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Vitamin E depletion (tocopherols, tocotrienols)

See my other article on how Vitamin E is protective against Poison/"Vitamin A" here (supplement suggestions at that link as well).

Based on current science, it is safe to say that there is a "Vitamin E Deficiency" epidemic going on, and animal studies (as well as human ones, to be added later) show that Vitamin E is greatly depleted by Poison/"Vitamin A":

Intake of alpha-tocopherol is limited among US adults.

OBJECTIVE:  To examine alpha-tocopherol intake and food sources of alpha-tocopherol in the US population relative to current Dietary Reference Intakes for vitamin E.
RESULTS:  Only 8.0% of men and 2.4% of women in the United States met the new EARs [Estimated Average Requirements] for vitamin E intake from foods alone. Regionally, only 5.8% of men and 2.1% of women in the South met these EARs, relative to 9.0% and 2.6%, respectively, in the Northeast. Top contributors of alpha-tocopherol for men and women included ready-to-eat cereal, sweet baked products, white bread, beef, oils, and salad dressing.

APPLICATIONS/CONCLUSIONS:  The majority of men and women in the United States fail to meet the current recommendations for vitamin E intake. Many of the top contributors are not particularly high sources of alpha-tocopherol but are consumed frequently. Greater inclusion of sources such as nuts, seeds, and vitamin E-rich oils, could improve intake of alpha-tocopherol.

More than 90% of people in the US are not getting the government's paltry recommendations for Vitamin E through their diet, and when they actually DO get some Vitamin E, it just so happens that many of their Vitamin E sources are fortified with Poison/"Vitamin A"!!!  If you didn't know already, "ready-to-eat cereal, sweet baked products, white bread" are all commonly fortified with added Poison/"Vitamin A".  If Poison/"Vitamin A" actually does deplete Vitamin E (it does, keep reading), the main Vitamin E foods people actually eat are fortified with Poison/"Vitamin A", and 90% of people aren't getting enough Vitamin E to begin you see the problem here???

Beta-carotene lowers the Vitamin E content of both skin and plasma in both humans and mice.

Beta-carotene supplements lowered Vitamin E in both the gut lining and blood, while also causing an accumulation of beta-carotene in the gut lining.

Vitamin A:  Vitamin Safety

Another area of attention has focused on whether or not excessive vitamin A can affect vitamin E status. Vitamin A has been reported to have a significant depressing effect on vitamin E status (Ching et al., 2002). Blair et al. (1996) indicated that a tolerable dietary range of vitamin A for young pigs in the range of 10 to 30 kg is up to 10 times the requirement. Ching et al. (2002) fed weanling pigs 6 times the vitamin A requirement (13,200 IU per kg or 6,000IU per lb). As dietary vitamin A level increased, serum and liver alpha-tocopherol concentrations declined, suggesting a reduced absorption and retention of alpha-tocopherol when weaned pigs were fed high dietary vitamin A concentrations. Fuhrmann et al. (1997) reported that 20,000 IU per kg (9,072 IU/lb) of diet vitamin A reduced plasma and tissue vitamin E levels, which in turn led to an increase of lipid peroxidation as indicated by a higher production of hydrocarbons. Blair et al. (1996) considered that this raised concern about further increases of vitamin A supplementation in early-weaned pigs. However, Anderson et al. (1997) concluded that during early gestation, the vitamin E status of gilts was not detrimentally influenced by three 350,000 IU injections of vitamin A shortly before, at and shortly after breeding. Anderson et al. (1995) reported that feeding a high level of retinyl acetate (20,000 IU/kg) did not influence animal performance or blood serum and tissue alpha-tocopherol concentrations in growing-finishing pigs. Weaver et al. (1989) reported a significant interaction for vitamin A and vitamin E for plasma tocopherol. Higher levels of vitamin A when supplied with a high level of vitamin E, lowered plasma tocopherol concentrations. Hoppe et al. (1992) indicated that dietary retinol at up to 10,000 IU per kg (4,536 IU per lb) of diet does not affect alpha-tocopherol concentrations in plasma or in tissues selected with the exception of cardiac muscle. Alpha-tocopherol levels in heart and liver displayed an inverse relationship with levels (5,000, 10,000, 20,000 or 40,000 IU per kg) of dietary retinol, while dietary retinol had no effect on levels of alpha-tocopherol in Longissimus muscle or backfat. Zomborszky-Kovacs et al. (1998) reported a numeric decrease in plasma vitamin E concentration in unsupplemented versus carotene-supplemented weaned pigs. Beginning one week prior to weaning, the supplemented group received 855 mg beta-carotene per kg (388 mg/lb) of diet (10 times the NRC [1988] recommendation). The carotene-supplemented pigs and control pigs had vitamin E concentrations in plasma of 2.12 and 5.58 mg/dl, respectively.

Differential effects of high dietary levels of vitamin A on the vitamin E-selenium nutrition of young and adult chickens.

Experiments were conducted to determine the nature of the interaction of high levels of vitamin A and vitamin E-selenium nutrition in the chicken. Results showed that chicks were protected from the vitamin E-selenium deficiency disease exudative diathesis (ED) by a high dietary level of vitamin A (1.0 X 10(6) IU/kg) which moderately depressed growth. A greater concentration (1.5 X 10(6) IU/kg) of vitamin A in the diets of hens fed a low vitamin E diet hastened their depletion of plasma tocopherols and increased plasma glutathione peroxidase (GSH-px) activity. At hatching the progeny of vitamin A-fed hens were severely depleted of plasma tocopherols but had normal plasma GSH-px activities. They showed increased susceptibility to ED when fed selenium-deficient, vitamin E-free diets for 2 weeks. Absorption studies using ligated duodenal loops or oral doses indicated that high-level dietary vitamin A promoted the enteric absorption of selenium but interfered with the absorption of vitamin E. The dual nature of these effects was related to the ED-protective influence of vitamin A when fed to chicks, and the ED-stimulative influence on progeny when vitamin A was fed to dams.

High dietary vitamin A interferes with tissue α-tocopherol concentrations in fattening pigs: a study that examines administration and withdrawal times.

This study aimed to assess the interaction between different dietary vitamin A (dVitA) levels and the same concentration of vitamin E (100 IU all-rac-α-tocopheryl acetate/kg feed) in growing-finishing pigs. In the first experiment, two fat sources × two dVitA levels (0 v. 100 000 IU) were used. The supplementation of 100 000 IU dVitA induced a range of 5.13 to 30.03 μg retinol/g liver, 62.78 to 426.88 μg retinol palmitate/g liver, and 0.60 to 1.96 μg retinol/g fat. Dietary fat did not affect retinol or retinyl palmitate deposition in pigs. The high concentration of dVitA produced lower fat and liver α-tocopherol concentrations, and increased susceptibility of muscle tissue to oxidation. A second experiment was carried out to study the retinol and α-tocopherol retention at different withdrawal times prior to slaughter (two dVitA levels; 0 v. 100 000 IU). A high dose of 100 000 IU vitamin A during a short 2-week period was enough to induce α-tocopherol depletion in liver and fat to a similar extent as when 100 000 IU were administered during the whole fattening. Muscle, fat and liver α-tocopherol concentrations were not affected by dVitA in the 1300-13 000 IU/kg range, but liver α-tocopherol concentration was higher when vitamin A was removed from the vitamin mix 5 weeks prior to slaughter (experiment 3).

Effects of dietary vitamin A supplementation or restriction and its timing on retinol and α-tocopherol accumulation and gene expression in heavy pigs

Certain vitamins such as vitamins A and E are related to meat quality and have been reported as antagonists. Thus, their tissue levels are of interest for swine producers and consumers. This experiment was undertaken to study the effect of dietary vitamin A supplementation or withdrawal duration and timing on the evolution of vitamin A deposition in tissues, α-tocopherol accumulation and gene expression in heavy pigs.
The results suggest that removing vitamin A from the diet for long or short periods in heavy pigs has the potential to reduce feed costs, increasing tissue α-tocopherol levels without affecting slaughter weight or feed efficiency.

Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona
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