Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by brenda, Mar 17, 2012.
Thanks a lot Rich for your detailed answer,
So basically what you are saying is, it's really not beneficial for "anyone" to be taking a high potency B-complex formulation due to it being overkill due to your body excreting out most of it and also the detrimental effects of lowering B-2 even further? What if someone were to only take <from the B group> only B-2 and B-12<for methylation help> would one not even have to adhere to the theory of "if you take seperate B's you have to make sure to take a B-complex along with it"? Maybe it is just hogwash marketing hype to get people to buy more vitamins.
I don't understand, B2 is already included in the SMP. The protocl includes already a multi with all the B's including B2. In the past there have been already posts about the need to supply coenzymes to support methylation.
Sorry but I'm confused at this point. Is the B2 too low and dosage needs to be upped or the Bs to be scaled down? The basic multi included in the SMP covers all the Bs as well as other nutrients. I was under the impression that multi had all the Bs in the proportion needed to support methylation.
Can somebody pls explain whether we're actually better off without it? (would save money).
And by taking all of them, as soon as they are absorbed, B2 activates them so that lowers the B2. Then the body realizes you don't need that quantity of them and you urinate them away. So you do not get any benefit of additional B's that aren't stored and you only tax the B2 storage locations in your body. by Dog Person Today at 12:33 PM.
Perhaps there are more nutrients/enzymes involved in excreting them from the storage locations.
Is there any evidence to support this?
Rand56, I think I can answer this. Been there. Done that.
I took 2x 18 mg of coenzymated B2 over 2hrs, followed by 25mg of riboflavin an hr later. Following morning, I took another 25mg.
(I know, I'm sort of cringing while I type this! I guess moderation is not in my DNA.)
I was ok, then I started to sweat & I got diarrhea, orange colored stools. I now realise this was too much.
Ok, so to back up, the reason I took so much is because I was in a crash due to what I now think is a B2 deficiency that I had made worse by taking very large dosages fo B6 for a couple of months.
Last year, I ran an OAT thru Great Plains. It showed high normal glycolic acid (thanks Rich) & also some other marker that the lab said indicated low B2. It also indicated low B6.
I began taking ramping up my intake of b6, & tried to make sure I had enough magnesium so it could be absorbed. I did feel better on it.
But a couple of days ago, I started with the vomiting, diarrhea & headache. It seemed my liver was backed up or malfunctioning.
I suspect, based on what dog person has shared, that the crash was because I tanked my already low b2 stores. Don't have any test results to back it up. But she described the same symptoms & they ameliorated with B2 supplmentation.. until this morning, when I got the sweating & nausea & orange stools. (It's worn off now but I will drop the dosage.)
Btw, I did seem to get better sleep last night so I was interested to hear what Brenda was saying about better quality sleep.
So I know this is anecdotal or sketchy but I just throw it out there FWIW.
I am my own personal lab rat. So far, it's been trial & error! Fun. NOT!
At the time that I had the hair test and Organic Acids which both showed B2 deficiency but failing to have them interpreted, I did not know. This was two years ago and I was on a B complex taking active B12 and eating a perfect diet with loads of organic fruit and vegetables, organic meat, green smoothies with parsley and dandelion leaves everything I put in my mouth was hyperhealthy.
hi Dog Person
This may be hard to determine based on how deficient someone is on stored levels of B-2, but do you atleast have a rough idea on the range of length of time it takes someone to get their stores of it up to optimum levels? Can it be done fairly quickly or would it take a good amount of time?
I've never heard this before. Please could you give some references in support of this statement?
Rand, I think there are some who have a defect that don't process B6 well - maybe that is something you could look into for yourself too re: your reactions to the B Complex.
Here is a good review article on B-2. Scrolling down the page more you will see a section of its interactions with folate, B-6, and B-12.
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.
A Human Client and her Four Dogs Quote
The dogs pooped some dark green again and are doing great. They sleep more soundly at night. Oh, by the way, I noticed one of Heidi's dark spots is flaking and has partially fallen off!!!! Eye discharge is much less, but not yet completely gone. Heidi used to excrete some residue, not much at all, when she would urinate that would discolor the hair around her genitals. It would sometimes cake and I would have to shave around her genitals to get it off so she wouldn't wind up with an infection. It's been two weeks, and there is no sign of it anymore. I also hesitate to say yet, but her fatty tumor is really shrinking. When it's all gone, I'll be thrilled. It was quite large as you recall. No change yet with Fritz' dark spots on his belly but he does not lick his penis anymore and has virtually stopped biting his paws. All the dogs lick their paws every once in a while though. All the dogs ears and gums are a bright pink now where before, Fritz and Liesl in particular were a grey color. They are all on 100mg B2 a day 4 doses of 25mg.
For me, I'm noticing a trend that tells me I'm going thru a major detox. I start to retain water, get cold sores in my nose, and get very congested. The stuff that comes out of my nose in the a.m. is unbelievable!! Then a couple of days later, my lips get very dry and I get tired. After a couple more days, my urine and stool get a horrible odor and then about 2-3 days later, my congestion clears, I loose the water retention, and when I start to get my energy back, my lips are most again. This last dry lip spell was as bad as it was before we increased the B2. If I have any dairy or wheat when my lips are so dry, they crack, get inflamed red and burn. But if I have dairy or wheat when my lips are moist, I have just a slight tingling whereas before, they would get very dry and I would get tired. I am taking the dose you suggested and sometimes 50 mg more (2 additional doses of 25 mg).
Right now, I'm coming out of a detox - my lips are moist and my energy is coming back. Isn't' it amazing that one vitamin could have such an impact!
hi Dog Person
Thank you for you very informative post. I'm like Brenda, I do not have the more obvious physical signs of B-2 deficiency, but funny you mentioned longitudinal ridges on the nails can be a sign. I've had them on my nails for as long as I can remember. Is this predominantly a sign of B-2 deficiency or could they appear from some other nutrient deficiency? The only other physical sign I have, and I don't know if this solely is from lack of B-2, but my eyes are constantly bloodshot. Not to the extreme, but I get jealous of other people who I see that their eyes are very clear and I wish mine were. I don't really suffer from allergies, other than occasional sneezing during pollen season but I don't get itchy eyes that often, so my bloodshot eyes doesn't really stem from this.
While I am waiting on my order of Douglas Labs Riboflavin 5 Phosphate, I decided to get some regular Riboflavin yesterday because I am antsy to start with it. I'm already starting to get more itching, predominantly on the back of my hands and forearms. Could this be a detox sign where I am already starting to rid myself of excess iron and copper thru my skin?
I have been on 3 X 12.5mg for 6 days and have had no itching or detox signs yet but am sleeping deeper and have more energy. I felt a difference soon after the first dose. I have eye problems which are common with riboflavin deficiency. Mine are dry and I get corneal rips when the eyelid sticks. I also have a patch of red bloodshot which has been there for a long time. I am thinking that I have been short for a long time but it got a lot worse when I started on high dose B complex.
Is it necessary to take riboflavin 5 phosphate or is ordinary riboflavin effective?
No immediate positive repsonse for me like you had for yourself. Could possibly have something to do with me still dealing with my low dopamine depression and/or maybe I have a bigger load of iron and copper to get rid of before I get a noticeable energy boost.
As a note, AOR makes an "Advanced B Complex" that contains all activated forms. I wonder if that would be less demanding for the Riboflavin stores but still allow us to get extra of the other b vitamins (if desired).
More Easy Reading
Riboflavin should not be taken by anyone with a B vitamin allergy or chronic renal disease. Other populations are unlikely to experience any difficulty from taking supplemental B2.
Taking supplemental riboflavin causes a harmless intense orange or yellow discoloration of the urine.
Riboflavin is extremely nontoxic. No cases of toxicity from ingestion of riboflavin have been reported. No toxic or adverse reactions to riboflavin in humans have been identified. A harmless yellow discoloration of urine occurs at high doses. The limited capacity of the gastrointestinal tract to absorb this vitamin makes any significant risk unlikely, and because riboflavin is water-soluble, excess amounts are simply excreted.
Interest in disorders of homocysteine metabolism has increased since moderate increases in homocysteine have been identified as a risk factor for vascular disease along with rare inborn errors attributable to severe deficiencies of cystathionine-[beta]-synthase, 5-methyltetrahydrofolate/homocysteine methyltransferase, and 5,10-methylenetetrahydrofolate reductase(MTHFR; EC 18.104.22.168). MTHFR is a flavoprotein (riboflavin enzyme) that catalyzes the NADPH-dependent conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate. Methyltetrahydrofolate is the most common form of folate in plasma and tissues and serves as the methyl group donor in the 5-methyltetrahydrofolate/homocysteine methyltransferase-catalyzed remethylation of homocysteine to methionine.
Gale Encyclopedia of Alternative Medicine | 2005 | Turner, Judith; Frey, Rebecca | COPYRIGHT 2005 The Gale Group, Inc. (Hide copyright information) Copyright
Recent research has found that riboflavin is one of three vitamins involved in the regulation of circadian (daily) rhythms in humans and other mammals. Riboflavin helps to activate certain light-sensitive cells in the retina of the eye that synchronize the animal's daily biological rhythms with the solar light/darkness cycle.
Recent studies done at the National Cancer Institute indicate that riboflavin deficiency increases a woman's risk of developing cervical cancer. Further studies of this connection are underway.
Some evidence indicates that impaired mitochondrial oxygen metabolism in the brain may play a role in the pathology of migraine headaches. Because riboflavin is the precursor of the two flavocoenzymes (FAD and FMN) required by the flavoproteins of the mitochondrial electron transport chain, supplemental riboflavin has been investigated as a treatment for migraine. A randomized placebo-controlled trial examined the effect of 400 mg of riboflavin/day for three months on migraine prevention in 54 men and women with a history of recurrent migraine headaches. Riboflavin was significantly better than placebo in reducing attack frequency and the number of headache days, though the beneficial effect was most pronounced during the third month of treatment. A more recent study by the same investigators found that treatment with either a medication called a beta-blocker or high-dose riboflavin resulted in clinical improvement, but each therapy appeared to act on a distinct pathological mechanism: beta-blockers on abnormal cortical information processing and riboflavin on decreased brain mitochondrial energy reserve. A small study in 23 patients reported a reduction in median migraine attack frequency after supplementation with 400 mg of riboflavin daily for three months. Although these findings are preliminary, data from most studies to date suggest that riboflavin supplementation might be a useful adjunct to pharmacologic therapy in migraine prevention.
Psychiatric disturbances can also be induced by a riboflavin (vitamin B2) deficiency. Six young men were maintained on a riboflavin deficient diet during a riboflavin deficiency study carried out under 24 hour medical supervision - the men were given whole sets of psychological tests during the trial. The young men experienced very significant levels of psychological change as soon as the deficiency started to manifest itself in the body. The young men became depressed and suffered from an increase in lethargy. Some of them complained about suffering from imaginary pains and illnesses - a medical condition called hypochondriasis. When measured on hysteria and psychopathic deviate scales - their scores were all high, and some of them underwent measurable personality shifts that were very significant. However, none of the classic symptoms seen during riboflavin deficiency - including problems like dermatitis and inflammation in the eyes affected the young men before the experiment ended. The men were again supplemented with riboflavin following the period of testing -which lasted about two months - the psychiatric symptoms took longer than two weeks to completely dissipate and the young men were restored to normal.
Carcinogens or cancer causing chemicals found in the human body are also actively detoxified by riboflavin. During one experiment, rats given such carcinogens were spared from developing liver tumors by giving them riboflavin in high doses. At the same time, a deficiency of the vitamin riboflavin can result in the stimulation of the growth of tumors in the body. One example of an increase in utilization and need of riboflavin is show in the fact that less amounts of riboflavin than normal is excreted if a person suffers from cancer of the stomach, breast cancer, uterine cancer, or cancers of the skin and the lungs. This connection between tumors and riboflavin excretion has been demonstrated in one study involving a thousand adults with various cancers, in eighty per cent of such people there was virtually no riboflavin excreted in the urine, notwithstanding the type of tumor they suffered from at the time.
In animals, riboflavin deficiency results in lack of growth, failure to thrive, and eventual death. Experimental riboflavin deficiency in dogs results in growth failure, weakness, ataxia, and inability to stand. The animals collapse, become comatose, and die. During the deficiency state, dermatitis develops together with hair loss. Other signs include corneal opacity, lenticular cataracts, hemorrhagic adrenals, fatty degeneration of the kidney and liver, and inflammation of the mucous membrane of the gastrointestinal tract. Post-mortem studies in rhesus monkeys fed a riboflavin-deficient diet revealed about one-third the normal amount of riboflavin was present in the liver, which is the main storage organ for riboflavin in mammals. About 28 million Americans exhibit a common sub-clinical stage. characterized by a change in biochemical indices (e.g. reduced plasma erythrocyte glutathione reductase levels). Although the effects of long-term subclinical riboflavin deficiency are unknown, in children this deficiency results in reduced growth. Subclinical riboflavin deficiency has also been observed in women taking oral contraceptives, in the elderly, in people with eating disorders, and in disease states such as HIV, inflammatory bowel disease, diabetes and chronic heart disease. The fact that riboflavin deficiency does not immediately lead to gross clinical manifestations indicates that the systemic levels of this essential vitamin are tightly regulated.
9^ a b Brody, Tom (1999). Nutritional Biochemistry. San Diego: Academic Press. ISBN 0-12-134836-9. OCLC 212425693 39699995 51091036 162571066 212425693 39699995 51091036.
10^ Powers J. Hilary. Riboflavin (vitamin B-2) and health, Review Article. Am J Clin Nutr 2003;77:135260
Because riboflavin is degraded by light, loss may be up to 50% if foods are left out in sunlight or any UV light. Because of this light sensitivity, riboflavin will rapidly disappear from milk kept in glass bottles exposed to the sun or bright daylight (85% within 2 hours).
Riboflavin is stable when heated and so is not easily destroyed in the ordinary processes of cooking, but it will leach into cooking water. The pasteurization process causes milk to lose about 20% of its riboflavin content. Alkalis such as baking soda also destroy riboflavin. Sterilization of foods by irradiation or treatment with ethylene oxide may also cause destruction of riboflavin.
A number of metals and drugs form chelates or complexes with riboflavin and riboflavin-5-phosphate that may affect their bioavailability (30). Among the agents in this category are the metals copper, zinc and iron; the drugs caffeine, theophylline and saccharin; and the vitamins nicotinamide and ascorbic acid; as well as tryptophan and urea. The clinical significance of this binding is not known with certainty in most instances and deserves further study.
30. D.B. McCormick, Riboflavin, in Present Knowledge in Nutrition, 6th ed. (M.L. Brown, ed), International Life Sciences Institute, Washington DC, 1990, p 146.
The Labratory Rat by Mark A. Suckow, Steven H. Veisbroth, Craig L. Franklin
American Colloge of Laboratory Animal Medicine Series, copyright 2006
Because flavoproteins are involved in the activation and tranformation of pyridoxine, folic acid and niacin, and vitamin K, riboflavin deficiency can be observed in conjunction with deficiencies of these vitamins (Rivlin, 1984).
Riboflavin deficiency in rats has been reported to induce eye signs varying in severity from an inflamed condition of the cornea to its complete opacity. The data are conflicting regarding the association between riboflavin deficiency and cataract formation (Bhat, 1982, 1987; Yagi et al., 1989; Dutta et al., 1990). Takemi et al (2004) examined the conjunctiva and cornea of riboflavin-deficient rats. Riboflavin deficiency resulted in a decrease of microvilli and microplicae in the cornea and conjunctiva epithelium. From these findings the investigators concluded riboflavin is essential in the development, maintenance and function of the ocular surface.
Villi morphometry and the kinetics of cell movement on the villi from riboflavin-deficient female Wistar rats were studied. Feeding a riboflavin-deficient diet to weanling rats resulted in a significantly lower number of villi, a significant increase in villus length, and an increased rate of transit of enterocytes along the villi compared to that with the controls (Williams et al., 1995, 1996a). The morphological and cytokinetic changes in duodenums from weanling rats fed a riboflavin-deficient diet for 5 weeks could not be reversed by a 21 day riboflavin-repletion period (Williams et al., 1996b). The earliest point at which riboflavin deficiency affects post-weaning bowel development in rats has been identified to be 96 hours after initiating the deficient diet. The changes affected duodenal crypt cell proliferation and bifurcation with no reduction in villus number (Yates et al., 2001).
Clinical signs of riboflavin deficiency in rats include unthrifty appearance with areas of alopecia on the skin, seborrheic inflammation, cheilosis, angular stomatitis, glossitis, anemia, hyperkeratosis of the epidermis, neuropathy, blepharitis, conjunctivitis, corneal opacity and vascularization, anestrus, and birth defects. (Cooperman and Lopez, 1984; NRC, 1995). The NRC estimated riboflavin requirements for growth and reproduction are 3 and 4 mg./kg diet, respectively (NRC, 1995).
This is interesting to me. Last time I had a blood test the dr. told me my iron saturation was only around 12%. I use to have nice long finger nails. For at least the last 5 years they have flattened out and little dents in them. I pointed this out to my dr. but he was not concerned about it. I have started taking B2, 50mg. I try to take it at least 3 time a day. So far I have not noticed any change at all. I usually take sub. b12 but today I gave myself an injection (cyano) instead of giving me energy I have been extremely tired all day. I have been slightly anemic my whole life, even as a child.
I guess my question is do I only take B2 or should I be taking it with P5P, b12 and folate? Iam so tired I can't even think straight right now. I'll have t check in tomorrow (not sure I got across what I wanted to point out)
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