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Fatty Acid Metabolism and Alpha XP Factor as Expressed in Autism

Fatty Acid Metabolism and Alpha XP Factor as Expressed in Autism

Dr. Brice E. Vickery
©2007 SuperNutrient Corporation

Fatty acid metabolism (FAM) is a complex process, which begins with digestion and ends with physiological regulation and energy production processes in the body. Autism has been reported as being associated with FAM:

  1. Studies have located FAM disorders ranging from maldigestion and taurine deficiency within the digestive system to beta oxidation malfunction within the cell
  2. This article will go through FAM starting in the stomach and ending in the cell, linking issues currently being investigated in autism with Alpha XP factor, critical deficiency of systemic protein in the body.

Dietary protein must be fully digested down to amino acids in order for the system to make systemic proteins such as enzymes, transporter proteins, repair proteins and binding proteins. When this digestive process stops happening, it becomes the limiting factor in a person’s ability to maintain their health. A continuing state of poor protein degradation will eventually cause systemic failure of various kinds. This limiting factor is the Alpha XP factor.

The Alpha XP Factor© was discovered in the early 1980’s by Dr. Brice E. Vickery. Clinical studies show it as the probable cause or major contributing factor to many unsolved conditions such as hypoglycemia, degenerative disk disease, chronic fatigue, fibromyalgia, arthritis, and even osteoporosis. The factor was named alpha; first, x; unknown, and P for protein, (which also means first nutrient.) Before Vickery’s discovery, doctors assumed that normal serum protein levels meant that the cells were receiving adequate amounts of amino acids for systemic protein production. Dr. Vickery found that in nine out of ten persons, this is not the case. Alpha XP is the rule rather than the exception.

Digestive system:

Major digestion of dietary fat occurs in the small intestine where it must mix with the protein lipase if it is to break down into fatty acids, which can then be used for the production of systemic fats such as phospholipids, which form the cell membrane and chylomicrons, which comprise lipoproteins such as HDL and LDL. Lipase is a protein which will quickly denature in the aqueous environment of the intestine and is protected from unfolding by other substances such as the protein colipase. Without this cysteine rich polypeptide, lipase would become destabilized by the action of bile salts and denature, becoming useless. However fat digestion also needs bile salts, which emulsify fats in preparation for their total degradation by lipase. When fats are completely broken down into free fatty acids and a mixture of mono- and diacylglycerols monoglycerolsl, they must be prepared for transport through the aqueous environment of the blood to the cells. They are absorbed into the intestinal wall where they are resynthesised back into triacylglycerols. Fats cannot tolerate aqueous environments such as blood or plasma unless the body first coats them with protein. Various types of apoproteins are manufactured in the liver and intestine that bind with these fats. The apoprotein B–100 is manufactured in the gut and binds with triacylglycerols, cholesteryl esters, phospholipids and free cholesterol to form chylomicrons (These lipoproteins reach the bloodstream via the lymphatic vessels. They pass fatty acids to adipose tissues until there are only chylomicron remnants left. These remnants are absorbed by the liver, repackaged as VLDL, and sent out to the tissues again. The VLDL loses fatty acids to tissue along the way and gradually becomes less dense becoming LDL and then HDL.) Free fatty acids are transported through the blood by the serum protein, albumin.

  1. Surveys of autistic children have found them deficient in the following amino acids: taurine, lysine, phenalalanine, methionine, cysteine tyrosine leucine, glutamine,isoleucine, and valine.
  2. Autisic children in general are found to have more essential amino acid deficiencies than control group children.
  3. The amino acid taurine, (a derivative of cysteine) is necessary for the synthesis of bile salts.
  4. The enzyme lipase contains the amino acids glutamine, leucine and lysine. If autistics don’t have enough amino acids to make lipase, how will they digest their fats?
  5. Seven of the eleven essential amino acids are necessary for the protein albumin: methionine, lysine, tryptophane, valine, phenalalanine, leucine.and arginine.(although some doctors only consider arginine to be semi-essential because it is synthesized by humans, most of it is hydrolyzed to urea and orthinine) If autistic patients are low in five of the seven essential amino acids required to make albumin, how can they make adequate amounts for fatty acid transport?
  6. Colipase is an enzyme rich in leucine and cysteine, in a segment of pancreatic colipase 112 amino acids long, all eleven amino acids were expressed with leucine expressed 11 times and cysteine 10 times. The next most frequently expressed were lysine and isoleucine. (7). If autistic patients are low in the amino acids needed to make colipse, how will their pancreatic lipase be able to function properly?
  7. Out of an Apo B100 fragment of 347 amino acids, 197 were essential amino acids, the most frequently expressed being leucine (40), isoleucine (38) and lysine(32), three of the amino acids deficient in autistic children. If autistic children have inadequate amino acids for Apo B–100, how will they make chylomicrons?

Cell:

For the most part, the body’s energy reserves are stored as triacylglycerides, which are broken down to free fatty acids and glycerol by lipases. Glycerol is metabolized by glycolosis, which occurs in the cell cytoplasm and is made up of nine reactions each catalyzed by a specific enzyme, ultimately resulting in ATP, or energy. Free fatty acids (FFAs) must get into the mitochondria in order to produce energy in the krebs cycle. First the FFAs are “activated” in the cytoplasm, which means they are converted into fatty acyl–CoAs of varying lengths. The short and medium chain fatty acids can pass directly through the mitochondrial membrane but the long chain acyl–CoAs must engage in a series of three reactions with carnitine, a special amino acid that is transported into the mitochondrial membrane by a specific membrane bound transport complex (afterwards free carnitine returns to the cytoplasm. Once fatty acly–CoA is inside the mitochondria it is ready to enter the beta-oxidation process, which produces the necessary acetyl–CoA for the krebs cycle. Beta-oxidation also requires a CoA dehydrogenase enzyme specific to the chain length of the fatty acyl–CoA (short, medium, long, or very long). Each round of B–oxidation produces 1 mole each of acetyl–CoA, NADH, and FADH2. The Acetyl–Coa then heads to the krebs cycle where it helps produce ATP.

  1. Autistic children are reported to have abnormally high levels of dietary peptides such as casein, gluten, lactalbumin ,and lactoglobulin in their systems showing that they are not breaking down their dietary protein. How will they be able to produce all the amino acids that they need to synthesize systemic proteins such as glycolytic enzymes or acyl-CoA.
  2. The acyl–CoA protein segment of the fatty acyl–Coa in the cell cytoplasm is also made up of amino acids, the sequences peppered through with essential amino acids. Studies also show that this protein is formed from lipids by enzyme activity Amino acids are needed to form these two proteins.
  3. Autistic children are frequently found to be deficient in carnitine, while new studies show that increases in carnitine levels improve FAM. If carnitine is low, how can the body produce three carnitine transport enzymes?
  4. Autistic children are frequently found to be deficient in carnitine, while new studies show that increases in carnitine levels improve FAM. If carnitine is low, how can the body produce three carnitine transport enzymes?

Fatty acids are also the building blocks of phospholipids. These are lipoproteins, which along with various membrane proteins, make up the cell membrane. Phospholipids are shown to be low in many autistic patients. The fatty acid component of these phospholipids is subject to wear and tear and so must be removed by a phospholipase enzyme. A fatty acid transferase/ligase enzyme then repairs the damaged membrane. These two enzymes have shown highly unstable activity in autism, resulting in leaky cell membranes, affecting the function of membrane proteins, causing inflammatory conditions and cell damage. Could it be that these proteins cannot work properly because the general balance of essential amino acids in the autistic body is so far off that all the other amino acids are drastically limited in their ability to perform and so proteins such as phospholipases and fatty acid transferases begin to malfunction?

Summary list of autistic symptoms suggesting Alpha XP factor:
Substance: Needed for:
Low taurine bile salts
Low glutamine, leucine lysine lipase
Low cysteine, leucine colipase
Low leucine, isoleucine, lysine apo B–100
Low methionine, lysine, tryptophane, valine, phenalalanine, leucine.and argenine albumin
Low carnetine membrane fatty acid transfer
Low LCAD cellular beta oxidation
Low leucine, lycine, LCAD
Low phospholipids cell membrane integrity
Unstable cell repair enzymes cell membrane integrity and function

The story of FAM is directly tied in with the story of protein metabolism. If dietary proteins cannot be broken down into amino acids then there cannot be adequate amounts of systemic protein to support FAM through the actions of digestive enzymes, protective protein coating, transport proteins, energy cycle proteins, and repair proteins. There are clinical studies that show if the correct balance of essential amino acids is administered, one that stays within the bounds of the essential limiting amino acid factor, then the basic protein deficiency now known as the primary unknown protein factor or the “Alpha XP Factor” can be overcome. The body’s supply of digestive enzymes picks up, and vitamin, mineral and fatty acid metabolism is supported more completely. Once Alpha XP is taken care of then the body can digest proteins down to amino acids thereby fulfilling the body’s primary need for systemic protein. The first guard against Alpha XP is adequate amounts of digestive enzyme production to fully digest dietary proteins into amino acids. When this is achieved, co–enzymes, such as vitamins, co–factors, such as minerals, and hydrophobic systemic fats, such as fatty acids have a much higher chance of working properly. Stress, illness, and aging are all precursors of Alpha XP and lead to lower and lower levels of systemic protein. Looking at the protein deficiencies and instabilities that research has uncovered in the disease, autism, it is quite plausible that Alpha XP factor may be a large part of the problem.

Research: