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I’ve been reading some of the Shute Brother’s Books recently about Vitamin E. Many of their principles and ideas line up very well with Ray Peat’s, and we know that Peat was familiar with the Shutes, as he referenced them in his article on Vitamin E, and in other places as well.
The Shute’s state that Vitamin E is antagonized by PUFA, iron, and estrogen, and vice versa. They advised against eating the high PUFA oils and iron supplements. They mention that Vitamin E is synergistic with many substances, including the B vitamins, Vitamin C, and thyroid hormone.
This is from Chapter 21, ESTROGEN and ANTAGONISTS, from “Vitamin E for Ailing & Healthy Hearts-
“AS EXPLAINED IN CHAPTER I, THE
whole concept underlying this work derived from the many
pathological conditions that accompany hyperestrogenism
and their correction by reducing the estrogen level to nor¬
mal. At first, it was menorrhagia and dysmenorrhea that
were successfully treated by my father and older brother
and later by myself and younger brother. Then it was found
that the alpha fraction of vitamin E could control the anti-
proteolytic factor found in the serum of aborting women
and that it could prevent abruptia placentae, this between
the years 1935 and 1937.“Gradually, it became apparent that there were at least
four estrogen antagonists, namely progesterone, thyroid
extract, alpha tocopherol, and testosterone and that these
could be used singly or in combination. The result was a
simple and effective method of treating the many conditions
associated with the overproduction of estrogen by the body.”Peat obviously talked at length about progesterone, thyroid, and Vitamin E. He didn’t talk as much about testosterone, but always seemed somewhat supportive, at least from the few times I’ve heard him mention it. Many bodybuilders that take steroids often add in an “anti aromatase.” Makes you wonder if base testosterone and a highish dose of Vitamin E might be the safest bodybuilding stack?
The Shutes often used higher doses of Vitamin E in their clinics, citing doses of 800 IU and 1600 IU frequently in their books, and mentioning a dose as high as 4800 IU. Peat was always conservative in his recommendations, but remember, he usually gave general, public recommendations. I think these recommendations should be seen more as a starting point, rather than a be all end all. Peat was always experimenting himself, and thought others should as well. He even suggested that with just one relatively safe substance, like aspirin or Vitamin E, one could experiment for years, trying a variety of doses and dosing schedules.
This has me thinking, since most people today have consumed large amounts of high PUFA oils (and likely have lots of PUFA in their tissues), and also consume high iron diets (thanks to fortification), could much higher doses of Vitamin E be beneficial?
Based on the Shute’s work, and some modern studies supporting their ideas, as well as Peat’s framework, I’m experimenting with a larger daily dose myself, 2000 IU. I’m going to add in a policosanol supplement, as that might have been a beneficial factor in the older versions of Vitamin E, and is certainly a beneficial item itself.
Vitamin E can lower prolactin levels. Dopamine Agonist drugs like bromocriptine and cabergoline do this, and they have been effectively used as weight loss drugs. Maybe Vitamin E can too? Here’s the study-
Effect of vitamin E therapy on sexual functions of uremic patients in hemodialysis
https://pubmed.ncbi.nlm.nih.gov/1490755/
Twenty-four uremic patients on hemodialysis who had never been treated with vitamin E or related drugs and 12 control patients with normal renal function were studied. Hemodialysis patients were randomly divided into two groups; 12 were treated with oral vitamin E (300 mg/day) for eight weeks and 12 uremic patients and 12 controls were given placebo. Serum vitamin E, prolactin, FSH, LH, and free testosterone levels were measured in all patients before and after treatment. After the vitamin E treatment serum prolactin levels were significantly decreased (50.8 vs 15.4 ng/ml, p < 0.01). Vitamin E levels were significantly increased (1.11 vs 1.22 mg/dl, p < 0.05). Serum FSH, LH and free testosterone were not affected. In the other two groups there were no significant changes. These results show that vitamin E treatment lowers prolactin levels in uremic hemodialysis patients. This might be due to inhibition of central prolactin secretion. Vitamin E inhibits pituitary gland hypertrophy in vitamin E-deficient rats.
Georgi Dinkov’s write up on series of studies by Hans Selye, on substances that slowed, and maybe even reverse, soft-tissue calcification (calciphylaxis), and possibly so called “aging” itself.
The even better news is according to [5] and [6] below a hefty dose of vitamin E (alpha-tocopherol acetate) was also able to fully block the calciphylaxis. Now, the dose of vitamin E used in that study was also quite high – an HED of about 4g-5g daily. However, the study used alpha-tocopheryl acetate, which is known to be only about 30% – 50% as effective as alpha-tocopherol. So, if one used pure alpha-tocopherol then a dose of 2g -2.5g daily should suffice. This is still a high dose but it has been used clinically in the 20th century for a variety if estrogen-related issues, especially by the Shute brothers. Perhaps just as importantly, study [7] below demonstrates that vitamin E protects from the side effects of high-dose anabolic steroids, which makes a combination of vitamin E + testosterone a rather good combination for blocking / reversing systemic soft-tissue calcification and possibly retarding the whole aging process.
The Shutes cautioned about using Vitamin E with hypertension. They stated that it increased the strength of the heart, and that this could increase hypertension, so only recommended using Vitamin E in high blood pressure patients if they were on some other sort of high blood pressure medication.
However, Ray Peat suggested that Vitamin E could be effective at regulating blood pressure in the longer term, and that it’s action shouldn’t be looked as commonly prescribed blood pressure drugs. This study in humans backs up Peat’s idea, it found that Vitamin E lowered blood pressure in mild hypertensive patients over a span of 6 months-
Vitamin E can Reduce Blood Pressure in Mild Hypertensives
https://econtent.hogrefe.com/doi/abs/10.1024/0300-9831.72.5.309
This triple-blind placebo-controlled clinical trial was performed to determine the effects of the antioxidant vitamin E on blood pressure and heart rate in patients with mild hypertension. A total of 70 new mild hypertensive subjects (systolic blood pressure, SBP: 140–160 mmHg; diastolic blood pressure, DBP: 90–100 mmHg) without secondary hypertension were selected from among people referred to the Hypertension Unit of Isfahan Cardiovascular Research Center and divided randomly into two groups of drug (DG) and placebo (PG). All subjects were aged from 20 to 60 years old, without any other cardiovascular risk factors. The drug group received vitamin E tablets (200 IU/day) and the placebo group received placebo only for 27 weeks. At the beginning and the end of the study, the blood vitamin E level was measured fluorimetrically in all subjects according to the Hansen and Warwick method [14, 15]. Blood pressure and heart rate were measured at the beginning, during, and at the end of the study. Blood pressure was measured by a physician using one random zero mercury sphygmomanometer. Personal information and dietary habits of subjects were collected by separate questionnaire. At the end of the study, it was found that the vitamin E supplement had caused a remarkable decrease in SBP (–24% in DG versus –1.6% in PG) and a less remarkable decrease in DBP (–12.5% in DG versus –6.2% in PG) (p < 0.05). The change in heart rate was –4.3% in DG, and –14.0% in PG (p < 0.05). It is concluded that a vitamin E supplement of 200 IU/day can be effective in mild hypertensive patients in the long term, probably due to nitric oxide, and improve their blood pressure status. Therefore, vitamin E supplement could be recommended to such patients.
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