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Gilbert's Syndrome


Senior Member
Sheffield UK
Has anyone ever been told they have Gilbert's Syndrome?

I got this on the subject from the Mayo Clinic:


Gilbert syndrome
By Mayo Clinic staff


Gilbert (zheel-BAYR) syndrome is a common, mild liver disorder in which the liver doesn't properly process a substance called bilirubin. Bilirubin is produced by the breakdown of red blood cells. Also known as constitutional hepatic dysfunction, unconjugated benign bilirubinemia and familial nonhemolytic jaundice, Gilbert syndrome typically doesn't require treatment or pose serious complications.

In fact, Gilbert syndrome is usually not considered a disease because of its benign nature. You most often find out you have the disorder by accident, when you have a blood test that shows elevated bilirubin levels.

Gilbert syndrome affects 3 percent to 7 percent of the U.S. population. Worldwide estimations vary, and no good measure exists. More males than females have the condition.

Usually no symptoms, sometimes jaundice
As an inherited condition, Gilbert syndrome is present from birth. Although it rarely causes symptoms, it may raise bilirubin enough to produce mild jaundice.

While the bilirubin does not reach a dangerous level, the appearance of jaundice may be unsettling. Typically, excess bilirubin turns the whites of your eyes yellow before affecting the color of your skin. If the bilirubin level keeps rising, your skin may develop a yellowish tinge.

Possible symptoms
You may experience episodes of:

■Abdominal pain
However, it's not known if Gilbert syndrome actually causes such symptoms, or if they're related to stress or other conditions.

Factors that may increase symptoms
A number of factors may increase bilirubin if you have Gilbert syndrome. These may include:

■Illness, including infections, such as a cold or the flu
■Fasting or skipping meals
If you have Gilbert syndrome, you have inherited an abnormal gene that controls the enzyme that helps break down bilirubin. Bilirubin is a yellowish pigment and is a normal waste product from the breakdown of old red blood cells. Bilirubin travels through your bloodstream to the liver. Normally an enzyme in liver cells breaks down the bilirubin and removes it from the bloodstream. The bilirubin passes from the liver into the intestines with bile. It's then excreted in stool. A small amount of bilirubin remains in the blood.

When you have Gilbert syndrome, you have a lower level of the enzyme that breaks down bilirubin. Consequently, excessive amounts of a form of bilirubin called unconjugated bilirubin can build up in your blood.

Risk factors
Other than the chance of inheriting abnormal genes, there are no known risk factors that increase the likelihood that you'll get Gilbert syndrome.

When to seek medical advice
If you notice a yellowish tinge to your skin or the normally white portions of your eyes, let your doctor know as soon as possible. A variety of conditions other than Gilbert syndrome can cause jaundice, and medical tests and exams can rule out serious illnesses.

Check with your doctor before taking new medications and take care not to consume higher than recommended doses of acetaminophen (Tylenol, others). You may be at greater risk of liver side effects for these or other drugs.

Tests and diagnosis
Often found by accident or if you have jaundice
If you have jaundice, your doctor may suspect that you have Gilbert syndrome or perhaps another condition. Often, though, Gilbert is found purely by accident when you have blood tests for other health reasons. Although it's present from birth, Gilbert syndrome usually isn't diagnosed until puberty or later, when bilirubin production increases.

Blood tests
Your doctor may do a physical exam and order additional blood tests. With Gilbert syndrome, unless you have an episode of jaundice, there are no physical signs or symptoms.

Common blood tests include:

■Complete blood count (CBC)
■Liver function tests
A diagnosis of Gilbert syndrome can usually be made from blood tests. With Gilbert syndrome, all of the results will typically be normal except for the mildly increased level of unconjugated bilirubin.

When you have Gilbert syndrome, the level of bilirubin in your blood may fluctuate. It's not always higher than the normal range. If your initial blood test shows a normal level of bilirubin, your doctor may suggest repeating the tests a couple of times.

Tests that help rule out other conditions
Rarely, your doctor may suggest other tests, including:

■An ultrasound of your liver
■Fasting for a 24-hour period to see if that increases bilirubin levels
■Genetic testing, which is not widely available, to check for the abnormal gene that causes Gilbert syndrome
When you have jaundice or a high bilirubin level, it's important to ensure that you don't have a more serious liver condition such as hepatitis or an obstructed bile duct. Your doctor may recommend other tests to check for such conditions.

Gilbert syndrome can cause episodes of jaundice. However, the jaundice is usually mild and goes away on its own. There are no other known complications of the condition, and it won't damage your liver.

More side effects with certain medications
The low level of the bilirubin-processing enzyme may cause increased side effects with certain medications because this enzyme helps eliminate these medications. In particular, irinotecan (Camptosar), a medication used to treat colon cancer, can reach toxic levels if you have Gilbert syndrome, causing severe diarrhea. Because of this potential effect with certain medications, talk to your doctor before taking any new medications if you have Gilbert syndrome.

Treatments and drugs
Because Gilbert syndrome is essentially a mild, harmless condition, it doesn't require treatment. The level of jaundice associated with Gilbert syndrome is typically harmless as well, and goes away on its own.

If you have Gilbert syndrome, you don't typically need long-term monitoring of your condition or repeat blood tests. But consult your doctor if you notice worsening jaundice or other symptoms.

If you're concerned about jaundice, the barbiturate medication phenobarbital may reduce bilirubin levels but can have side effects such as sedation and lightheadedness.

Gilbert syndrome is an inherited genetic disorder. Getting the disorder isn't related to lifestyle habits or environment.

The only way to theoretically prevent the condition is to keep parents from passing the abnormal gene that causes it on to their children. But more than half the people in the general population carry one copy of this abnormal gene, making it very common. If two people with this abnormal gene have a child, they may pass along the genetic defect that causes Gilbert syndrome — but not always. Not everyone who has two copies of this abnormal gene gets Gilbert syndrome. This means you may have the condition without a family history of it. In contrast, everyone with Gilbert syndrome does have two copies of this abnormal gene.

Lifestyle and home remedies
Certain events in your life can trigger episodes of higher bilirubin levels in Gilbert syndrome, leading to jaundice. Doing what you can to manage those situations can help keep bilirubin under control and perhaps prevent bouts of jaundice.

These steps include:

■Avoiding infectious illnesses, such as colds and the flu
■Managing stress
■Eating a nutritious diet, and avoiding fasting and skipping meals

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Parent Liver problems
April 18, 2008

I was told I had 'it' when I was at Oldchurch Hospital (2001?), a CFS in patient ward in London, by Professor Lindley. He said it had been noted as more prevalent in PWCFS (2 patients in the six bed ward had it). I looked it up on Wikipedia.


It seems only a few studies have been done on this minor 'syndrome'.

Peter White and Anthony Cleare looked at in relation to CFS in 1993.

Any thoughts anyone?


Senior Member
My husband has it and only found out through a blood test for liver function which the doctor took because he was feeling ill. It doesn't seem to affect him a lot.


Has anyone ever been told they have Gilbert's Syndrome?

I was told I had 'it' when I was at Oldchurch Hospital (2001?), a CFS in patient ward in London, by Professor Lindley. He said it had been noted as more prevalent in PWCFS (2 patients in the six bed ward had it). I looked it up on Wikipedia.


It seems only a few studies have been done on this minor 'syndrome'.

Peter White and Anthony Cleare looked at in relation to CFS in 1993.

Any thoughts anyone?

When I first became ill I had a number of tests done and the doctor told me I had Gilbert's. So I have it, that's about all I can say really.


I do to. Cytochrome p450. It explains why we are chemically sensitive and have detox pathway issues. Genova labs has a good gene detox profile test. Gluthathione deficiency plays a role.....It explains why we are so toxic w heavy metals, etc. Our blood is toxic acidic perfect place for viral reactivation. The viruses are just a side effect. We are the canaries in the coal mine.



Senior Member
Very interesting thank you!

Here what I found:

Pathology of bilirubin conjugation


Is due to a very mild deficiency of glucuronyl transferase.It is a very frequent disorder. It affects 5 to 7% of the general population. More common in males. It consists of mild fluctuating jaundice due to non- hemolytic unconjugated hyperbilirubinemia in the range of 5 to 7mg/dl or rarely higher. The liver is morphologically normal. State of health and life-span are normal. Hemolysis, low caloric diet, nicotinic acid will increase the jaundice.
A lipid diet will decrease the jaundice.
Phenobarbital and other enzyme inducing agents are beneficial....


I always had a skin with a yellowish tendancy, I wonder if I may be concerned...

If this is the case, I may stop my supplementation with Nicotinamide!




Senior Member
Hi Adam,

I have it too.Dr Myhill informed me that probably about 10 years ago.It is not serious as far as I recall.However one may suffer from more body toxin problems as a result(?).

yes it does!

"Unconjugated bilirubinin is lipophilic. Its conjugation with glucuronic acid renders it hydrophilic, thus, it can be eliminated in the bile.

The glucuronidation of bile proceeds in two steps: first glucuronic acid (GA) is synthesized from cytosolic glucose that is complexed with uridinediphosphate (UDP) ad forms udpglucuronic acid (UDPGA).
From this compound, the glucuronic acid is transferred to blirubin.
The first reaction is catalyzed by a UP- glucose dehydrogenate,
the second reaction is catalyzed by bilirubin- DUGAN- transferees that is synthesized by microsomes.
Any deficiency of these two enzymes will result in defective conjugation and elimination of bilirubin.
On the other end, administration of microsomal enzyme inducers such as phenobarbital, glutethimide and antipyrine favor bilirubin conjugation and elimination by increasing blirubin transferase activity. Conjugation occurs in the endoplasmic reticulum and consists of forming an ester between glucuronic acid and one or both propionic side-chains of bilirubin.
The result will be formation of bilirubin mono and di-glucuronides. In general, about 80% of the di and less than 20% of the mono are formed. Human bile cotains also small amounts of unconjugated bilirubin.
In summary:



The most specific Glucuronyltransferase for bilirubin is UGT1A1:

"UGT1A1 is the only enzyme (?) catalyzing the generation of water-soluble bilirubin glucuronides in hepatocytes, thus mutations in this gene lead to deficiencies in bilirubin conjugation and excretion. To date, 130 UGT1A1 mutations, in both coding and non-coding regions of the gene, have been identified that decrease or abrogate enzymatic function (24). Conversely, UGT1A1 activity can be increased by phenobarbital administration, which induces UGT1A1 gene expression by activating the distal phenobarbital response enhancer element (25)."


"Gilbert syndrome (GS)
First described in 1901 by Gilbert and Lereboulet (26), GS is the most common hereditary hyperbilirubinemia syndrome, occurring in 3–13% of the population (27,28). It is typically associated with at least 50% decrease in hepatic bilirubin UGT activity (29). GS is now regarded as an autosomal recessive disorder, with affected patients being either homozygotes or compound heterozygotes (i.e. two different recessive alleles at a particular locus) (30). More than 100 different mutations have been implicated in GS and their frequencies differ among different ethnic groups (31)."

"UGT1A1 is involved in the breakdown of bilirubin, estrogen, and several carcinogens.
UGT1A1 is also responsible for the breakdown of BPA (in plastics)

rs8175347 (not in 23andMe) is associated with UGT1A1*28"


UGT1A6 is also involved in transforming bilirubin, hormones, and certain drugs (aspirin, acetaminophen) into water-soluble metabolites that can then be excreted from the body. Studies on this gene also look at the polymorphisms in association with benzene poisoning.