Vitamin C

Volume I

Alan B. Clemetson

• Publisher: CRC Press
• Year: 2018
• Print ISBN: 9781315898469
• eBook ISBN: 9781351094467
• Topic: Medicine
• Subtopic: Nutrition, Dietics & Bariatrics

The factors affecting blood vitamin C levels are described in detail in this series. Many factors such as aging, smoking, infection, trauma, surgery, hemolysis, hormone administration, heavy metals, pregnancy, alcohol, ionizing radiation and several medicines have been found to cause a disturbance of ascorbic acid metabolism and to reduce blood vitamin C levels. Indeed, abnormalities of ascorbic acid metabolism, due to factors such as smoking, occur much more frequently than does dietary vitamin C deficiency today.It is now known that low blood vitamin C levels are associated with histaminemia (high blood histamine levels), and also that ascorbate-responsive histaminemia is common in apparently healthy people. High blood histamine levels are believed to cause small hemorrhages within the inner walls of the blood vessels and these may lead to the deposition of cholesterol, as an aberrant form of wound healing. Ascorbic acid not only reduces blood histamine levels, but also aids the conversion of cholesterol to bile acids in the liver. The clinical pathological and chemical changes observed in ascorbic acid deficiency are discussed in detail. Several diseases and disorders associated with low blood vitamin C levels are also described. Possible toxic effects resulting from the oxidation of ascorbic acid are noted, and reasons for the use of D-catechin or other chelating fiber to prevent or minimize the release of ascorbate-free radical are detailed. An excellent reference for physicians, nutritionists and other scientists

Factors Affecting the Economy of Ascorbic Acid

Chapter 3

INADEQUATE ASCORBIC ACID INTAKE

Many workers studying the vitamin C requirements of human subjects, monkeys, and guinea pigs have been struck by the wide disparity between the findings in different laboratories. Some find guinea pigs do well on 1 or 2 mg of ascorbic acid a day, while others find them to have a requirement of 20 mg/d. Some of the reasons for these wide disparities are now evident, as ascorbic acid can be lost by oxidation and subsequent hydrolysis when traces of heavy metals like copper are present in the drinking water; conversely ascorbic acid can be preserved when there is sufficient protein or chelating fiber in the food to bind and inactivate heavy metals.

Prolonged storage or cooking may destroy vitamin C in food before it is consumed. There are also many factors which can alter the requirements of an individual animal or an individual patient, so it is difficult to define an adequate or an inadequate intake of vitamin C.

Parsons (1938) observed that, “occasionally scurvy occurs even when the diet contains considerable quantities of vitamin C; an infant admitted to the Children’s Hospital with frank scurvy was having daily orange juice containing 60 mg of ascorbic acid. We have suspected that this might be due to lack of absorption, though we have not been able to demonstrate this chemically. Indeed, in the case to which I have just referred, cure was actually obtained by giving large doses of ascorbic acid by mouth. It is probable that some children require more vitamin than others.”

Kline and Eheart (1944) studied nine normal young women living in the same dormitory and eating an experimental diet; they reported that the ascorbic acid intake requirements to achieve saturation in these women mostly ranged between 1.4 and 1.8 mg/kg/d, but one subject had a requirement of only 0.6 mg or less per kilogram, while two had ascorbic acid requirements of 2.2 mg/kg or above.

One of the world’s most experienced investigators of vitamin C deficiency must surely be Dr. John Crandon of Boston, Massachusetts, who abstained from all foods containing ascorbic acid for nearly 7 months; he took daily supplements of all other known vitamins to make sure that he developed a pure vitamin C deficiency and that the clinical picture was not confused by other deficiencies, as is so often the case with naturally occurring maladies. Crandon et al. (1940) made a detailed report of all the laboratory and clinical findings in this experiment. Ascorbic acid (reduced form), estimated by the method of Mindlin and Butler (1938), was no longer detectable in the blood plasma after 41 d on the diet, at which time the white blood cell and blood platelet (buffy coat) ascorbic acid level had fallen from 28 to 10 mg/100 g. Thereafter, the plasma readings remained at 0, whereas the buffy coat readings did not reach 0 until 121 d had elapsed; 2 weeks later, small perifollicular hyperkeratotic papules (raised reddened hair follicles) began to appear over the buttocks. Not until after 161 d of the diet, or after the plasma ascorbic acid had been 0 for 120 d and the buffy coat 0 for 40 d, did the perifollicular hemorrhages, so characteristic of scurvy, appear over the lower legs. Then, 3 weeks later an experimental wound made in the back of the subject showed no signs of healing after 10 d. Previously, a similar wound made at the end of 3 months of diet, after the plasma had been 0 for 44 days and the buffy coat reading was 4 mg/100 g, showed reasonably good healing both clinically and microscopically.

Subsequently, Crandon et al. (1953), reviewing the results of this experiment wrote as follows: “Although ultimate failure of wound healing was the more striking result of this experiment, equally significant were the results of fatigue tests performed just before the cessation of the diet. In the completely scorbutic state the subject was able to run on a motor-driven tread-mill at a rate of seven m.p.h. for only 16 sec, at the end of which time he was completely exhausted, with a sensation of impending collapse. Following ascorbic-acid therapy, the subject was able to run for 66 sec, without the sensation of impending disaster experienced in the first test. The subjective phenomena associated with the prescorbutic state were vague and difficult to describe. There was certainly an increased lassitude and desire for sleep. There was a marked disinclination to exertion.”

These authors also reported at the same time a study of blood samples from 561 selected surgical patients at the Boston City Hospital. Here they measured total ascorbate (by the method of Roe and Kuether, 1943) in blood plasma, in the buffy coat, and in specimens of abdominal muscle sheath; they found blood plasma ascorbate levels to be closely related to tissue levels and to be more valuable than buffy coat levels in prediction of wound healing. Ideal blood plasma ascorbate levels range from 1.0 to 1.3 mg/100 ml and may be found in healthy young persons receiving 75 to 100 mg of ascorbic acid a day in their diet (viz., one orange and one tomato a day). When the diet contains only 15 to 25 mg/day, plasma values range from 0.1 to 0.3 mg/100 ml: in this study they found 24 patients with plasma ascorbate levels below 0.2 mg/100 ml and were able to follow 18 of them for 2 years; 12 of the 18 had serious wound complications including evisceration in 1, massive bleeding into the wound in 1, wound dehisced down to the peritoneum in 2, incisional hernia in 3, poor or no healing in 2, and persistent draining sinus in 3. There is no proof that all of these wound complications were due to a lack of ascorbic acid, but the very high rate of wound complications would seem to be more than coincidental.

Among patients with almost totally deficient plasma, who were receiving no vitamin C, a precipitous drop in buffy coat ascorbic acid was frequently noted with the onset of infection, evisceration, or other serious complications. It is thus evident that there may develop a vicious cycle wherein the problem may compound itself. Ascorbic acid deficiency predisposes to serious complications, and these in turn may hasten depletion of ascorbic acid stores.

Crandon et al. studied seven patients with frank scurvy. All seven showed traces of ascorbate in the buffy coat, and five showed traces in the plasma as well. They concluded that scurvy, in many cases, appears to be a manifestation not of complete absence of ascorbic acid alone, but of marked ascorbic acid deficiency plus local tissue stress.

Actually, the difference between the original findings of Crandon et al. (1940), where ascorbic acid disappeared from both plasma and platelets before the onset of scurvy, and the subsequent studies of Crandon et al. (1953), where small amounts of ascorbic acid were still found in the blood of patients with scurvy, may be partly due to the different methods of chemical analysis used. The method of Mindlin and Butler measures only the reduced (most active) form of the vitamin, while the method of Roe and Kuether measures the reduced form plus the small amount of the oxidized form, dehydroascorbic acid (DHAA), which is normally present in the blood, as well as possibly traces of inactive diketogulonic acid derived from the latter. Only DHAA is detectable in the blood plasma and tissues in scurvy.

Lind (1753) also believed that stress and various other factors in the form of hardships would hasten the onset of scurvy and noted that half of Lord Anson’s crew died of scurvy rounding Cape Horn, even though they had only been at sea for 3 months. Of course, we do not know how their diet had been before they set sail, but it is undoubtedly true that many facotrs, even smoking, as noted by Maynwaringe (1668), can hasten the onset of scurvy.

However, Crandon speaks of local tissue stress, which raises the very interesting question as to whether a damaged or infected tissue or organ can develop scurvy while the rest of the body remains relatively healthy. There is insufficient evidence on this point and it does deserve further study. Indeed, the recently discovered inverse relationship between histamine and ascorbic acid makes it conceivable that inflammation is in one respect similar to local scurvy.

Dodds and MacLeod (1947) studied 41 healthy young women students at the University of Tennessee in Knoxville; all the women were maintained on a low-ascorbic acid diet containing approximately 7 mg of ascorbic acid a day, and all received an ascorbic acid supplement increasing stepwise from 25 to 50 to 75 and to 100 mg/d at 7- to 10-d intervals, with a view to establishing the plasma ascorbic acid level associated with each intake level. However, it was observed that there was a wide range in the plasma ascorbic acid values at each of the controlled intake levels; the authors concluded that any estimation of the vitamin intake of a population based on a plasma ascorbic acid survey cannot be narrowly defined.

Salomon (1957) studied the biological half-life of ascorbic acid in nine guinea pigs and found a range from 70 to 144 h. Likewise, Williams and Deason (1967) reported great variability in the amount of ascorbic acid required to maintain the body weight of guinea pigs under experimental conditions and gave reasons for believing that there may be an even greater variation between the needs of individual human beings. These authors postulated that guinea pigs, monkeys, and human beings may have varying abilities (hitherto undetected) to produce ascorbic acid endogenously, but cannot produce it fast enough to maintain heal...

Table of contents

• Cover
• Title Page
• Copyright Page
• Table of Contents
• Vitamin C Deficiency
• Factors Affecting the Economy of Ascorbic Acid
• Index