Hello Rand,
The length of time to restock the bodys stores depends on how much iron and copper your body needs to eliminate, and how much energy you need to produce in the time that you are eliminating it (like mowing the yard, riding your bike, swimming, etc.), what you eat, and how much stress you have either mental or physical, while this process occurs. The following are my observations, not all scientifically proven statements though some are.
A 9 year old boy client was blood tested as high ferritin and several of his lymph nodes in his neck were enlarged. His brown hair had become orange as well, and he was easily angered and a problem at school, because he would get into fights daily. Iron goes to a section of the brain called the amygdala, where you can react aggressively on instinct, before rational thought occurs. As I wrote previously, if you are tested as high ferritin then you can be 99% certain you have high iron stored in the liver and possibly elsewhere.
However, if you have a low serum ferritin, it is not accurate to say you have low iron stores. This is because there are two types of ferritin. One is the serum ferritin protein that contains little or no iron. Serum ferritin is formed on the endoplasmic reticulum (ER) in the liver. The other form is storage ferritin which is formed on free ribosomes.
When the body is deficient in manganese, these ER structures become swollen and elongated and unable to adequately produce serum ferritin. Thus, a low serum ferritin reading may be indicative of malfunctioning ER structures, which has been shown to track back to riboflavin deficiency in the dogs (and one human client that was blood tested as manganese deficient) that I did liver biopsy research with. All the dogs had over accumulated iron and copper in their livers, but could not release it from storage due to the malfunctioning ER structures.
A 90 pound German shepherd client, age 9, had severe niacin deficiency, as observed by the black deposits under the skin. All his life, he was very aggressive and required additional training to keep him under control. His tan fur also turned an orange color, which the breeder told the owner was just like all the others from his lineage, not knowing this was a sign of inability to use copper. Everywhere he licked turned a plum or bronze color.
The dog was started on just 2 doses of B2, at 6.25mg/dose. He very slowly and gradually was increased to his current dosage of 25 mg. of B2, 8 times a day and twice during the night for the past 3 months. If we increased his dosage too quickly, he would again become extremely aggressive and agitated, the discharge from the ears would worsen, he could not stop itching and chewing at the black spots on his belly and his stools would turn orange and very loose. Currently, he continues to improve as his black deposits are fading, hes stopped having a black discharge from his ears, he no longer licks and chews at his groin and can now be peaceful when at the grooming salon where the owner works. His retest chart indicates that his stores of B2 have not begun to improve. However, his iron and copper indicate much better usage by the liver. Better usage = elimination as well as ability of the liver to manufacture more carrier proteins to work with the extra iron. His manganese level is coming up, indicating that he has enough B2 to convert Folic acid to its active form, which activates choline, which allows the liver to store manganese. When you can retain manganese, the ER structures in the liver keep healing and as they heal more iron and copper can be released.
The body makes 5 million red blood cells per second at rest. This process requires B2 enzyme reactions to let the iron out of the liver, put it in myoglobin and send it to the bone marrow to stimulate hemoglobin production and put it into the Red Blood Cells with iron to carry oxygen. The bone marrow produces the precursor cell called a protoporphryn in anticipation of myoglobins arrival, needed for heme synthesis. When iron is not available for heme synthese protoporphyrin combines with zinc to form zinc protoporphyrin. The amount of zinc protoporphyrin (EZP) increases in riboflavin deficiency due to inability to mobilize iron from the liver. This is when you start to see zinc decreasing on a hair test because it is being used in these blood cells along with lead. This is why I believe all the CSF charts Ive received indicated deficiency of zinc and very high levels of lead. This protoporphyrin carries oxygen, but not nearly as well.
Lack of adequate usable iron has been shown to cause gastritis in about 75% of patients. This is associated with a reduction in gastric secretion. With progression of gastric damage is the loss of ability to secrete intrinsic factor which is critical to absorption of Vitamin B 12.
Visible features associated with lack of usable iron affect the finger and toe nails. They can become brittle and fragile with longitudinal ridges. These are due to the change in the bodys Na/K ratio, allowing calcium to precipitate out of suspension from the blood and accumulate in the soft tissues like the nails. Also can be observed are transverse recessed grooves in the nails. These reflect inability to use iron; changing back and forth from a high degree of deficiency to a more moderate degree of deficiency. The nail normally grows from beginning to end in 6 months so where you see the indents, can normally indicate a more stressful period in your life, which drops the level of B2, leading to less use of iron, which the nails (thumb or toe nails) indicate. In continuous, severe deficiency, the nails become thin, flattening and finally develop koilonychia, concave or spoon-shaped nails.
Many changes are seen on the epithelial layer of the tongue: soreness or burning, with varying degree of redness. In severe cases, fungiform papillae may also be affected, leaving the tongue completely smooth and waxy or glistening. There may be ulcerations or fissures at the corners of the mouth called angular stomatitis the later is also a common symptom of Riboflavin deficiency. See how the two go hand in hand?
B2 travels with bile, which continuously gets reabsorbed at the end of the small intestines and re-circulated called enterohepathic circulation. As the dog began supplementation with B2, his liver immediately sensed it contained too much iron which it wanted to release. So it increased bile production to release the iron that it could (which this is scientifically proven). This iron travels with the bile but if too much is released, when the bile is taken back into blood circulation, it will take some of that released iron back into the blood with it. This then, will require more usage of B2 enzymes. So if he was given too much B2 this is why you would see the same symptoms that he exhibited prior to B2 supplementation as after B2 supplementation. His liver is slowly repairing the ER structures which is where the carrier proteins are assembled. But when first staring the B2 very few structures are working well, so only a small amount of iron must be released so that only a small amount would be reabsorbed or he still could not make enough transferrin to handle the extra circulating iron.
In addition, by adding riboflavin, the body can now send the myoglobin to the bone marrow for production of hemoglobin to be placed into red blood cells to carry oxygen. This requires B12 as well. But as shown above, its absorption was compromised so when the body looks for B12 (normally 2-5 mg, 50%. is stored in the liver), it may find little to none. This can quickly case a person or animal to experience symptoms of B12 deficiency which also cause painful tongue, gums, teeth, dry skin and lower energy production and memory loss. Thus additional supplementation is normally needed. If you take too much B12, the body knows that red blood cells are deficient in iron (heme), thus it looks for B2 to release iron from the liver in an effort to make more. So if you take too much B12, you may lower the already low B2. Again, small amounts of B12 are advised in this nutritional situation.
The question was asked how does riboflavin affect B6: To convert pyridoxol-5-phosphate and pyridoxamine-5-phosphate need pyridoxal oxidase (requires FMN) to be converted to pryidoxal-5-phosphate, the active form of B6.
Also to be absorbed, P5P (more commonly called PLP) must be dephosphorylated to pyridoxine. These is an enzyme in our intestines that does this. Phosphorylated compounds rarely cross membranes, including the intestinal epithelium, so taking PLP is just a very expensive way to give pryidoxine.
You also require B2, usable B6 and usable iron to create niacin from tryptophan. In the energy cycle, you require many reactions that require niacin, so again you can see adequate B2 is required to run the reaction because it is needed to convert B6 and produce niacin and convert folic acid to its usable form as well as allow absorption of B12 all needed in the citric acid cycle. You also need B12 to recycle Folic Acid. You also require the usable form of FA to convert choline to its usable form, which allows the liver to store manganese and the citric acid cycle to use choline.
Many have asked me why was this not easily found by researchers if it is just riboflavin deficiency. My answer is that it is not just riboflavin deficiency and it did not start as riboflavin deficiency, thus it does not present symptoms that would normally be observed by professionals looking for only riboflavin deficiency.
There clear as mud?
Im writing why this has occurred all over the world. Sadly, the WHO (World Health Organization) actually has a sentence in their 2006 food enrichment guide that says they knew they were not supplying adequate levels of riboflavin. Ill post it as soon as I can finish it.
