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"The Fallacy Of Administering Mixtures Of Crystalline Vitamins Alone In Nutritional Deficiency"

Discussion in 'Water-Soluble Vitamins' started by Amazoniac, May 1, 2018.

  1. Jennifer

    Jennifer Member

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    Well said, Ella! :):
    Mmm...yeah. It's sad when you learn that the people who you would do anything for if they were in need don't share that same attitude toward you. But then I found people who didn't know me from Adam who were really supportive and tried to help — Amazoniac always sending me info, Blossom, tara, Sue, Diane, Charlie, Narouz, pboy etc. and their kind words, and VoS. VoS was unbelievably supportive, always checking up on me and trying to help. I have a lot of love for members here and the support I was given (and still get) and thanks to them, it makes resentment hard to hold onto. It doesn't replace the need for physical help, but I hope you've found some support and comfort over the years with the forum, also. ❤️
     
  2. OP
    Amazoniac

    Amazoniac Member

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    Riboflavin - Wikipedia
    "FAD is [also] required to convert retinol (vitamin A) to retinoic acid via cytosolic retinal dehydrogenase"

    I'm not((

    I guess the correction of vitamin deficiencies (especially the wasser-solubles) should precede that of trace minerals, otherwise the person can't do anything productive with those minerals and so they can become problems. It's the coral reef state.

    Gerson*:

    "To the great complexity of the biological functions of the body belongs also its capacity of adaptation. A healthy body can adapt itself to different types of nutrition. It reabsorbs the necessary minerals, vitamins and enzymes as we know from experiments to determine the time for the clinical appearance of one or another vitamin deficiency. A sick body has lost this capacity. The deficiencies cannot be restored as long as the essential organs are poisoned. That is true in cancer also, as demonstrated by clinical observations."

    "When intermediate substances are left in the body, they work as carcinogenic substances."​

    Koch often wrote similar things:

    "[..]various tissues of the body become overloaded with incompletely assimilated food products. These in turn serve as material for the support of germ growth, and for the production of poisons. They also blunt the body chemistry, cutting down its efficiency, and hampering the immunity process."

    It might sound as if that's only meant for unabsorbed nutrients, but it's not:

    "These materials are not effectively handled, they are only incompletely metabolized and remain absorbed in the cell where they hamper its normal chemistry, cut down its efficiency and serve as material for the nutrition of germs and the production of germ poisons."​

    After vitamins and electrolytes have been addressed, and there's a need for specific trace minerals that are difficult to be met by diet, then I guess the safest way to supplement is very little more often; or better yet, one or two times a week to give the body a chance to correct any imbalance. These can also be lessened by supplementing only when eating nutritious foods (example, per calorie but still useful). I'm mentioning this because it's not uncommon for people to supplement trace minerals along with meals that are poor in them, sometimes even on empty stomach, which is a waste of chance to prevent imbalances. The exception here is perhaps selenium, which doesn't seem to interact as much with the others.

    Ps: *"I found that almost all of the arthritis cases have a weak liver or damaged liver. This is also true of coronary disease."​

    It makes more sense to blame the children then. Janelle, consider hating your family.

    The Body's Vitamin B12 Store | Dr. Schweikart

    "Our bodies store greater amounts of vitamin B12 than they do for any other vitamins; an estimated 2000-4000 µg, the majority of which is found in the liver.[1-4] Theoretically speaking, the body could function on a minimum provision of 1 µg per day for up to 10 years. This is one reason why the serious effects of a vitamin B12 deficiency can take several years to become apparent."​

    But it's common to be depleted in disease.
    Buying the ways, I had this link on hold:
    https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.0954-6820.1962.tb04231.x
     
  3. Captain_Coconut

    Captain_Coconut Member

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    Good luck with the ACV! Sometimes it takes a couple different approaches before that kind of thing really is defeated.

    A few worth trying:
    Before any of the following, I suggest you pre-treat area with isopropyl alcohol, helps to kill fungus and open up pores.

    1. Castor oil with baking soda, mixed to pancake batter consistency, applied as a compress and left on for a day.

    2. Bentonite clay and ACV, mix to paste consistency and apply as compress and leave on for as long it feels comfortable.

    3. Grapefruit seed extract, a couple drops in a couple ounces of water applied and allowed to dry.

    4. Pepto bismul, painted on the skin and allowed to dry.

    5. Compress of 3% hydrogen peroxide.
     
  4. Janelle525

    Janelle525 Member

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    Yes I did have some good friends on the forums, it made my situation less lonely. And gratefulness has been a big part of my recovery. Sometimes I can get caught up on woe is me, and turning back to what I am thankful for always helps. I'm glad you found the forum supportive for you!
     
  5. Janelle525

    Janelle525 Member

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    Haha, well I could never hate my family,but we have been through a lot together.

    Yeah I agree vitamins are absorbed better with other nutrients. But I don't think I'll be making veggies a big part of my diet anytime soon! Maybe boiled and the water drank. I actually like the taste of parsley juice. Kale not so much bleck!
     
  6. Janelle525

    Janelle525 Member

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    Wow thanks for the list! Those are some good ideas.
     
  7. OP
    Amazoniac

    Amazoniac Member

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    Greens must have been part of people's diet on almost every part of the planet because if you think about it, even in various harsh of the climates they're still available. So if people were subsisting, greens were the least likely food to be disappearing from the diet. As long as they were edible, you would expect that there were efforts to include them to increase nutrition.
     
  8. Janelle525

    Janelle525 Member

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    That's a huge generalization!
    I disagree plants are necessary for health, especially vegetables. I agree with Peat on this issue that they are famine food. I feel worse when I include lots of vegetables, even carrots.
    "Poor people, especially in the spring when other foods were scarce, have sometimes subsisted on foliage such as collard and poke greens, usually made more palatable by cooking them with flavorings, such as a little bacon grease and lots of salt. Eventually, "famine foods" can be accepted as dietary staples. The fact that cows, sheep, goats and deer can thrive on a diet of foliage shows that leaves contain essential nutrients. Their minerals, vitamins, and amino acids are suitable for sustaining most animal life, if a sufficient quantity is eaten. But when people try to live primarily on foliage, as in famines, they soon suffer from a great variety of diseases. Various leaves contain antimetabolic substances that prevent the assimilation of the nutrients, and only very specifically adapted digestive systems (or technologies) can overcome those toxic effects."
    Vegetables, etc.—Who Defines Food?
     
  9. OP
    Amazoniac

    Amazoniac Member

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  10. OP
    Amazoniac

    Amazoniac Member

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  11. OP
    Amazoniac

    Amazoniac Member

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    Early Infant Exposure to Excess Multivitamin: A Risk Factor for Autism?

    "It is known that to ensure normal functioning of the nervous, immune, and digestive systems, the monoamines released from the nervous system and the gastrointestinal tract must be inactivated/degraded and eliminated in time. Monoamine-neurotransmitters, like xenobiotics (substances foreign to the body, such as pollutants, food additives, pesticides, and drugs), are metabolized through enzymatic phase I (oxidation, reduction, and hydrolysis) and phase II reactions (conjugation, e.g., methylation, sulfation, acetylation, glucuronidation, and glutathione conjugation) [18]. The characteristics of monoamine degradation are as follows:

    (1) enzymatic degradation: the degradation of all the monoamines and their precursor amino acids is enzymatic multipathway and multistep processes (Figure 1)."

    "(2) Need for methyl groups and sulfate: as shown in Figure 2, methyl groups and sulfur amino acids (e.g., methionine and cysteine) are required for the body’s detoxification and antioxidant activities (Figure 2). An adequate supply of methyl groups and sulfate is prerequisite for methylation- and sulfation-mediated monoamine-neurotransmitter inactivation. Since both the biotransformation of exogenous chemicals and the degradation of monoamine neurotransmitters share the same pool of methyl groups [22] and sulfate [23], in theory, any chemicals (such as vitamins, see the following) that consume methyl groups and/or sulfur amino acids in their biotransformation may competitively inhibit the methylation and sulfation of monoamine neurotransmitters."

    "(3) Gender differences in monoamine-neurotransmitter inactivation: as mentioned above, monoamine neurotransmitters can be inactivated either by deamination, by methylation, or by sulfation. The redundant nature of monoamineneurotransmitter metabolism enables one pathway to compensate for blockade of the other. For example, reduced or absent activity of MAO leads to a decrease in the production of deaminated metabolites and an increase in that of O-methylated amine metabolites [24, 25], while inhibition of COMT increases the production of 3,4-dihydroxyphenylacetic acid [25], a deaminated metabolite of dopamine (Figure 1). Thus, if methylation and sulfation cannot take place (e.g., due to depleted methyl-group and sulfate pools by exogenous chemicals) [22, 23], the inactivation of monoamine neurotransmitters will depend mainly on the activity of MAO.)) Importantly, the genes encoding the two isoforms of MAO are X-linked [26], and their activity is lower in males than in females [27, 28], suggesting a biological basis of sex differences in monoamine degradation. Such a sex difference in MAO activity also suggests that males might have less ability to compensate for blockade of methylation- and sulfation-mediated monoamine inactivation than females. Therefore, it is conceivable that similar levels of exogenous chemical exposure may disturb the inactivation of monoamine neurotransmitters in males more than in females."

    "Excess vitamins, like xenobiotics and monoamine neurotransmitters, are also degraded through phase I and phase II reactions and thus may increase the consumption of labile methyl-groups and sulfate. Moreover, some vitamins are known to play a role in the synthesis of monoamine neurotransmitters. For example, vitamin B6 is a cofactor for aromatic L-amino acid decarboxylase that catalyzes the formation of serotonin and dopamine (Figure 1), while 5-methyltetrahydrofolate, the active form of folate, also stimulates the synthesis of monoamine neurotransmitters [29]. Therefore, excess vitamins can increase the levels of monoamine neurotransmitters either by competing for the same biotransformation system or by facilitating the synthesis, or by both. Indeed, evidence shows that high doses of vitamin C decrease plasma-conjugated dopamine and norepinephrine levels by competing for sulfation [30], whereas nicotinamide increases the levels of plasma of norepinephrine [31], serotonin, and histamine [32], presumably due to a decrease in methylation-mediated degradation of the monoamines. Vitamin B6 supplementation can increase the blood serotonin levels of newborn babies [33]. Interestingly, Berman and colleagues [34] found that maternal supplementation with vitamin B6 during the last 3 to 5 weeks of pregnancy increased the maternal blood levels of serotonin at parturition but did not increase the cord blood serotonin level or urinary 5-hydroxyindoleacetic acid output in the newborn infants, suggesting that the placenta may protect the fetus from the risk of excess vitamin exposure. Although little is known about the effect of excess vitamin exposure on the neurotransmitter metabolism in the human infant brain, evidence from animal studies has shown that some vitamins can affect the metabolism of central monoamine neurotransmitters. For example, vitamin C [35] and vitamin B6 [36, 37] increase the levels of serotonin in the brain of rats. Recently, Tekes and colleagues [38] found that neonatal vitamin A or vitamin D treatment has significant influence on the metabolism of monoamine neurotransmitters in the adult rat brain. Therefore, excess vitamin exposure may be a potential risk factor for neurotransmitter metabolism disorders."

    "It has been known for over a century that the dose-response curve for many micronutrients is nonmonotonic, having an initial stage of increasing benefits with increased intake, followed by increasing costs as excesses become toxic [39]. Both vitamin deficiency and vitamin excess are known to cause toxicity, including neurotoxicity [15, 40]. A meta-analysis of randomized trials of antioxidant supplements for primary and secondary prevention suggests that supplementation of vitamin A and E may increase mortality [41]. Supplemental folic acid (the synthetic form of folate) was also found to be associated with increased mortality [42, 43]. Davis and colleagues [44] found an association between high serum thiamine levels and sudden infant death syndrome (SIDS, a sudden and unexplained infant death most likely to occur between 2 and 4 months of age), and they further demonstrated that high doses of thiamine could cause death in rabbits and mice due to respiratory failure. Moreover, there is evidence suggesting an association between early infant vitamin supplementation and an increased risk of allergic diseases later in life [45, 46]. Although these data are not conclusive, they at least suggest the possibility that excess vitamin exposure may lead to serious health outcomes."

    "To date, little is known about the relationship between early infant exposure to excess vitamins and autism, except a recent hypothesis that suggests that excess folic acid supplementation may be a risk factor for autism [47]. There are two studies that examine the relationship between early vitamin exposure and learning development in rats. One found that neonatal vitamin A exposure may induce a long-lasting defect in learning [48], and the other showed that niacin supplementation induced spatial learning impairment in rats [49]. These observations suggest that early excess vitamin exposure may have adverse effects on neurodevelopment. It should be noted that the neurological effects of vitamin deficiency and vitamin excess may be similar [15]. Such a similarity could be a common cause for a wrong diagnosis. For example, SIDS was initially suggested to be related to a thiamine deficiency. To test this hypothesis, Davis and colleagues [44] compared serum thiamine levels between 233 SIDS infants and 46 control infants dying from other causes. Unexpectedly, they found that most of the SIDS infants had significantly higher serum thiamine levels. Therefore, to avoid making a wrong diagnosis, the levels of vitamins and their metabolites should be monitored."

    "It should be pointed out that some cofactors, although not belonging to vitamins, may also play an important role in the synthesis of monoamine neurotransmitters."

    Autism:
    "Among the possible risk factors in infant foods, such as nutritional imbalances (deficiencies and excesses) and food additives and contaminates, excess multivitamin exposure may be the most common and important."

    "For example, the content of niacin, folic acid, vitamin B6, thiamine, and vitamin C in a premature infant formula (see, http://abbottnutrition.com/products/similac-special-care-20-with-iron) is about 20 (5,000 versus 250 g/100 kcal), 9 (37 versus 4 g/100 kcal), 7 (250 versus 35 g/100 kcal), 6 (250 versus 40 g/100 kcal), and 4 (37 versus 8mg/100 kcal) times the lower limit value, respectively. The level of thiamine in some manufactured milk-based formulae (2160 g/L) was found to be about 20 times that of human breastmilk (mean 178 g/L) [44]. In addition to the vitamin supplementation of infant formula, multivitamin use in infants and toddlers is very common [16]. Thus, high-vitamin feeding may increase the risk of vitamin overload. Indeed, many studies have shown that formula-fed infants have higher levels plasma/serum of vitamins than human milk-fed infants [59–62]. Unmetabolized folic acid, a sign of folic acid overload, is observed in the serum of 4-day-old infants fed with formula [63]. Porcelli and colleagues [62] found a several times increase in the plasma levels of riboflavin and pyridoxine and a more than 10 times increase in the urine riboflavin and pyridoxine concentrations in very low-birth-weight neonates after being fed with preterminfant formula. Baeckert and colleagues [64] showed that very low-birth-weight infants who received the recommended parenteral vitamin supplement as part of their total parenteral nutrition developed elevated plasma riboflavin concentrations during their first postnatal month with peak concentrations 100-fold above baseline umbilical cord plasma vitamin concentrations. Moreover, there are two studies finding high plasma levels and urinary excretion of methylated metabolites of niacin in autistic patients [65, 66], which suggests a niacin overload, because excess niacin is rapidly degraded after ingestion, but its methylated metabolites remain longer in the circulation [31, 67]. Given that excess vitamins may lead to neurotoxicity and disturbances in monoamine neurotransmitter metabolism, as mentioned earlier, it is possible that high multivitamin exposure may play a role in the increased prevalence of autism."

    "Current understanding of the rates of maturation of metabolic capability indicates that human infants up to approximately 6 months of age are typically more sensitive to chemical toxicity than adults due to their immature detoxification systems [71]. This suggests that newborn infants, especially premature infants, may have a low tolerance to excess vitamins. Indeed, available evidence, although limited, has shown an association between high levels of some vitamins (thiamine [44] and vitamin C [72]) and apparent life-threatening events and SIDS in infancy. A randomized controlled trial on vitamin C supplementation in very preterm infants also showed that infants who died during the trial were those who had significantly higher vitamin C concentrations before randomization than surviving infants [73]. Evidence from animal studies suggests that high exposure to vitamin A [48] and niacin [49] in the early life has adverse effects on the behaviors of adult rats. Thus, it appears that high multivitamin feeding in the first few months of life may be particularly harmful. Although there is little information on the role of excess vitamins in infant brain injuries, it is common knowledge that chemical exposure-induced neurological injury may have a variety of manifestations, depending on the length and degree of exposure [74]. Notably, preterm birth is associated with increased risk for both autism and other neurological conditions, such as cognitive, visual, and hearing impairments; and there is considerable cooccurrence of autism with other neurological and cognitive disorders [75]. We therefore postulate that autism might be one of chemical/excess-vitamin exposure-induced neurological sequelae (which may range from neurological deficits to death) in early infancy. What is worthy of note is that with the maturation of metabolic function and age-related changes in feeding foods, the causal exposure present in infancy and resultant metabolic and neurological manifestations may no longer exist. This may account for why there is lack of consistent biological markers in autism. Even elevated blood serotonin, the most consistent serotonin-related finding in autism, may not be observed in adolescent autistic patients [76]."
     
  12. Janelle525

    Janelle525 Member

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    This is interesting. How were they able to study this in humans when we have never even had studies of safety of vaccines?? I mean just testing blood levels after death doesn't tell us they were overdosing at 2 months old with thiamine! Between 2-4 months is when the first round of vaccinations are given. I have found from many articles that vaccines are a plausible reason for SIDS. But autopsy reports try to leave it out.

    Also millions of babies are essentially being fed multivitamins and minerals every single feeding through formula which I believe is one of the most unnatural way of feeding a baby, but I guess some babies are so sickly they need food separated down into their parts already. I still think even the most fragile babies would benefit from donor breastmilk and some hospital NICU's would agree.

    I do agree both high and low nutrients could be an issue if given artificially, but we must be cognizant that researchers want to blame anything but vaccines for causing autism, not that I think that is the only reason but when you have thousands of parents saying how their child changed after vaccines we can't just ignore it.
     
  13. MrSmart

    MrSmart Member

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    Uh-oh, buzzword @Travis

    Prepare for sum aluminum talk.
     
  14. OP
    Amazoniac

    Amazoniac Member

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    They're just speculating as The Reader can confirm by inspecting the title. After a tiresome discussion, the authors reached a consensus that it was indeed a sagacious move to complement it with a question to deflect Janelles in the future. It's also possible to note from further careful inspection that the word 'cause' wasn't used, they opted for 'risk' instead.
     
  15. Janelle525

    Janelle525 Member

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    Haha. Yes I just wanted a reason to talk about vaccines.
     
  16. OP
    Amazoniac

    Amazoniac Member

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    And I'm using your post right now to officialize that I have quoted his entire book with the following one:
     
  17. Janelle525

    Janelle525 Member

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    Very smart. I haven't taken anything in two days. I am proud of myself. I will now do muscle testing to see what my body wants. It did test okay for ascorbic acid this morning but I am seeing what happens if I take none.

    I just found out my Grandpa who is turning 96 in a week has throat cancer. :cry: He has declined treatment. I don't blame him! He's lived a long life. We all gotta go at some point.
     
  18. OP
    Amazoniac

    Amazoniac Member

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    But how do you define how long is enough living? It seems to me that if the person resists society's enormous pressure in an expected death range, then the person is forgiven to live further, turning into a family's cherished mascot.
     
  19. Janelle525

    Janelle525 Member

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    I would say he was our mascot for a long time. He thought if he got to 90 he was good! So he made it another 6 yrs and who knows how long he will survive with cancer.
     
  20. OP
    Amazoniac

    Amazoniac Member

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    But a cherished mascot isn't let go.