Bio-Resonance Results Glossary Vitals Liver and Gall Bladder Health


The alkaline phosphatase test (ALP) is used to help detect liver disease or bone disorders. In conditions affecting the liver, damaged liver cells release increased amounts of ALP into the blood.
Higher-than-normal ALP levels can indicate: biliary obstruction, bone conditions, osteoblastic bone tumors, osteomalacia (a fracture that is healing), liver disease or hepatitis, eating a fatty meal if you have blood type o or b,  hyperparathyroidism, leukemia, lymphoma, paget disease, rickets, sarcoidosis.
Lower-than-normal ALP levels: hypophosphatasia, malnutrition, protein deficiency, or Wilson disease.
Other conditions for which the test may be done include: alcoholic liver disease (hepatitis/cirrhosis), alcoholism, biliary stricture, gallstones, giant cell (temporal, cranial) arteritis, multiple endocrine neoplasia (men) ii, pancreatitis, renal cell carcinoma.


ALT (Alanine Aminotransferase)

This is present primarily in liver cells. In viral hepatitis and other forms of liver disease associated with hepatic necrosis, serum ALT is elevated even before the clinical signs and symptoms of the disease appear. Although serum levels of both aspartate aminotransferase (AST) and ALT become elevated whenever disease processes affect liver cell integrity, ALT is a more liver-specific enzyme. Serum elevations of ALT are rarely observed in conditions other than parenchymal liver.

Moreover, the elevation of ALT activity persists longer than does AST activity. Elevated alanine aminotransferase (ALT) values are seen in parenchymal liver diseases characterized by a destruction of hepatocytes. Values are typically at least ten times above the normal range. Levels may reach values as high as one hundred times the upper reference limit, although twenty to fifty-fold elevations are most frequently encountered. In infectious hepatitis and other inflammatory conditions affecting the liver, ALT is characteristically as high as or higher than aspartate aminotransferase (AST), and the ALT/AST ratio, which normally and in other condition is <1, becomes greater than unity. ALT levels are usually elevated before clinical signs and symptoms of disease appear.


AST (Aspartate Aminotransferase)

A test measures the amount of this enzyme in the blood. AST is normally found in red blood cells, liver, heart, muscle tissue, pancreas, and kidneys. Low levels of AST are normally found in the blood. When body tissue or an organ such as the heart or liver is diseased or damaged, additional AST is released into the bloodstream. The amount of AST in the blood is directly related to the extent of the tissue damage. After severe damage, AST levels rise in 6 to 10 hours and remain high for about 4 days.  

The AST test may be done at the same time as a test for alanine aminotransferase, or ALT. The ratio of AST to ALT sometimes can help determine whether the liver or another organ has been damaged. Both ALT and AST levels can test for liver damage.  

An aspartate aminotransferase (AST) test is done to: Check for liver damage, Help identify liver disease, such as hepatitis (liver disease may produce symptoms such as pain in the upper abdomen, nausea, vomiting, and sometimes jaundice). Check on the success of treatment for liver disease, find out whether jaundice was caused by a blood disorder or liver disease, and keep track of the effects of medicines that can damage the liver.


Bile Secretion Function

Bile is a digestive juice that is secreted by the liver and stored in the gallbladder. Bile does not contain enzymes like other secretions from the gastrointestinal tract. Instead it has bile salts (acids) which can emulsify fat and break it down into small particles with its detergent-like action. And then help the body absorb these broken-down products of fat in the gut. Bile salts bind with lipids to form micelles. This is then absorbed through the intestinal mucosa. The other important function of bile is that it contains waste products from hemoglobin break down. This is known as bilirubin and is normally formed by the body as it gets rid of old red blood cells which are rich in hemoglobin. Bile also carries excess cholesterol out of the body and ‘dumps’ it into the gastrointestinal tract where it can be passed out with other waste matter.


The liver cells (hepatocytes) produce bile which collects and drains into the hepatic duct. From here it can enter the small intestine to act on fats by traveling down the common bile duct, or it can enter the gallbladder through the cystic duct, where it is stored.


The liver manufactures between 600ml to 1 liter of bile in a day. As bile travels down the ducts, the lining of these passages, secrete water, sodium and bicarbonate ions into the bile, thereby diluting it. These additional substances help to neutralize the stomach acid which enters the duodenum with partially digested food (chyme) from the stomach. 



A bilirubin test is used to detect an increased level in the blood. It may be used to help determine the cause of jaundice and/or help diagnose conditions such as liver disease, hemolytic anemia, and blockage of the bile ducts. Bilirubin is an orange-yellow pigment, a waste product primarily produced by the normal breakdown of heme. Heme is a component of hemoglobin, which is found in red blood cells (RBCs). Bilirubin is ultimately processed by the liver to allow its elimination from the body. Any condition that accelerates the breakdown of RBCs or affects the processing and elimination of bilirubin may cause an elevated blood level. Two forms of bilirubin can be measured or estimated by laboratory tests:

Unconjugated bilirubin is when heme is released from hemoglobin, it is converted to unconjugated bilirubin. It is carried by proteins to the liver. Small amounts may be present in the blood.

Conjugated bilirubin- Is formed in the liver when sugars are attached (conjugated) to bilirubin. It enters the bile and passes from the liver to the small intestines and is eventually eliminated in the stool. Normally, no conjugated bilirubin is present in the blood. 

In adults and older children, bilirubin is measured to:

  • Diagnose and/or monitor diseases of the liver and bile duct (e.g., cirrhosis, hepatitis, or gallstones).
  • Evaluate people with sickle cell disease or other causes of hemolytic anemia; these people may have episodes called crises when excessive RBC destruction increases bilirubin levels.

In newborns with jaundice, bilirubin is used to distinguish the causes of jaundice.

  • In both physiologic jaundice of the newborn and hemolytic disease of the newborn, only unconjugated (indirect) bilirubin is increased.
  • In much less common cases, damage to the newborn’s liver from neonatal hepatitis and biliary atresia will increase conjugated (direct) bilirubin concentrations as well, often providing the first evidence that one of these less common conditions is present.

It is important that an elevated level of bilirubin in a newborn be identified and quickly treated because excessive unconjugated bilirubin damages developing brain cells. The consequences of this damage include mental retardation, and developmental disabilities, hearing loss, eye movement problems, and death.


Detoxification Function, Phase I

Your body doesn’t like to keep any molecules around for a long time. Even “good” molecules, such as hormones, are constantly being disassembled and reconstructed to prepare them to be recycled or eliminated. Thanks to detoxification enzymes, the liver is able to break up most molecules, even toxic and dangerous ones. Enzymes are molecules that act as catalysts in the transformation process. There are thousands of different enzymes, each with a unique role.

Think of this detoxification process as a two-phase wash cycle. Enzymes are like the soap that liberates grease into little droplets, removing impurities that the water can’t remove on its own. 

In the first part of the wash cycle (Phase 1), enzymes break toxins down into intermediate forms. Some toxins are ready for elimination at this stage, but others require a second wash cycle. In Phase 2, these intermediate compounds are routed along one of six chemically driven detoxification pathways, where they are further broken down, and then bound to specific types of protein molecules which act as “escorts” to guide them out of the body, allowing them to exit through the kidneys (in the form of urine) or the bile (in the form of feces). This process is called conjugation.

When the liver is “sluggish,” Phase 1 of the detoxification cycle may not be processing toxins at a normal and necessary speed. This causes toxins to accumulate in the bloodstream. If the hormone estrogen, for example, is not dismantled during Phase 1, the buildup can reach potentially harmful levels. Premenstrual tension can be an expression of this. Many factors can cause Phase 1 to become sluggish. As we age, our detoxification processes slow. Use of medications such as anti-ulcer drugs (cimetidine) and oral contraceptives; exposure to cadmium, lead, and mercury; and consumption of large amounts of sugar and hydrogenated fats hinder Phase 1 detoxification.

Substances that slow down Phase 1 detoxification, setting the stage for a toxic buildup, are called Phase 1 inhibitors. They affect the DNA of the liver cells, causing less detoxification enzymes to be produced. In addition to those mentioned previously, Phase 1 inhibitors include:

  • Grapefruit
  • Turmeric
  • Capsicum (found in hot peppers)
  • Cloves
  • Drugs containing benzodiazepenes and antidepressants 
  • Antihistamines
  • Ketoconazole (used in antifungal medications)
  • Toxins from bacteria in the intestines

A different type of detoxification problem develops if Phase 1 breaks down toxins at so fast a rate that Phase 2 cannot keep up. In this situation, the toxic intermediates produced during Phase 1 waiting to be washed out in Phase 2 flood the system. Many of these intermediate compounds-stuck in between Phase 1 and Phase 2-are more dangerous than the original toxin. This bottleneck can become a biochemical nightmare, damaging the liver, brain, and immune system.

Some of the substances that accelerate the breakdown of toxins in the liver by increasing the production of Phase 1 enzymes, without a concurrent increase in Phase 2 enzymes, are known carcinogens-pesticides, paint fumes, and cigarette smoke. Others are well known for their detrimental effects, such as alcohol and steroids. Even some otherwise harmless substances such as limonene from lemons, increase Phase 1 detoxification. But unlike cigarette smoke, limonene does not create dangerous intermediate molecules. As you read the following list, keep in mind that it is not strictly a list of “bad” things, but of those that increase the rate of Phase 1 detoxification, and that this becomes a problem only when Phase 2 can’t keep up.

  • Phenobarbital
  • Steroids
  • Sulfonamide medications
  • Foods in the cabbage family
  • Charbroiled meats
  • High-protein diets
  • Citrus fruits
  • Vitamin B1
  • Vitamin B3
  • Vitamin C
  • Environmental toxins (exhaust fumes, paint fumes, dioxin, pesticides)
  • Cigarette smoke
  • Alcohol
  • Endotoxins from intestinal bacteria in the bloodstream

Exposure to a toxin, when coupled with exposure to another substance that speeds up Phase 1, is especially dangerous. The combination of alcohol and acetaminophen provides a good example. It’s not uncommon to drink heavily, and later take acetaminophen for the headache that follows. The intermediate compound (from acetaminophen) is an extremely toxic substance called n-acetyl-p-benzoquinoneimine (NAPQI). Under normal conditions, NAPQI is removed quickly during Phase 2, but alcohol intake forces more NAPQI into the liver than Phase 2 can handle.

Research has shown that specific foods and nutrients not only have a beneficial effect on detoxification capability, but can also provide a safe and viable approach to treating a variety of immune disorders and toxicity syndromes.

If two or more detoxification accelerants are combined, they can interact, with serious consequences. An individual on a prescription medication who smokes, for example, actually needs higher dosages of the medication because smoking causes the medication to be broken down faster than it normally would be during Phase 1. If Phase 2 can’t handle the extra burden, a detoxification bottleneck results. 

You can take steps to keep your liver detoxification system running smoothly. Diet has a strong effect on detoxification enzymes, and foods can help “regulate” or balance Phase 1 and 2 activity. Eating foods that support the liver can reduce your susceptibility to damage from toxins and to conditions such as multiple chemical sensitivity syndrome, chronic fatigue syndrome, and cancer. Research has shown that specific foods and nutrients not only have a beneficial effect on detoxification capability, but can also provide a safe and viable approach to treating a variety of immune disorders and toxicity syndromes.

Essential fatty acids are vital for Phase 1 detoxification, and the standard American diet does not provide an adequate supply of these vital nutrients. Essential fatty acid intake in the form of cold-water fish and flaxseed oils have a demonstrated ability to heighten detoxification. Other sources of essential fatty acids include edible oils, such as those made from sunflower seeds, walnuts, and sesame seeds; wheat germ; and supplements of black current seed, borage, or evening primrose oil. 

Eating fresh fruits and vegetables daily is a good way to continually replenish your body’s store of glutathione, necessary for one of Phase 2 pathways. High-quality protein nourishes both the amino acid and the sulfation pathways. Vegetable sources of sulfur for the sulfation pathways include radishes, turnips, onions, celery, horseradish, string beans, watercress, kale, and soybeans. Eggs, fish, and meat are also excellent sulfur sources.

Cabbage, brussels sprouts, broccoli, citrus fruits, and lemon peel oils support Phase 2 activity. Studies have shown dramatic results from consuming broccoli sprout extract, which inhibits the activity of Phase 1 enzymes and, simultaneously enhances the Phase 2 glutathione pathway. Broccoli sprout extracts are especially beneficial for people who have frequent or high-level exposure to pesticides, exhaust fumes, paint fumes, cigarette smoke, or alcohol. Anyone who is exposed to known carcinogens will benefit from broccoli sprout extract.

Foods to Support Liver Detoxification

  • Cabbage family
  • Cold-water fish
  • Flaxseed oil
  • Fruits (fresh)
  • Garlic
  • Nuts and seeds
  • Onions
  • Safflower oil
  • Sesame seed oil
  • Sunflower seed oil
  • Vegetables (fresh)
  • Walnut oil
  • Wheat germ and wheat germ oil

Nutritional Supplements to Support Liver Detoxification

  • Bioflavonoids
  • Black currant seed oil
  • Borage oil
  • Carotenes
  • Coenzyme Q10
  • Copper
  • Evening primrose oil
  • Folic acid
  • Iron
  • Lecithin
  • Magnesium
  • Manganese
  • N-acetyl-cysteine
  • Niacin
  • Riboflavin
  • Selenium
  • Silymarin (milk thistle)
  • Trace minerals
  • Vitamin A
  • Vitamin B6 (pyridoxine)
  • Vitamin B12
  • Vitamin C (ascorbic acid)
  • Vitamin D
  • Vitamin E
  • Vitamin K
  • Zinc

Tests that measure Phase 1 and Phase 2 enzymes take much of the guesswork out of estimating the severity of liver detoxification dysfunction, and can to some extent indicate whether a person is at special risk for cancer, neurological disease, chemical and drug sensitivity, and immune problems.     Source

Detoxification, Phase II, Acetylation

Conjugation of toxins with acetyl-CoA is the primary method by which the body eliminates sulfa drugs. This system appears to be especially sensitive to genetic variation, with those having a poor acetylation system being far more susceptible to sulfa drugs and other antibiotics. While not much is known about how to directly improve the activity of this system, it is known that acetylation is dependent on thiamine, pantothenic acid, and vitamin C.

Detoxification, Phase II, Amino Acid Conjugation

The body manufactures five different types of amino acids that form this detoxification pathway: glycine, taurine, glutamine, arginine, and ornithine. Of these, glycine is the most important for the neutralization of toxins. In some cases, the body cannot make enough glycine to keep up with its own detoxification needs. Though not considered an essential amino acid because the body can make it, glycine production depends on an adequate intake of dietary protein. Individuals who eat a protein-deficient diet have trouble detoxifying environmental pollutants.

Glycine supplies can be depleted by lifestyle stresses. Benzoates for example, found in soft drinks, bind with glycine and rob the body’s store of it. One study found that people who consumed a large number of soft drinks had problems breaking down toluene, a common industrial organic solvent. Aspirin also slows down this detoxification pathway because it competes for available glycine in the liver. When the diet is supplemented with glycine, as well as the other nonessential amino acids, there is a noticeable improvement in the detoxification capabilities of many people.


Detoxification, Phase II, Glucoronidation Pathway

Glucuronidation, the combining of glucuronic acid with toxins, in Phase II can be reversed by Beta glucuronidase enzymes produced by pathological bacteria and cause toxins to be reabsorbed increasing toxicity. Many of the commonly prescribed drugs are detoxified through this pathway. It also helps to detoxify aspirin, menthol, vanillin (synthetic vanilla), food additives such as benzoates, and some hormones. Calcium d-glucurate, a natural ingredient found in certain vegetables and fruits can inhibit beta glucuronidase activity resulting in increased elimination of toxins.


Detoxification, Phase II, Glutathione Conjugation

One of the most important systems in Phase 2 is the glutathione conjugation pathway, which utilizes glutathione for the detoxification of deadly industrial toxins such as PCBs, and the breakdown of carcinogens. Its activity accounts for up to 60 percent of the toxins excreted in the bile. Glutathione also circulates through the bloodstream combating free radicals. No other conjugating substance is as versatile as glutathione and the body’s supply of it, most of which is produced by the liver, is easily depleted. Exposure to high levels of toxins exhausts reserves of glutathione, possibly increasing susceptibility to cancer. Chronic disease, HIV, and cirrhosis use up reserves of glutathione. Excessive exercise, which increases oxidative stress and free radical production, and alcohol consumption, which blocks glutathione production, also deplete glutathione in the blood.


Detoxification Function, Phase II, Methylation Pathway

Methylation and glutathione are very tightly intertwined. There is a critical metabolic intersection-a fork in the road-where cells must decide to either make more glutathione, or support more methylation. The overall balance between these two options is crucial to health. Your body can take homocysteine and convert it back to cysteine. Homocysteine is a metabolite of the essential amino acid methionine, and elevated levels have been associated with vascular disease. Homocysteine is created when methionine donates its methyl group to another molecule in a process known as methylation.

Methylation is a fundamental process of life which is intimately linked to redox status. In chemistry, a methyl group is a hydrocarbon molecule, or CH3. When a substance is methylated, it means that a CH3 molecule has been added to it. Methylation can regulate gene expression, protein function, even RNA metabolism. It can suppress viruses, even latent viruses or cancer viruses we are born with and can help us handle heavy metals. In the liver in particular, methylating a toxin helps change it to a form of the compound that can be more easily processed and excreted.

Methylation is an extremely broad and fundamental action that nature uses to regulate all kinds of processes. It regulates epigenetic changes-changes to gene expression that occur because of environmental factors-by affecting how DNA unravels during development. Some changes can be permanent for the whole lifespan and can even be passed down as many as three generations. That shows that the environment, through the process of methylation, can be quite a profound influence. There are 150-200 methyl transferase enzymes, and each enzyme can methylate multiple targets. So you can imagine methylation as a spider’s web within each cell, and that web branches out in many directions.

Methylation and glutathione are very tightly intertwined. There is a critical metabolic intersection-a fork in the road-where cells must decide to either make more glutathione, or support more methylation. The overall balance between these two options is crucial to health, and this occurs with homocysteine. When methionine gives away its methyl group, we’re left with homocysteine. And the body has to decide, should homocysteine be methylated, and go back into methionine, or should it be converted into cysteine, so that the body can make more of the antioxidant glutathione? This fundamental decision is made again and again by the body, and the overall balance is crucial to health. Too little glutathione and we will end up with free radical, oxidative damage. Not enough methylation, and many genes and viruses will not be properly regulated. Excess homocysteine, and the risk of vascular disease goes up.


Detoxification, Phase II, Sulfation Pathway

The weakest pathway in most people, from a dietary standpoint, is sulfation, the one responsible for the transformation of neurotransmitters, steroid hormones, drugs, industrial chemicals, phenolics (compounds derived from benzene, commonly used in plastics, disinfectants, and pharmaceuticals), and especially toxins from intestinal bacteria and the environment. Intake of too little dietary sulfur, a molecule that must come from our diets, is a cause of ineffective detoxification. If your exposure to substances that need to be detoxified via the sulfation pathway is high, but your sulfate reserves are low due to an inadequate diet, you will not be able to break down these toxins.
Studies have established a strong association between the function of the sulfation pathway and a variety of illnesses including Alzheimer’s disease, Parkinson’s disease, motor neuron disease, autism, primary biliary cirrhosis, rheumatoid arthritis, food sensitivity, and multiple chemical sensitivity. A comprehensive detoxification profile test identifies alterations in this pathway.


Energy Production Function

Understanding the liver’s role in energy production clarifies how a compromised liver can result in fatigue. The liver is intimately involved in supplying the body with energy. The liver converts glucose into glycogen, storing it for later use. When the body needs energy, liver glycogen can release glucose to provide fuel for creating a burst of energy. Additionally, if the body is low in carbohydrates, the liver can manufacture more from fat or proteins.

By producing, storing and supplying the body with glucose, the liver is a key player in preventing fatigue. A liver unaffected by disease releases glucose between meals, or whenever the cells need nourishment and energy. While a healthy liver maintains a steady level of energy throughout the day, one hampered by disease has a reduced ability to produce glucose, and less space to store it.

For those will liver disease, the continued, long-term response of the immune system contributes to fatigue. The release of neurotransmitters (chemicals in the brain) is part of a healthy immune system response. When the body is physically or emotionally stressed, the immune system activates, causing the brain to release the appropriate substance for self-protection. Liver disease causes a chronic, uncontrollable stress to the patient, weakening the immune system and decreasing the release of certain neurotransmitters.


Liver Fat Content

Fatty liver is a condition in which the cells of the liver accumulate abnormally increased amounts of fat. Although excessive consumption of alcohol is a very common cause of fatty liver (alcoholic fatty liver), there is another form of fatty liver, termed nonalcoholic fatty liver disease (nonalcoholic fatty liver disease), in which alcohol has been excluded as a cause. In nonalcoholic fatty liver disease, other recognized causes of fatty liver that are less common causes than alcohol also are excluded.

Nonalcoholic fatty liver disease is a manifestation of an abnormality of metabolism within the liver. The liver is an important organ in the metabolism (handling) of fat. The liver makes and exports fat to other parts of the body. It also removes fat from the blood that has been released by other tissues in the body, for example, by fat cells, or absorbed from the food we eat. In nonalcoholic fatty liver disease, the handling of fat by liver cells is disturbed. Increased amounts of fat are removed from the blood and/or are produced by liver cells, and not enough is disposed of or exported by the cells. As a result, fat accumulates in the liver.

Nonalcoholic fatty liver disease is classified as either fatty liver (sometimes referred to as isolated fatty liver or IFL) or steatohepatitis (NASH). In both isolated fatty liver and NASH there is an abnormal amount of fat in the liver cells, but, in addition, in NASH there is inflammation within the liver, and, as a result, the liver cells are damaged, they die, and are replaced by scar tissue.

Nonalcoholic fatty liver disease is important for several reasons. First, it is a common disease, and is increasing in prevalence. Second, NASH is an important cause of serious liver disease, leading to cirrhosis and the complications of cirrhosis–liver failure, gastrointestinal bleeding, and liver cancer. Third, nonalcoholic fatty liver disease is associated with other very common and serious non-liver diseases, perhaps the most important being cardiovascular disease that leads to heart disease and strokes. Fatty liver probably is not the cause of these other diseases, but is a manifestation of an underlying cause that the diseases share. Fatty liver, therefore, is a clue to the presence of these other serious diseases which need to be addressed.     Source 



Protein Metabolism The liver synthesizes non-essential amino acids from other amino acids, glucose and fatty acids. The enzymes alanine and aspartate transaminases convert amino acids that are in abundance to others that are needed by the body. A high concentration of these enzymes in the blood indicates liver damage. The liver makes most plasma proteins including albumin and produces coagulation factors. The liver breaks down proteins and removes the toxic ammonium ion by converting it to urea.  Serum Globulin; a globulin or mixture of globulins occurring in blood serum and containing most of the antibodies of the blood. The serum globulin electrophoresis test measures the levels of proteins called globulins in the fluid part of a blood sample. This fluid is called serum, one of a group of proteins in blood serum with antibody qualities. The various types of serum globulins, designated alpha, beta, and gamma, have different specific properties.  Serum total bile acid; Serum total bile acid (TBA) levels are used clinically as a sensitive and reliable index of hepatobiliary diseases. In the present study, to assess the clinical usefulness of determining TBA in interferon (IFN)-treated patients, changes in liver function test values, including TBA and liver histology, were examined in 36 chronic hepatitis C patients for 3 years after a sustained response to IFN treatment.  Total bilirubin Bilirubin is a brownish yellow substance found in bile. It is produced when the liver breaks down old red blood cells. Bilirubin is then removed from the body through the stool (feces) and gives stool its normal color. A bilirubin test measures the amount of bilirubin in a blood sample. Total bilirubin and direct bilirubin levels are measured directly in the blood, whereas indirect bilirubin levels are derived from the total and direct bilirubin measurements. When bilirubin levels are high, the skin and whites of the eyes may appear yellow (jaundice). Jaundice may be caused by liver disease (hepatitis), blood disorders (hemolytic anemia), or blockage of the tubes (bile ducts) that allow bile to pass from the liver to the small intestine.