated the safety of statins in most patients taking them.

    Simvastatin is currently one of the most commonly used statins. One of the world’s largest studies, the Heart Protection Study (HPS), has shown that daily use of simvastatin at a dose of 40 mg / day in patients at high risk of cardiovascular disease reduces the risk of myocardial infarction and stroke, and also the need for 1/3 revascularization, even in patients with normal cholesterol levels.Simvastatin provides a significant reduction in cardiovascular morbidity, primarily by reducing vascular disease by about 25% compared to a placebo control group.

    It should be noted the scale of the study (20 536 people were included), as well as the fact that the HPS, in contrast to other similar studies, included patients not only with already diagnosed coronary heart disease, but also people without coronary heart disease, suffering from cerebrovascular disorders, peripheral arterial disease, diabetes mellitus (thus, women and elderly people were included in the study) 18.Positive results were observed in all selected subgroups, including men and women, regardless of age, and also, which is especially important, regardless of the baseline level of total cholesterol and LDL cholesterol. The most important result of the HPS study was a decrease under the influence of simvastatin therapy in the number of cardiovascular complications (including heart attacks, strokes) in patients with coronary artery disease and other manifestations of atherosclerosis in the presence of normal values ​​of total cholesterol and LDL cholesterol.

    One of the most significant studies at the moment is also the Scandinavian study – 4S (Scandinavian Simvastatin Survival Study).His goal was to confirm the hypothesis that lowering serum cholesterol levels reduces mortality from cardiovascular disease. The study involved 4,444 patients with coronary artery disease with high cholesterol (from 213 to 310 mg / dl) and triglycerides (220 mg / dl). Patients were randomized to receive placebo or simvastatin. The initial dose of the drug was 20 mg / day, under the control of lipid metabolism in some patients, it was increased to 40 mg. Patient follow-up lasted about 5.4 years on average.The main result of the study was a decrease in the overall mortality rate by 30%, mortality from cardiovascular diseases by 42%, and myocardial infarction by 34% under the influence of simvastatin therapy.

    Statins contribute not only to a decrease in LDL, but also to an increase in HDL. A comparative study of the efficacy and safety (Comparative HDL Efficacy and Safety Study – CHESS) of atorvastatin and simvastatin was conducted in 917 patients with hypercholesterolemia who took one of the drugs at 80 mg / day.Since at these doses in most patients, both drugs lower LDL cholesterol levels below 100 mg / dL, the main task of CHESS was to determine which drug is most effective in raising HDL levels, which, according to the NCEP (National Cholesterol Education Program), is the second by the importance of a task in the treatment of dyslipidemia. After 24 weeks of treatment in the group of patients taking simvastatin, HDL increased by 8.3% from the initial level, and in patients taking atorvastatin – by 4.2%.At the same time, both groups showed a decrease in LDL cholesterol below 40 mg / dL. In the study of the safety of the use of these statins, it was found that an increase in the level of liver enzymes by more than 3 times was observed in 2.8% of patients taking atorvastatin, and only 0.4% of those taking simvastatin.

    So, based on the foregoing, it can be argued that statins, in particular simvastatin, are highly effective antihyperlipidemic drugs that can significantly reduce the risk of cardiovascular diseases.

    On the other hand, statins have a number of serious side effects that cannot be ignored when prescribing therapy. Chief among these is hepatotoxicity, which should be especially considered when prescribing statins to patients with preexisting NAFLD. However, hepatotoxicity should not be regarded as a contraindication to the use of statins, which in this case should be prescribed under constant monitoring of hepatic transferases.

    Although clinically significant liver damage with statins is extremely rare, asymptomatic elevations in liver enzymes are common (in 1-3% of patients).Thus, in connection with the potential hepatotoxicity of statins, liver diseases are noted as contraindications in the instructions for use of the drug.

    The mechanisms of liver damage when using antihyperlipidemic drugs are complex. Usually the hepatocellular component of the injury predominates; the picture of isolated cholestasis is extremely rare, sometimes there is a mixed type. The mechanisms of hepatotoxicity differ depending on the drug and its group, among them: effect on the cytochrome P-450 system, impairment of bile acid transport, immune inflammatory process on drug administration or on its metabolites, immune-mediated cell apoptosis under the action of TNF-α, oxidative stress and intracellular damage.

    It is believed that hepatotoxicity with simvastatin is due to drug interactions. There have been several cases of hepatotoxicity with the combined use of simvastatin and amiodarone. This information is potentially very significant, since these drugs are usually used together with each other in the treatment of patients with cardiovascular diseases. There are also reports of hepatotoxicity when using simvastatin in conjunction with flutamide, troglitazone and diltiazem.The simultaneous use of simvastatin with diltiazem is likely to cause a significant increase in the level of serum simvastatin due to inhibition under the influence of diltiazem of the isoenzyme CYP3A4 (a component of cytochrome P450), with the participation of which statins are metabolized. Recovery usually occurs within a few weeks or months after drug withdrawal.19

    Other authors believe that the mechanism of asymptomatic elevation of aminotransferase levels is related to the pharmacodynamic effect of lipid-lowering drugs in general, rather than to the statins themselves.Indeed, an asymptomatic increase in the level of aminotransferases is characteristic of all antihyperlipidemic drugs, including ezetimibe, which does not affect hepatic cholesterol synthesis and bile secretion.

    Initial toxicology studies indicated that statins can cause serious liver damage. In large doses, statins cause hepatocellular necrosis of the liver in rabbits. Similarly, high doses of simvastatin induce hepatocellular liver necrosis in guinea pigs.However, liver damage in these animals can be prevented by administering mevalonate. From this it can be concluded that it is the depletion of mevalonate or its potential metabolites that can lead to liver damage in these animals 20. In humans, however, no cases of hepatocellular necrosis as a result of statin use have been identified.

    The most common manifestation of the liver in medical practice when using statins is an asymptomatic increase in the level of hepatic aminotransferases, which is a typical effect when using statins.In clinical studies evaluating the effectiveness of statins, an increase in the level of alanine aminotransferase 3 times higher than normal was used as a safety criterion. It has been shown that such an increase was observed only in very rare cases.

    The data of clinical studies have shown that an increase in the level of transaminases to clinically significant values ​​(3 times higher than the upper limit of normal) is observed in approximately 0.5–2% of patients receiving statins. This increase is dose-dependent and, as a rule, appears within 3 months from the beginning of the course of treatment.A recent meta-analysis of 49,275 patients enrolled in 13 large placebo-controlled statin trials showed that low-dose statin therapy was not associated with significant increases in liver enzymes compared with placebo: both groups had increased aminotransferase levels occurs at the same frequency. Thus, a comparison of the cases of elevated liver enzymes in the group of patients taking statins and in the placebo group raises the question of the possibility of spontaneous fluctuations in the level of transaminases, regardless of the use of statins 21.

    The general consensus that statins should not be used in patients with active liver disease or persistent elevations in aminotransferases of unknown origin is questionable, since it remains unclear in which patients liver disease should be regarded as active and which elevations in aminotransferases of unknown origin are persistent.

    For the first time, the question of the ability of statins with long-term use to cause deterioration of liver histology in patients with NAFLD was raised by Caldwell et al.This question is important not only because NAFLD is common in patients with hyperlipidemia and type 2 diabetes, but also because the presence of fatty liver in itself increases the risk of cardiovascular disease. Currently, only a limited number of studies have been conducted to investigate the safety of statins in patients with preexisting NAFLD, in whom the use of statins is necessary for the primary or secondary prevention of cardiovascular disease.

    A study by Chalasani et al.22, 25, aimed to study cases of liver damage in patients with preexisting abnormalities in liver biochemical parameters, using an extensive medical database of 3 hospitals and 30 clinics. The study included atorvastatin, simvastatin, pravastatin and fluvastatin. We compared cases of hepatotoxicity caused by statins in 342 patients with hyperlipidemia and elevated liver enzymes who received statins, 1,437 patients with hyperlipidemia, normal aminotransferase levels who received statins (statin control), and 2,245 patients with elevated liver enzymes. not receiving statins.Increases in biochemical parameters over 6 months of observation were classified as moderate and significant. The criterion for the presence of serious liver damage was considered to be an increase in the level of aminotransferases 10 times higher than the upper limit of normal (and more) in patients without mention of an increase in liver tests in history and more than 10 times from the initial level in patients with an increased level of liver tests. Compared with the statin control group, patients with elevated liver enzyme levels had an increased risk of moderate elevations in aminotransferases (4.7% vs 1.9%), but not serious elevations (0.6% vs 0.2%).However, in patients with elevated liver enzymes who received statins, there were no more frequent increases in liver enzymes of moderate degrees (4.7% vs 6.4%) or severe increases (0.6% vs 0.4%) compared with patients with elevated liver enzyme levels, but not receiving statins. Thus, it has been shown that in some patients with an increased initial level of liver enzymes, changes in biochemical parameters can occur regardless of whether they receive statins or not.

    Despite the often discussed issue of hepatotoxicity of statins, it has been established that acute hepatic failure with statins is extremely rare. Among 51,741 patients who underwent liver transplants in the United States during 1990–2002, only 3 cases were recorded in which acute liver failure was caused by statins. In two of these three cases, liver failure was caused by the use of Cerivastatin, which is no longer in use.

    There is also no evidence that higher doses of statins increase the risk of clinically significant liver damage compared to lower doses.

    So, hepatotoxicity caused by the use of statins manifests itself in 1-3% of patients, is characterized by an increase in the level of aminotransferases, an asymptomatic course, is dose-dependent and, as a rule, is reversible after a reduction in the dose of a statin or upon its withdrawal. After normalization of indicators, re-administration of statins may not lead to an increase in aminotransferases.

    At the same time, care must be taken when prescribing statins to patients with liver disease, and the possible toxic effect on the liver during treatment should be monitored constantly. For simvastatin, it is recommended to perform liver function tests before starting treatment and then when any clinical symptoms appear. When the dose is increased to 80 mg / day, patients should undergo additional tests immediately before the dose increase, 3 months later, and periodically during the subsequent period during the first year of treatment.

    The safety of statins in patients with pre-existing NAFLD is an important consideration. It should be noted that NAFLD deserves attention not only as a component of MS, but also as an independent factor and marker of an increased risk of developing cardiovascular diseases.

    NAFLD is associated with an increased risk of death from various causes and is a predictor of future diseases of the cardiovascular system, regardless of age, gender, LDL cholesterol levels and manifestations of MS.

    Since MS therapy is generally aimed at reducing the risk of cardiovascular diseases, and in patients with NAFLD this risk is especially high, it is advisable to carry out therapy aimed also at improving liver condition.

    In recent years, a series of works has been published on the advisability of using statins in NAFLD. Since NAFLD is one of the complications of MS and is closely related to its pathogenesis, these studies consider the possibility of using statins in the combination therapy of NAFLD.
    Although there are doubts about the toxicity of drugs in patients with NAFLD, increasing evidence indicates that commonly used drugs such as metmorphine and statins do not harm the liver.23

    The effect of statins on liver histology in patients with NAFLD is not well understood. Mattias et al. 24 examined the histology of liver tissue in patients with preexisting NAFLD before and after starting treatment with statins. The data obtained were compared with a group of patients who did not receive statins.At the start of the study, patients who were later prescribed statins had significantly higher BMI values ​​and more pronounced hepatic steatosis than patients who did not receive statins. In the course of further follow-up, patients taking statins maintained higher BMI values, as well as diabetes and severe insulin resistance with a greater frequency. However, this group of patients showed a significant reduction in the degree of hepatic steatosis compared with patients who did not take statins.And although these patients were more at risk of liver fibrosis progression, only 4 patients taking statins had steatosis progressed to the fibrotic stage. Based on the data obtained, the authors argue that statins can be prescribed to patients with elevated liver enzyme levels as a result of NAFLD.

    A similar study of pravastatin showed that taking it in small doses (20 mg / day) for 6 months led to the normalization of liver enzymes and weakened inflammatory processes in the liver in patients with NAFLD.A preliminary study of atorvastatin also showed improvements in aminotransferase levels and lipid levels in patients with NAFLD, suggesting its efficacy and safety.
    Thus, in response to the question about the hepatotoxicity of statins, there is more and more evidence that their prescription in standard therapeutic doses in patients with elevated levels of liver aminotransferases is not associated with a significant risk of its development.

    You can request a complete list of references in the edition

    one.World Health Organization. Obesity and Overweight. 2003.
    2. Alberti K. G., Zimmet P., Shaw J. IDF Epidemiology Task Force Consensus Group. The metabolic syndromea new worldwide definition. Lancet 2005; 366: 1059-62.
    3. Kaplan N.M. The deadly quartet: upper-body obesity, glucose intolerance,
    hypertriglyceridemia and hypertension // Arch.Intern. Med. 1989. V. 149. P. 1514-1520.
    4. Loria P., Lonardo A., Carulli L., Verrone A.M., Ricchi M., Lombardini S., Rudilosso A., Ballestri S., Carulli N. Review article: the metabolic syndrome and non-alcoholic fatty liver disease. Aliment Pharmacol Ther. 2005 Nov; 22 Suppl 2: 31-6.
    5. Tim CMA Schreuder, Bart J Verwer, Carin MJ van Nieuwkerk, Chris JJ Mulder; Nonalcoholic fatty liver disease: An overview of current insights in pathogenesis, diagnosis and treatment; World J Gastroenterol 2008 April 28; 14 (16): 2474-2486.
    6. Laclaustra M., Corella D., Ordovas J.M. Metabolic syndrome pathophysiology: the role of adipose tissue. Nutr Metab Cardiovasc Dis 2007; 17: 125-139.
    7. Bergman R.N., Kim S.P., Catalano K.J., Hsu I.R., Chiu J.D., Kabir M., Hucking K., Ader M. Why visceral fat is bad: mechanisms of the metabolic syndrome. Obesity (Silver Spring) 2006; 14 Suppl 1: 16S – 19S.
    8. Chavez-Tapia N.C., Mendez-Sanchez N., Uribe M. The metabolic syndrome as a predictor of nonalcoholic fatty liver disease. Ann Intern Med 2006; 144: 379; author reply 380.
    9. Hae Jin Kim, MD; Hyeong Jin Kim, MD; Kwang Eun Lee, MD; Dae Jung Kim, MD; Soo Kyung Kim, MD; Chul Woo Ahn, MD, PhD; Sung-Kil Lim, MD, PhD; Kyung Rae Kim, MD, PhD; Hyun Chul Lee, MD, PhD; Kap Bum Huh, MD, PhD; Bong Soo Cha, MD, PhD; Metabolic Significance of Nonalcoholic Fatty Liver Disease in Nonobese, Nondiabetic Adults; Vol. 164 No. 19, October 25, 2004 Arch Intern Med. 2004; 164: 2169-2175.
    10. Hamaguchi M., Kojima T., Takeda N., Nakagawa T., Taniguchi H., Fujii K., Omatsu T., Nakajima T., Sarui H., Shimazaki M., Kato T., Okuda J., Ida K. The metabolic syndrome as a predictor of nonalcoholic fatty liver disease; Ann Intern Med. 2005 Nov 15; 143 (10): 722-8.
    11. Eduardo Alegría Ezquerra, José M. Castellano Vázquez, and Ana Alegría Barrero; Obesity, Metabolic Syndrome, and Diabetes: Cardiovascular Implications and Therapy; Departamento de Cardiología, Clínica Universitaria de Navarra, Pamplona, ​​Navarra, Spain
    12. Raszeja-Wyszomirska J, Lawniczak M, Marlicz W, Miezyńska-Kurtycz J, Milkiewicz P.Non-alcoholic fatty liver disease – new view; Pol Merkur Lekarski. 2008 Jun; 24 (144): 568-71
    13. Adams LA, Angulo P. Recent concepts in non-alcoholic fatty liver disease; Diabet Med. 2005 Sep; 22 (9): 1129-33.
    14. Kivici M, Gulten M, Gurel S, Nak SG, Dolar E, Savci G, et al. Ursodeoxycholic acid and atorvastatin in the treatment of nonalcoholic steatohepatitis. Can J Gastroenterol. 2003, 17: 7 13-8
    15. Wisse BE. The inflammatory syndrome: the role of adipose tissue cytokines in metabolic disorders linked to obesity; J Am Soc Nephrol.2004 Nov; 15 (11): 2792-800
    16. Ryuichi K., Hitomi T., Nobuyuki O., Ai Inoue, Atsushi K .; Metabolic syndrome, diabetes and subclinical atherosclerosis as assessed by carotid intima-media thickness. Juornal of atherosclerosis and thrombosis Vol. 14, No.2
    17. Lennernäs H, Fager G .; Pharmacodynamics and pharmacokinetics of the HMG-CoA reductase inhibitors. Similarities and differences. Clin Pharmacokinet. 1997 May; 32 (5): 403-25
    18. Heart Protection Study Collaborative Group.MRC / BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomized placebo-controlled trial. Lancet 2002; 360: 7-22.
    19. Naga Chalasani, Sidharth S. Bhardwaj, Lipid Lowering Agents That Cause Drug-Induced Hepatotoxicity; Clin Liver Dis. 2007 August; 11 (3): 597-vii.
    20. Horsman Y, Desager JP, Harvengt C. biochemical changes and morphological alterations of the liver in guinea-pigs after administration of Simvastatin / Pharmacol Toxicol 1990; 67: 336-339.
    21. de Denus S, Sprinler SA, Miller K, Peterson AM. Statins and liver toxicity: a meta-analysis. Pharmocotherapy 2004; 24: 584-591.
    22. Chalasani N, Aljadhey H, Kesterson J, Murray MD, Hall SD. Patients with elevated liver enzymes are not at higher risk for statin hepatotoxicity. Gastroenterology 2004; 126: 1287-1292
    23. Ahmed MH, Byrne CD; Current treatment of non-alcoholic fatty liver disease; Diabetes Obes Metab. 2008 Jun 16
    24.Mattias T Ekstedt, Lennart E T Franz Y n, Ulrik L. T Mathiesen, Marik T Holmqvist, Guzhran T Bodemar, Stergios T Kechagias; Statins in non-alcoholic fatty liver disease and chronically elevated liver enzymes: A histopathological follow-up study; Volume 47, Issue 1, Pages 135-141 (July 2007)
    25. Naga Chalasani; Statins and Hepatotoxicity: Focus on Patients With Fatty Liver; HEPATOLOGY, Vol. 41, No. 4, 2005
    26. Dominguez EG, Gisbert JP, et al. A pilot study of atorvastatin treatment in dyslipidemia, non-alcoholic fatty liver patients.Aliment Pharmacol Ther 2006; 23: 1643-7.

    what to eat and what to give up in order to save them

    Our biological life depends on enzymes, without them our food chain would not work, reports Sputnik Belarus.

    Why are enzymes so important to us?

    A certain amount of enzymes is stored in our body from birth. We have more than 3 thousand types of them.

    Without enzymes, neither digestion nor breathing is possible, without them the heart will never contract, and the thought processes in the brain will not work.Enzymes are involved in pregnancy and childbirth, reduce inflammation, improve the immune system, and are also involved in DNA synthesis and intracellular digestion. We are composed of cells, life boils in each of them 24 hours a day thanks to enzymes. It is safe to say that life management is an enzymatic reaction.

    Enzymes are protein structures consisting of chains of amino acids. They participate in the splitting of the necessary and in the destruction of the unnecessary.

    Each enzyme, like a key, opens only its own lock.Enzymes are plant, animal and those that are produced by our body. They always work in a specific environment and conditions. For them, the pH environment, temperature, the presence of trace elements, vitamins and amino acids are important. Since enzymes are a protein structure, at a temperature of about 48 ° C they coagulate (break down). Animal-derived enzymes are essentially a dried enzyme from an animal’s gland. And the trouble is that the enzymes of animal origin, our body recognizes how its own and, over time, the functions of the glands that produce their own enzymes are significantly reduced, and in case of organ disease, they can even approach zero.

    Pelmeni – shock for enzymes

    The acid-alkaline environment is of great importance for enzymes. Some enzymes work in an acidic environment, while others work in an alkaline environment. That is why doctors recommend a separate diet, and sometimes an additional intake of enzymes.

    Let’s give an example: many of you have probably noticed that after a good portion of dumplings, belching often torments. Because dumplings are minced meat and dough. To break down meat, you need enzymes that work in an acidic environment, and to break down dough, enzymes from an alkaline environment.Remembering chemistry. Acid + alkali = new product and gas that comes out in the form of belching! So dumplings are more of a reason to pamper the taste buds than a benefit to the body. It is better to eat any meat with vegetables and herbs, which contain their own enzymes and help the body to cope with the protein product.

    How to make digestive enzymes work properly?

    Having eaten a certain food, we must translate it into an accessible form for our body. And enzymes act here as catalysts for processes.At each stage of digestion, their own groups of enzymes work. Let’s take a look at the main ones.


    Produced by the salivary gland. Due to this, the primary fermentation process, the breakdown of food, begins in the oral cavity. Therefore, proper digestion begins with thoroughly chewing food.

    Amylase converts starch to glucose. This enzyme is not active in gastric juice, so it is better to eat sugar with a bite – this is how its primary breakdown will begin in the oral cavity.

    For example, if you chew a piece of brown bread for 2-3 minutes, it acquires a sweetish taste, which means that the amylase enzyme has broken down starch into glucose. One stage of digestion has been overcome. Continue chewing.

    The longer you chew, the longer your life will be.

    If the amylase has not worked enough, starch or sugars are not broken down by other enzymes. When they enter the large intestine, they become food for fungi, in particular the genus Candida. So badly chewed sugar, in addition to flatulence, can also give you candidiasis.


    A class of enzymes that break down proteins. Produced by the stomach, pancreas and intestinal secretions. The enzyme pepsin starts its work in the stomach. It is active at pH 2, that is, in an acidic environment, degrades proteins to peptides. If a person has gastritis, then there is a failure in the production of other stomach enzymes involved in the breakdown of proteins. Special attention of physicians was attracted by the ability of this group of enzymes to break down proteins that cause inflammation.

    If there is a lack of proteases, this leads to the fact that proteins cannot be completely degraded and some of the proteins enter the large intestine.

    More than 500 active species of microflora live in our intestines. Some of its representatives are useful to us, others are neutral until they receive the necessary nutrition. Unbroken proteins are just the kind of food they need. Having refreshed itself, the neutral flora begins to actively multiply and becomes pathogenic, dangerous for us. There is a sharp change in microflora and dysbiosis develops.


    It is secreted by the small intestine, for the breakdown of milk sugar, it turns into glucose.


    The enzyme is synthesized by the pancreas for the duodenum and small intestine, where fats are broken down into glycerol and higher fatty acids.

    Also, the liver secretes bile, which allows you to break down fat from large drops into small ones and further, under the action of lipase, into tiny forms. Passing into nutrients, they are absorbed in the intestines and carried by the blood to the cells. Enzymes in liver cells work a million times in 1 second.

    With a lack of lipase, fats are not completely broken down and in the form of large drops reach the large intestine, causing irritation of its walls, irritable bowel syndrome is formed.

    How to understand that there are not enough enzymes in the body?

    We can feel a lack of enzymes on a physical level, if for 30 minutes – an hour we feel a heaviness, aching pain in the abdomen, a fullness in the abdomen, or if you feel sleepy – analyze the contents of your plate and what was next to it!

    Maybe this is a banal lack of enzymes, because the consequences can be different: from a lack of nutrients as a building material to serious diseases.

    To always be in shape, it is imperative to remember that food is also a pleasant tasty medicine. Almost everything can be adjusted with proper nutrition and a sensible approach!

    What destroys enzymes?

    Temperature, sugar, salt, vinegar, contact with metal, time. But if frozen fruits are whipped into sorbet, then within 15 minutes you will get an amazing cocktail of enzymes. True, it is advisable to eat it faster, otherwise the reverse processes will go in it.

    There are many products on earth that contain enzymes.

    Products containing highly active detoxifying enzymes : bananas, mango, papaya, pineapple, avocado, kiwi, lingonberry, grapefruit.

    With care – garlic, onions, raw and sauerkraut, raw carrots and beets without chemicals, radishes, sprouted grains other than wheat, soft cheeses. But nuts, on the contrary, are inhibitors (blockers) of enzymes, therefore, when preparing vegetable salads with nuts and seeds, think what is your prerogative: pleasure or benefit?

    Substances that destroy enzymes : egg white, sprouted potatoes, peas, beans, lentils, seeds, so these products are best used with cooked food, where there will be no enzymes a priori.

    With a lack of enzymes, in addition to the fact that bacteria and fungi begin to grow in the intestines on undigested food debris, constipation begins, diseases associated with metabolic disorders (phosphorus-calcium metabolism): joint pain and gout, crystals of uric acid are formed, which accumulates in the joints.

    Proper digestion is the basis for both health and disease development. Do not forget about this every time you think about what to eat.

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    90,000 Healthy lifestyle

    The human digestive system performs the tasks of grinding, digesting food, assimilating nutrients and removing undigested residues from the body.In order for it to successfully realize its functions, nature has created it rather complexly arranged. Unfortunately, a large number of aggressive factors acting on the digestive organs provide their increased vulnerability to various diseases.

    The structure of the human digestive system

    The digestive system includes the gastrointestinal tract and accessory organs.

    The gastrointestinal tract begins with the oral cavity, in which the salivary glands, teeth, and tongue are located.In the mouth, food is chopped, its taste is determined, a food lump is formed and its digestion begins.

    Further, through the pharynx, food enters the esophagus, through which it enters the stomach. In the stomach, digestion continues. It produces hydrochloric acid and enzymes (pepsin, chymosis, lipase), and making contractions, the walls of the stomach mix food with digestive juices.

    From the stomach, the food lump enters the small intestine, which has several sections: the duodenum, the jejunum and the ileum.The excretory ducts of the liver and pancreas open into the small intestine, and in it, with the help of enzymes and bile, fats, carbohydrates and proteins are broken down.

    The last section of the gastrointestinal tract is the large intestine, which in turn is divided into the blind, colon (ascending, transverse and descending), sigmoid and rectum. The absorption of water and nutrients continues in the large intestine, and the bacteria inhabiting this part of the intestine contribute to the complete digestion of the incoming food.Feces are formed in the large intestine. Undigested residues are excreted through the rectum.

    The human digestive system includes auxiliary organs: liver, gallbladder, pancreas and salivary glands. All of them are necessary to improve the digestion of food, as they produce enzymes that break down proteins, carbohydrates and fats.

    Diseases of the human digestive system

    Depending on the cause of the occurrence, all diseases can be divided into several large groups:

    • inflammatory;
    • parasitic;
    • infectious;
    • food poisoning by toxic compounds;
    • resulting from metabolic disorders;
    • autoimmune;
    • tumor.

    Gastrointestinal problems are also classified by location.

    • Oral cavity, pharynx: stomatitis, tumors, pharyngeal diverticula.
    • Esophagus: esophagitis, cancer;
    • Stomach: gastritis, polyps, ulcers, esophageal reflux disease;
    • Small intestine: enteritis, ulcerative lesions, tumors, autoimmune diseases;
    • Colon: colitis, colon cancer, benign tumors, autoimmune diseases (ulcerative colitis, etc.).
    • Liver: alcoholic, viral, toxic and other hepatitis, liver cirrhosis, cancer, cysts, hemangioma, etc.;
    • Gallbladder: cholecystitis, gallstone disease, dyskinesia;
    • Pancreas: pancreatitis, cysts, pancreatic tumors.

    Also, diseases are divided along the course, they are acute and chronic.

    Many diseases of the digestive system are similar in symptoms.It is also important to note that sometimes different disorders of the digestive tract are combined with each other. All this does not always make it easy to diagnose a person. Therefore, in order to determine the cause of anxiety, the patient should definitely consult a qualified doctor.

    Diseases of the digestive system and sleep disorders

    Any serious disturbance in well-being negatively affects the quality of sleep. Abdominal pain, diarrhea, nausea make it difficult to fall asleep, and sleep intermittent and shallow.Insomnia and nightmares are also common in liver disease.

    There are other situations when it is not diseases of the digestive system that cause sleep disorders, but vice versa. For example, with obstructive sleep apnea syndrome due to the appearance of respiratory stops during sleep and the disruption of the diaphragm, which occurs in this case, patients develop belching and heartburn.

    Any sleep problems can be quickly and successfully solved by the specialists of the Barvikha sanatorium.Read more on the website.

    Back to list

    90,000 Diet for chronic pancreatitis: nutritional rules for exacerbation

    Table of Contents

    Diet for pancreatic disease such as pancreatitis is no less important than drug therapy . It is thanks to constant proper nutrition that patients manage to avoid exacerbations of pathology. A balanced diet makes it possible to eliminate a number of unpleasant symptoms of the disease (severe pain, nausea and vomiting, fever, etc.)).

    Factors of onset and symptoms of pancreatitis

    Pathology is characterized by inflammatory relapses, as a result of which the normal functioning of the pancreas and the release of a sufficient amount of enzymes and hormones are disrupted. The disease is dangerous because of its progression. With the development of pancreatitis, the tissues of the organ are destroyed, which leads to irreversible consequences for the whole organism.

    Important! Inflammatory phenomena can be a consequence of the acute stage of the disease or an independent manifestation if the patient suffered from jaundice, cirrhosis of the liver, atherosclerosis, abuses alcohol or fatty, junk food.

    The main symptoms of pancreatitis include :

    • Severity in the stomach (mainly after eating)
    • Severe pain syndrome on the right side in the navel
    • Burp
    • Heartburn
    • Bloating
    • Acute hunger
    • Sweetish taste in the mouth
    • Bad breath
    • Nausea
    • Frequent oily and liquid stools
    • Swelling of the eyelids
    • Dry lips
    • Skin redness

    Also, the disease is characterized by the accumulation of toxic substances in the patient’s body and disruption of insulin production.

    Features of the special diet

    Diet for pancreatitis should contain a large amount of protein, but with a minimum amount of fat . Such components should be eliminated from the diet during exacerbations completely or minimized. This will improve the condition of the pancreas and gallbladder. In some cases, a small amount of vegetable oil is allowed. The need for protein is due to the fact that it allows you to quickly renew the injured areas of the pancreas.Patients can also consume carbohydrates, but provided there is no predisposition to diabetes. If there is such a predisposition, you should refuse products that contain sugar.

    Diet for chronic pancreatitis (with exacerbations) also means reducing salt intake. Reducing the swelling of the gland will allow the complete exclusion of salty foods for only 2-3 weeks. If, with severe exacerbations, the patient suffers from severe symptoms of the disease, he is prescribed only liquid and pureed food.Any food should be consumed warm. You need to give up too hot and cold drinks and food.

    Food for the patient should be prepared without seasonings and spices. It is important to carefully monitor the freshness of the products used. If the patient eats porridge, they need to be cooked exclusively in water. Vegetable purees, low-fat cottage cheese, tea (without sugar and weak), puree soups will be useful.

    Gradually, egg proteins, lean meat and fish, slightly dried bread, jelly can be introduced into the diet.Portions should be small, but you need to eat food often enough to prevent the feeling of hunger, in which many patients complain of severe discomfort in the area of ​​the organ. It is best to switch to six meals a day.

    When is the pancreatitis diet prescribed?

    Typically, patients’ nutrition is adjusted immediately after diagnosis. It is especially important to pay attention to the diet during an exacerbation. With severe symptoms of pancreatitis, experts advise adhering to the principle of “cold, hunger and rest.”In the first 2-3 days after the attack, it is allowed to drink weak and unsweetened tea, non-carbonated mineral water and rosehip broth. When you come out of fasting, they gradually include in the diet dishes that have a good effect on the condition of the inflamed organ. These include oat broth and vegetable broths.

    In case of exacerbations, special sparing fractional nutrition is recommended for at least 6-12 months. During this period, the body can fully recover. At the same time, the patient himself will have time to get used to healthy nutrition.The diet for pancreatitis will not become too rigid for him and requiring a high level of self-control. Moreover, she will be the key to recovery. Thanks to it, it is possible to avoid not only surgical intervention, but also long and often tedious conservative therapy.

    Important! Both treatment and diet for pancreatic pancreatitis in men and women, regardless of symptoms, should be prescribed exclusively by a doctor. Only a gastroenterologist has accurate information about the condition of the pancreas, as well as has special professional skills and knowledge.

    Foods that are recommended and not recommended for sickness

    For pancreatitis, foods such as should be consumed:

    • Lean meat: lean pork, veal, chicken, rabbit, turkey
    • Lean fish: pike, flounder, pollock and cod
    • Groats: oat, semolina and rice
    • Durum wheat pasta
    • Fermented milk products
    • Vegetables: potatoes, zucchini, beets, carrots

    Milk is allowed to be consumed only as part of cereals, milk soups and jelly.If the condition improves, you can supplement the diet with mild and low-fat types of cheese. Eggs can be used in steaming omelettes. Of fruits, it is better to give preference to non-acidic apples. They can be baked and mashed.

    Strongly prohibited :

    • Onions
    • Sorrel and spinach
    • Radish, radish, horseradish and rhubarb
    • Bell pepper
    • Condiments and hot spices
    • Alcoholic products
    • Coffee and cocoa
    • Carbonated drinks

    During a diet for chronic pancreatitis, you should try to exclude goose and duck meat, lamb and bacon.You cannot eat fried meat, kebabs, sausage products and meat delicacies. All types of canned fish and meat, rich broths on meat, jellied meat are also forbidden to the sick. Fatty cottage cheese and sour sour cream, spicy and smoked cheeses, legumes, tomatoes, cakes and pastries, ice cream and chocolates should be removed from the diet.

    It is not recommended to use margarine, as well as beef and pork fat when preparing dishes. At least for the duration of exacerbations, oils in any form should be abandoned.

    Benefits of treatment at MEDSI

    • Experienced gastroenterologists. Our doctors have the necessary knowledge and skills for the complex management of patients with chronic pancreatitis (including exacerbation). Gastroenterologists can choose the right diet that takes into account all the characteristics of the patient’s lifestyle and his current condition
    • Modern diagnostic methods . Laboratory and instrumental techniques are used for examinations.We have the necessary expert-level equipment, which allows us to quickly diagnose and prescribe adequate therapy in any situation (including in case of complications)
    • Modern methods of treatment . We use both proven methods and our own author’s developments that allow for the treatment of chronic pancreatitis during an exacerbation quickly and competently, with minimal discomfort for the patient, using effective and safe medicines.Special attention is paid to proper nutrition
    • Connecting other specialists to work with the patient . If necessary, patients can be observed not only by gastroenterologists, but also by nutritionists, endocrinologists, etc.

    If you want our gastroenterologist to carry out the necessary treatment and select the optimal diet for you, call + 7 (812) 336-33-33.

    Enzyme deficiency in children

    Enzymes are protein catalysts, the production of which is regulated in the body by heredity.If, for some reason, these substances are not enough, ordinary products do not decompose into constituent substances, or do not turn into other necessary ones. Enzyme deficiency is called a common word – fermentopathy.

    Malabsorption syndrome

    is a syndrome of malabsorption of food components in the small intestine. Absorption or absorption of monomers (fatty acids, amino acids, monosaccharides, etc.) is preceded by hydrolysis – the breakdown of food polymers (proteins, fats and carbohydrates) under the influence of digestive enzymes.Violation of the hydrolysis of polymers with a deficiency of digestive enzymes (digestive enzymes) is called maldigestion syndrome or digestive insufficiency syndrome. The combination of both types of disorders, malabsorption and maldigestion, which is often encountered in clinical practice, was proposed to be designated as malassimilation syndrome. However, in the medical literature, all disorders of intestinal absorption are traditionally called malabsorption, caused by both the pathology of the absorption process itself and the lack of digestive enzymes.Malabsorption syndrome is accompanied by a whole group of diseases, the development of which is based on hereditary or secondary (with pathology of the pancreas or other organs of the digestive system) enzyme deficiency.

    In the first year of life, malabsorption syndrome is most often a genetic hereditary pathology, the most famous hereditary fermentopathies are disaccharidase deficiency, celiac disease and cystic fibrosis.

    Disaccharidase deficiency.

    Disaccharides are components of most carbohydrates. Their digestion processes are provided by special intestinal enzymes – disaccharidases. After the breakdown of disaccharides, monosaccharides are formed, which can then be absorbed by the intestinal transport systems. Intolerance to disaccharides in children is caused by the hereditary absence or decrease in the activity of one or more intestinal disaccharidases, resulting in incomplete breakdown of disaccharides in the small intestine. By peristaltic bowel movements, incompletely split disaccharides move to the lower parts of the digestive tract, where, under the action of natural microflora, they are converted into organic acids, sugars and hydrogen.These substances reduce the absorption of water and salts from the intestinal cavity, that is, the food gruel (chyme) liquefies, and this leads to the development of diarrhea in the child. Symptoms of primary disaccharidase deficiency usually appear in a baby immediately after birth. This group of diseases is characterized by the fact that with age, there is some compensation for the disturbed enzymatic functions, and the symptoms of the disease are mitigated or even disappear altogether. Among the hereditary defects of disaccharidases, the most famous are the deficiency of lactose, sucrose, isomaltase, trehalase.Lactase deficiency is explained by a mutation of the gene that is responsible for the synthesis of lactose, as a result of which this enzyme is either not synthesized at all (alactasia), or its inactive form is synthesized (hypolactasia). Therefore, when lactose enters the intestine, it is not completely broken down by defective lactose, and a characteristic symptom of malabsorption, diarrhea, develops.

    Lactose is the main component of milk, including female milk, therefore, the treatment of severe forms of lactose deficiency in infants is a rather difficult task.Lactase deficiency manifests itself from the first days of a child’s life, as soon as he begins to eat. There are two forms of lactose deficiency. The first form (congenital lactose intolerance of the Holcel type) is distinguished by a more benign course. Newborns with this form of the disease develop frothy, watery stools with a sour smell of vinegar or fermented wine, and streaks of mucus in the stool are possible. A rumbling is heard in the stomach, flatulence is expressed, gases are released abundantly. The general condition of the child is usually satisfactory, the appetite is not disturbed, the children suck well, the body weight increases normally.Some children tolerate small amounts of lactose well enough, they develop diarrhea only when it is received in quantities that lactose with reduced activity cannot cope with. With a favorable course, the symptoms of the disease completely disappear after the exclusion of milk from the diet of newborns. By 1-2 years of life, lactose deficiency is compensated to one degree or another. With a severe course, the addition of a secondary infection, it is possible to form metabolic disorders and chronic eating disorders that do not go away with age.The second form (congenital lactose intolerance of the Durand type) is characterized by a more severe course. After the first feeding, the child develops watery stools, vomiting. Growth and weight gain are slowed down. Over time, severe metabolic disorders develop, the kidneys and the nervous system are affected. There may be hemorrhagic disorders. In some cases, vomiting is persistent (resembles vomiting with pyloric stenosis), leading to dehydration of the child. Treatment with a lactose-free diet is ineffective. The main component of lactose deficiency treatment for breastfed babies is the intake of enzymes (containing lactose), and for bottle-fed babies – the use of special formulas (lactose-free).

    Parents need to be aware that lactose is found not only in whole women’s, cow’s and goat’s milk, but also in all types of milk powder, in many fermented milk products (sour cream), condensed milk, and also in some medicines as a filler. Therefore, when prescribing a medicine, the doctor should be informed about the existing lactose deficiency and carefully read the annotation of the drug. In mild cases of lactose intolerance, milk products and milk treated with B-galactosidase preparations are given instead of milk.Children with lactose deficiency are shown products containing fructose (vegetable and fruit purees), which is well absorbed and does not undergo bacterial fermentation. In addition to medical nutrition, in the first days of the disease, a short course (5-7 days) is prescribed enzymatic preparations. Within 30-45 days, probiotics are used to normalize the intestinal. Sucrose and isomaltase deficiencies are more common together. In children who are bottle-fed, there are no signs of a deficiency of these enzymes.Symptoms of the disease appear after the child eats food containing sucrose and starch (sugar, potatoes, semolina, flour products) when transferring it to artificial feeding or after the introduction of complementary foods. After taking such food, a child has foamy watery stools, vomiting. With a severe form and the child being artificially fed with mixtures containing sucrose, vomiting becomes persistent, the child loses weight. The diagnosis of sucrose intolerance is confirmed by a sucrose-loaded test.Treatment consists in adherence to a diet with the exclusion of foods containing sucrose and starch. You can eat fruits and vegetables in which the amount of sucrose is small (carrots, apples). The prognosis is favorable. With age, enzyme deficiencies are compensated for, and the diet can be expanded.

    Celiac disease (celiac disease)

    is a chronic hereditary disease that develops due to a deficiency of enzymes involved in the digestion of gluten. In recent years, in connection with the improvement in the quality of diagnostics, celiac disease is being detected more and more often.Gluten is a gluten component of a number of cereals – wheat, rye, barley, oats. When gluten breaks down, a toxic product is formed – gliadin, which has a damaging effect on the mucous membrane of the small intestine. However, in normal healthy children, gliadin does not damage the mucous membrane, since specific enzymes break it down to non-toxic substances. With celiac disease, a deficiency of these enzymes is observed to varying degrees (up to their complete absence). As a result, gluten is not hydrolyzed in the intestine, but accumulates together with the products of its incomplete breakdown, exerting a toxic effect on the mucous membrane of the small intestine, the cells of the mucous membrane of the small intestine die, and the digestive and absorption functions are impaired.In typical cases of celiac disease, the disease has a chronic course with periods of exacerbation and remission.

    The first signs of celiac disease appear in a child in the second half of life after the introduction of complementary foods, which include cereal gluten (semolina, wheat, oatmeal).

    If a child is artificially fed with mixtures containing wheat flour, then the symptoms of the disease appear earlier. From the moment gluten-containing foods are introduced into a child’s diet until symptoms appear, it usually takes 4-8 weeks.The main signs of celiac disease are dystrophy, weight loss and stunting, diarrhea, steatorrhea (the presence of undigested fats in the stool), and damage to the central nervous system. The celiac disease clinic develops gradually. First, the child’s appetite decreases, lethargy, weakness, and frequent regurgitation appear. In the future, regurgitation turns into vomiting, diarrhea develops. Stool in celiac disease is sharply offensive, abundant, frothy, pale with a grayish tinge, shiny. The child stops gaining weight, and then his body weight decreases.Children are very stunted. The abdomen is enlarged, which, in combination with thin limbs, gives the child a characteristic appearance – “a backpack with legs”. The child’s expression is sad, mimicry is poor (“unhappy look”). Over time, other organs of the digestive system are affected – the liver, pancreas, duodenum. Cirrhosis of the liver may develop. There is a moderate increase in the size of the liver and spleen. Violation of the enzyme-forming function of the pancreas leads to an even greater suppression of the digestive process.The development of secondary insulin deficiency is possible, which explains the symptoms of diabetes mellitus (increased urine output and thirst) during an exacerbation of the disease. All types of metabolism suffer, especially protein. Amino acid deficiency develops, the concentration of total lipids, cholesterol decreases, and the number of ketone bodies in the blood serum increases. Metabolic disorders are manifested by rickets, polyhypovitaminosis, anemia. In children, baldness of the scalp (alopecia) may occur, and fractures of long bones are frequent.A secondary immunodeficiency state develops, children are prone to frequent colds, which are more difficult and long-lasting. All children have disorders of the central nervous system (metabolic-toxic encephalopathy), children are irritable, capricious, lagging behind in psychomotor development. To confirm the diagnosis of celiac disease, a provocative gluten test and a biopsy of the mucous membrane of the duodenum or jejunum are used.

    The main method of treating celiac disease is diet therapy – exclusion from the diet of a sick child of all products containing gluten (bread, bakery, confectionery and pasta, semolina, oatmeal, pearl barley, wheat and barley groats and industrial cereals from these cereals).Since flour and other processed products of gluten-containing cereals are often added to sausages, sausages, wieners, canned meat and fish (including those intended for baby food), they are also excluded from the child’s diet. In the acute period of the disease, enzymes, vitamins, and probiotics are also used.

    In extremely severe forms of celiac disease and low effectiveness of diet therapy, glucocorticoids (hormones) are used in a short course with a gradual cancellation in the future.Parents should remember that a gluten-free diet should be followed for life, even if the symptoms of the disease completely disappear. Failure to comply with the diet can lead to a more severe relapse of the disease, and the resulting violations will be difficult to compensate.

    Intestinal form of cystic fibrosis.

    A genetic defect in this hereditary disease disrupts the reabsorption of sodium chloride by all exocrine glands, as a result of which their secret becomes viscous, thick, and its outflow is difficult.The secret stagnates in the excretory ducts of the glands, they expand, and cysts are formed. Death of glandular cells occurs. Most often, there are intestinal and pulmonary forms of cystic fibrosis, in which the glands of the intestines or bronchi are predominantly affected, respectively. Combined forms may occur. The defeat of the intestinal glands in cystic fibrosis leads to the fact that the processes of digestion and absorption of food components are significantly impaired (maldigestion and malabsorption syndromes). The digestion of fats suffers to a greater extent, which is associated with inhibition of the enzymatic activity of the pancreas, which also suffers from cystic fibrosis.

    In newborns, the intestinal form of cystic fibrosis can manifest itself as meconium ileus – intestinal obstruction as a result of blockage of the intestinal lumen with thick and viscous meconium. Normally, in newborns, meconium should leave in the first day of life. If this does not happen, there should be alertness about cystic fibrosis, especially if the parents or close relatives of the child have signs of this disease. Complications of meconial ileus are perforation (hole formation) of the intestinal wall and the development of a serious condition – meconial peritonitis (inflammation of the peritoneum).

    In the first year of life, a child with cystic fibrosis, despite good care, rational feeding and good appetite, does not gain weight well. Signs of cystic fibrosis are especially pronounced when switching from breastfeeding to mixed or artificial feeding. The appearance of children with cystic fibrosis is characteristic: a “doll” face, a deformed chest, a large swollen abdomen, and often an umbilical hernia. The limbs are thin, there is a deformation (thickening) of the terminal phalanges of the fingers in the form of drumsticks.The skin is dry, its color is grayish-earthy. The child’s stool is abundant, liquid, grayish in color, with a fetid, specific smell of rancid fat (“mouse smell”), greasy and shiny, poorly washed off the pot and diapers. A common symptom of “slippage” is when a baby has stool immediately after a feed. In some cases, there may be constipation, a putty stool consistency, or the release of liquefied stool is preceded by the release of a stool. Against the background of constipation, prolapse of the rectal mucosa often occurs (as a rule, surgical correction is not required in this case).Sometimes undigested fat flows out of the baby’s anus in the form of an oily liquid, leaving a greasy mark on the diapers. If bowel movements and urination occur at the same time, fat floats on the surface of the urine in the form of oily films. Due to the constant long-term disturbance of the digestive processes, the child, against the background of a usually good or increased appetite, loses weight (up to the development of severe forms of exhaustion), signs of deficiency of various vitamins (polyhypovitaminosis) appear, metabolic processes suffer.Children are lagging behind in physical development. Diagnosis of cystic fibrosis is carried out by examining feces (determination of undigested food debris), determination of trypsin in feces, sweat samples (sodium and chlorine content in sweat fluid) and using a specific genetic study with the identification of a mutant gene. Treatment for the intestinal form of cystic fibrosis is aimed at improving the digestive processes. In a severe and moderately severe child’s condition, when malabsorption syndrome is combined with dehydration and severe toxicosis, the diet begins with a water-tea break.The child is soldered at the rate of 100-150 ml / kg of body weight per day with 5% glucose solution, rehydron, green tea, etc. In a serious condition, glucose-salt solutions are also administered intravenously. In the hospital in the acute period, hormonal therapy is prescribed with a short course, vitamins. After relieving the exacerbation, the child is transferred to a diet with a feeding frequency of 8-10 times a day. Babies in the first year of life continue to receive breast milk, which is the optimal type of food for them. For artificial feeding, preference should be given to formulas that contain fats in the form of medium chain triglycerides.These components of fats do not require the participation of pancreatic enzymes for their digestion and therefore are easily absorbed. After the introduction of complementary foods and in later life, the child’s diet should include a minimum amount of fat and a large amount of protein. Patients with cystic fibrosis need an increased amount of protein, since it is lost in a significant amount due to malabsorption syndrome. Therefore, it is necessary to include such high-protein foods as meat, fish, eggs and cottage cheese in the diet of a child from 7 months of age.In addition to the diet, individually selected dosages of enzyme preparations are prescribed. To normalize the intestinal biocenosis, preparations of normal intestinal flora are used in courses of 2-3 months or more.