Introduction: Persons allegedly abducted by ET Aliens have been reported to experience the vitamin A deficiency induced abnormality Nyctalopia (night blindness) despite diets providing adequate Vitamin A (1). This non-dietary vitamin A deficiency may be due to the mechanism of implant mediated vitamin A destruction. Vitamin A is involved in  steroidogenesis (biosynthesis of steroid hormones by the adrenal cortex) and evidence is presented for steroid hormonal deficiencies in abductees, presumably related to vitamin A deficiency.

Salt craving and anesthetic difficulties in abductees have also been previously reported (1). Salt craving is logically due to excessive urinary salt loss, due to deficiency of the adrenal steroid mineralocorticoid hormone Aldosterone, which functions primarily to reduce salt loss. 

This Report briefly presents four abductee cases, one each in support of non-dietary Nyctalopia, low Aldosterone level, transient low adrenal glucocorticoid hormone level, and one case of evident deficiency involving the female sex hormone Estrogen. The Estrogen deficiency signs and symptoms were reversed by adding carrots and Vitamin E to the diet. 

Adding carrots and vitamin E (which, both being antioxidants, has a sparing action on vitamin A) to the daily diet will safely and markedly increase body vitamin A, and by doing so in theory might thereby work towards reestablishment of normal hormonal levels, by facilitating steroidogenesis, and/or competing for implant mediated hormonal destruction.

Signs and symptoms of estrogenic deficiency in a pre-menopausal abductee taking Estradiol and vitamins without benefit, were promptly eliminated by adding carrots and vitamin E to her diet. This non-toxic inexpensive dietary addition may be of benefit to other alleged abductees with physiologic abnormalities.  Persons adding the carrot vitamin E (CE) regimen to their daily diets are requested to inform me concerning procedures and results.

Background. In Derrel Sims’ study of 250 alleged abduction cases about 50% of the subjects suffer from night blindness (Nyctalopia). About 90% of the female portion of the study suffer from Nyctalopia.  All subjects exhibited a compulsion to consume salty substances and applied large amounts of common table salt to meals. All subjects showed abnormal reactions to procaine (dental) local anesthetics, in that either the normal amount was not sufficient or there were frank outright allergic reactions to these compounds (1). By my personal interviews with alleged abductees these reported results of Mr. Sims’ studies have been essentially completely confirmed. These phenomena are as published on.

Visual Abnormalities. Nyctalopia (night blindness) is manifested by vision deficiency in dark adaptation.  The person with night blindness typically cannot see adequately in dim light, where persons with normal vision can. Or when adaptation is still possible an abnormally long time is required. By making personal inquiries I have confirmed that females with a history of multiple abductions frequently cannot drive at night, crave salty foods, and may exhibit the described procaine anesthetic phenomena. One such alleged abductee informed me that night blindness was so common among her circle of alleged abductee friends it was assumed by them to be a female (sex linked genetic) trait. It is not.  In theory genetically determined inability to employ vitamin A would be lethal. There are no genetic vitamin A deficiencies.

Nyctalopia is due to a deficiency in vitamin A. New vitamin A is constantly required (in small amounts) to produce the visual substance retinene as part of the normal visual cycle. Vitamin A is stored, primarily in the liver. Without adequate vitamin A intake the body stores eventually become depleted, and a deficiency occurs, resulting in Nyctalopia (2). Vitamin A is specific for the cure and prevention of the vitamin A deficiency states Nyctalopia and Hemeralopia (day blindness), and the severe vitamin A deficiency disease Xeropthalmia (3). Xeropthalmia refers to the more advanced clinical manifestations of severe Vitamin A deficiency which can lead to blindness, cell metaplasia, prominent in the lungs, and possibly even death.

Nyctalopia with adequate vitamin A intake. All the alleged abductees interviewed had more than adequate intake of vitamin A and precursors. One person I call Jane who by my evaluation is an abductee with implant stated she takes a Vitamin A tablet (5000 Units) and cod liver oil (another good source) daily.  She also likes to eat carrots, broccoli and other good sources of carotenes, which are normally converted to Vitamin A. Her fat and protein (mostly chicken) intake (necessary for Vitamin A absorption and use respectively) were normal. Her digestion is normal and she is relatively healthy, though with Nyctalopia, salt craving, dental anesthetic problems, low resistance to infection, etc. There is no history of liver disease (carotene is converted to vitamin A in the liver). Therefore it is evident her Nyctalopia, salt craving, and anesthetic problems are not due to inadequate intake of Vitamin A. It appears that despite more than adequate intake the vitamin A in her body is not adequate to allow normal night vision.

Possible mechanism of vitamin A deficiency. It is reported that under black (long wavelength) ultraviolet (UV) light some implants fluoresced green (5). Vitamin A fluoresces a characteristic green (6).  Therefore a possible simple mechanism explaining both vitamin A deficiency and implant fluorescence would be implant adsorption of vitamin A. Presumably followed by inactivation of vitamin A. 

According to this concept, the implant induces Nyctalopia by inactivating vitamin A. Then despite apparently adequate intake, abductees with implants may have varying degrees of vitamin A deficiency caused by their implants. Warning- excessive amounts of vitamin A are dangerous. Its carotene precursors (carrots) are believed safe to eat in quantity.

There are alleged abductees without Nyctalopia, who drive satisfactorily at night, but also report frequently experiencing abnormal sensitivity to sunlight. At such times it hurts their eyes and produces tearing. This transient sensitivity might conceivably be due to a transient corresponding vitamin A deficiency. In my opinion such extreme visual sensitivity to sunlight, which might conceivably result over time in Hemeralopia (day blindness), is a more reliable indicator of possible abduction than is non-dietary Nyctalopia. Of course both conditions may have medical causes other than abduction, which causes must be ruled out before taking them for example as possible indicators of abduction.

Hormones of the Adrenal Cortex. The possibility exists that alleged abductees’ common complaints of fatigue, susceptibility to infection, autoimmune type disorders, allergic reactions etc. may be related to sub-clinical vitamin A deficiency, which in addition may possibly result in deficiencies of hormones of the adrenal cortex. According to the literature Vitamin A is implicated in steroidogenesis (steroid production) in the adrenal glands. (9). Implants may conceivably destroy these hormones as well as vitamin A. Then vitamin A deficiency may conceivably manifest in a variety of clinical problems related to decreased levels of the adrenal hormones, which include the mineralocorticoid Aldosterone (electrolyte regulation via sodium retention, sodium/potassium balance), and the glucocorticoids such as Cortisol (metabolic, antistress and antiallergic affects, and others.) (10).

Electrolyte Abnormalities. Salt craving is most commonly due to excessive loss of salt. Salt loss occurs in heavy sweating, due to elevated temperature, or in urinary excretion.  The persons interviewed worked and lived in air conditioned spaces and were without fevers. Excessive salt loss into the urine is commonly associated with disease of the kidney or adrenal cortex. No history or evidence of kidney or adrenal cortex disease was presented. The adrenal cortex mineralocorticoid hormone Aldosterone normally regulates body salt retention by stimulating sodium ion retention. In uncompensated clinical Aldosterone deficiency the body suffers from markedly increased salt (sodium and chloride ion) loss into the urine, and there is also increased body potassium ion retention (4). This results in abnormally high potassium to sodium ratios in extracellular body fluids. This condition has been found among abductees (7). 

In a recent case reported to me by Dr. Roger Leir a male abductee’s 24 hour urine showed an Aldosterone level of 3.0 mcg/dL. The normal ranges are: Normal sodium intake 100- 200 mEq daily 6- 25 mcg/dL, High sodium intake greater than 200 mEq daily 0-6 mcg/dL, Low sodium intake less than 25mEq daily 17-44 mcg/dL Aldosterone. Sodium intake was normal, therefore the test result indicates low Aldosterone concentration.