What Happens With Vitamin C Deficiency

Ascorbic Acid Deficiency

Ascorbic acid deficiency might be associated to a lower absorption of nutrients, an insufficient intake, a higher metabolic requirement, and a rapid destruction of the GI tract [137].

From: Gastrointestinal Tissue , 2017

SCURVY

T.K. Basu , D. Donaldson , in Encyclopedia of Food Sciences and Nutrition (Second Edition), 2003

Pathophysiology

Vitamin C deficiency causes failure to maintain the cellular structure of the supporting tissues of mesenchymal origin, such as bone, dentine, cartilage, and connective tissues. As a consequence, vitamin C deficiency is characterized by weakness and fatigue, hyperkeratosis of the hair follicles, perifollicular hemorrhages, petechiae and ecchymoses, swollen bleeding gums, delayed wound healing, and the easy fracturing of bone. These are the characteristic clinical features of scurvy.

The clinical manifestations of scurvy are the result of complete vitamin C deprivation of 100–160 days' duration (Table 2). During deficiency the vitamin C pool of the body is depleted at a daily rate of about 2.6% of the existing pool; 92% is lost after 100 days and symptoms of mild scurvy are evident when the pool is less than about 300 mg.

Table 2. The consequences of withdrawing vitamin C from the diet

Day	Plasma ascorbic acid		Buffy coat ascorbic acid – in leukocytes (WC)		Body pool of ascorbic acid
Day	mg l⁻¹	μmol l⁻¹	μg 10⁻⁸ WC	nmol 10⁻⁸ WC	g	nmol	Clinical state
0	8–15	45–85	21–57	119–323	0.6–1.5	3.4–8.5	Adults
20	3	17	10–38	57–216
40	1–3	6–17	2–10	11–57	0.3–0.6	1.7–3.4	Subclinical deficiency
60	<1	<6	<5	<28	0.3–0.6	1.7–3.4
80	<1	<6	<5	<28	0.3–0.6	1.7–3.4
100	<1	<6	<5	<28	0.3–0.6	1.7–3.4
120	<1	<6	<2	<11	<0.3	<1.7	Perifollicular hyperkeratosis
140	<1	<6	<2	<11	<0.3	<1.7
160	<1	<6	<2	<11	<0.3	<1.7	Petechiae and ecchymoses of the skin and failure of wounds to heal
180	<1	<6	<2	<11	<0.1–0.3	0.6–1.7	Gingival changes
200	<1	<6	<2	<11	<0.1	<0.6	Dyspnea, edema, and very rapid progression

Fibroblasts play a central role in the wound-healing process. In vitamin C deficiency the fibroblasts proliferate but in an unimpeded manner. These proliferating cells generally remain immature, however, and fail to synthesize collagen molecules, which are the 'building blocks' of tissue repair. The impaired fibroblastic activity is essentially responsible for the delayed wound healing in vitamin C deficiency. Moreover, in vitamin C deficiency cartilage cells of the epiphyseal plate, at the end(s) of the diaphysis of long bones, continue to proliferate and line up in rows. The cartilage between these rows is calcified where osteoblasts do not migrate, resulting in the development of compressed and brittle bone.

Ultrastructural studies in scurvy show distinct alterations of the ribosomal and polyribosomal pattern. The endoplasmic reticulum shows considerable dilation and loss of ribosomal granules. The polyribosomes are disaggregated, unbeaded fibrillar material being seen in the extracellular space.

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Vitamins, minerals and trace elements

Richard K. Miller , Paul Peters , in Drugs During Pregnancy and Lactation (Third Edition), 2015

Pharmacology and toxicology

Vitamin C is important in cellular metabolism for the maintenance of oxidation–reduction balance. The daily requirement is set at 100 mg.

Vitamin C deficiency leads to scurvy, with disturbances in the collagen metabolism, and to a tendency to bleed. Vitamin C concentration in the fetal blood is three times as high as in the maternal blood because vitamin C accumulates in the fetus after the placental transfer of dehydroascorbic acid (Malone 1975). It is not known whether giving vitamin C affects the fetal reduction–oxidation balance. Recently, the association of vitamin C deficiency with gestational diabetes has been discussed (Zhang 2004a, 2004b), as has vitamin C supplementation during second and third trimesters to prevent premature rupture of membranes (Casanueva 2005, Tejero 2003) and most recently with selected birth defects (limb, cleft palate and heart defects) and exposure to notrosatable drugs (Shinde, 2013). This association with drug/chemical induced birth defects is among the first for human exposures and certainly requires further study. A recent meta-analysis did not find that supplementation with Vitamins C and E could prevent or improve maternal preeclampsia (Conde-Agudelo 2011).

Recommendation

Vitamin C supplementation is not necessary during pregnancy, if the diet is balanced.

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Vitamin C: Deficiency States

CJ Bates , in Encyclopedia of Human Nutrition (Third Edition), 2013

Abstract

Ascorbic acid deficiency has been traditionally recognized by the characteristic (scorbutic) signs and symptoms of clinical scurvy, which respond to (i.e., can be cured by) rich dietary sources of vitamin C such as citrus fruits or a dietary vitamin C supplement. Milder deficiency results in low or negligible concentrations of vitamin C in serum, plasma, and many tissues without causing overt clinical abnormality. Vitamin C occurs in several forms, of which the fully reduced form, ascorbic acid, is responsible for a variety of redox roles in the body, for example, in certain key enzymes and reactions. An intake of 10 mg day⁻¹ in adult humans can cure and prevent clinical scurvy, but higher intakes are required to replete body stores and optimize functionality.

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Biochemical Indices

C.M. Pfeiffer , ... K.L. Caldwell , in Encyclopedia of Human Nutrition (Third Edition), 2013

Diseases of Blood

J. PHILIP SAPP DDS, MS , ... GEORGE P. WYSOCKI DDS, PHD , in Contemporary Oral and Maxillofacial Pathology (Second Edition), 2004

Vitamin C Deficiency (Scurvy)

VITAMIN C DEFICIENCY (SCURVY): A systemic disease caused by lack of vitamin C dietary intake in which vascular wall integrity and wound repair mechanisms are defective.

Vitamin C deficiency (scurvy) is rarely seen in the industrialized world, because most individuals have sufficient vitamin C in their diets. Citrus fruits and tomatoes are the primary sources of this vitamin. Therefore scurvy is usually encountered in third world countries, where adequate nutritional intake is not available.

CLINICAL FEATURES

Purpura is one of the main manifestations of scurvy and occurs because of vascular wall fragility. The purpuric lesions may occur in the oral mucosa and on the skin and are represented by petechia and ecchymosis. Although the bruising usually occurs after traumatic provocation, in severe scurvy, spontaneous purpura may be identified.

Because the collagen fibers of the periodontal ligaments may also be defective, severe periodontal disease may be encountered and spontaneous tooth loss will occur.

Scorbutic changes may also evolve in bone matrices, leading to pathologic fractures.

Because vitamin C is important during healing, ulcerations or lacerations may persist and become secondarily infected. These ulcerations can involve the oral mucosa.

HISTOPATHOLOGY

Microscopically, vascular wall changes are not discernible in scurvy; although pathologic changes are identifiable with electron microscopy. Skin or mucosal biopsies show extravasation of erythrocytes, extravascular clot formation within tissue, and hemosiderin pigment deposition. The disease is diagnosed by assessing the patient's history, clinical findings, and serum ascorbic acid levels.

TREATMENT

Scurvy is reversed by adequate dietary intake of ascorbic acid. The vascular changes are reversible. Periodontal tissue breakdown, however, is permanent; lost alveolar bone will not regenerate after adequate vitamin intake.

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CHINKS IN THE ARMOUR; THINGS THAT GO WRONG WITH OUR DEFENCES

Cedric Mims , in The War Within Us, 2000

Vitamin C

Vitamin C deficiency causes the disease scurvy, as Captain Cook discovered in the 18th century when he gave limes to his sailors. The person with scurvy suffers bleeding into the gums, round the hairs in skin, and in muscles. Wounds don't heal and there is anaemia. A French priest who had been in the Crusades described it thus '… the gums and teeth were attacked by a sort of gangrene, and the patient could not eat any more. Then the bones of the leg became horribly black and so, after having suffered continual pain, during which they showed the greatest patience, a large number of Christians went to rest in the bosom of the Lord'.

Increased susceptibility to infection, however, is not a feature of scurvy. For 20 years the Nobel Prize winner Linus Pauling campaigned for massive doses of vitamin C as a remedy for the common cold, although the official view is that most of us get enough vitamin C from our diet, and giving extra amounts serves no useful purpose. The take home message from many studies is that the effect on respiratory infections is minimal, but vitamin C does seem to have an action on polymorph phagocytes. Those who suffer from chronic boils and whose polymorphs are not working normally can be helped by one gram of vitamin C a day.

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Elderly: Nutrition Requirements

R. Chernoff , in Encyclopedia of Food and Health, 2016

Vitamin C (ascorbic acid)

Vitamin C deficiency disease, scurvy, is rare but as new metabolic properties of vitamin C are described, an AI of vitamin C-rich foods remains a key for health maintenance, especially in elderly adults. There are no age-related changes in absorption and metabolism at median level intakes; it can be assumed that any deficiency is related to poor intake. Dietary vitamin C intakes vary mainly as a function of the presence of illness associated with overall poor nutrient intake, institutionalization, and age.

The intake of different dietary supplements, especially including vitamin C, has increased and contributes considerably to the nutrient intake of large segments of the elderly population. Institutionalization, hospitalization, and illness lead to a decrease of vitamin C intakes contributing to low plasma levels.

It has been reported that lower ascorbic acid levels are seen more frequently in elderly men than in elderly women; sex differences in plasma ascorbic acid concentration might be caused by a lower tubular reabsorption of vitamin C in elderly men. Healthy centenarians had significantly lower vitamin C plasma concentrations because of lower intakes.

Low levels of vitamin C in healthy elderly people can be corrected easily by the administration of oral ascorbic acid supplements, but when stopped, there may be a rapid decrease in the blood levels. Elderly people with low vitamin C levels do not necessarily show clinical symptoms, so it has been concluded that there is no real need to raise the ascorbic acid levels in the blood through supplementation. Because of the functions of vitamin C, this conclusion might be incorrect. In view of what is known or not yet known about the significance of low plasma levels, a continuous, adequate daily intake should be ensured.

Ascorbic acid can be important in the pathogenesis of chronic diseases of aging. Ascorbic acid has been found to be potentially important in the prevention of atherosclerosis, cancer, senile cataract, lung diseases, cognitive function, and various degenerative diseases. Vitamin C supplements are promoted to decrease lipid levels, thereby reducing the risk of atherosclerosis. However, a 5-year vitamin C supplementation trial had no markedly favorable effects on the serum lipid and lipoprotein profile in an adult population.

Vitamin C supplements do not prevent any of the chronic diseases of aging, but neither do pharmacological doses of vitamin C have a protective effect. The current recommendation for ascorbic acid seems to be adequate for older adults, although some individuals might find it difficult to achieve this intake level from diet alone. Nevertheless, intake should be strongly encouraged in elderly individuals who are institutionalized, ill, or of lower socioeconomic status. An increased consumption of fresh fruits and vegetables should be encouraged in elderly people.

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The Obese Gunshot Patient: Injury and Septic Shock

Susan Ettinger , in Nutritional Pathophysiology of Obesity and its Comorbidities, 2017

2.8.6 Vitamin C (Ascorbate) Requirements in Critical Care (Refer to Essentials I: Life in an Aerobic World. Ascorbate)

Ascorbic acid deficiency (in scurvy) is characterized by hemorrhage, impaired secretory functions, vasomotor instability, hematologic alterations, impaired wound healing, depressed immune response, and psychological disturbances. Since the critical care patient displays many of these symptoms, the ascorbate requirements of these patients have recently been reviewed ( Berger and Oudemans-Van Straaten, 2015). A major factor in the trauma patient is oxidative damage, derived from complications of the initial injury including septic shock and ischemia/reperfusion injury, as well as from emergency treatment such as oxygen therapy (Cornet et al., 2013). The arsenal of defenses against oxidative damage includes the enzyme cascades, superoxide dismutase, catalase and glutathione peroxidase, as well as proteins (albumin), bilirubin, uric acid, and other lipid- and water-soluble metabolites. Vitamin C was identified as the primary plasma antioxidant defense during sepsis; ascorbate also reduces vitamin E radicals and protects biomembranes from lipid peroxidation (Stocker et al., 1987). Ascorbate levels in the serum fall precipitously following trauma; the fall is greater if the patient develops septic shock (Oudemans-van Straaten et al., 2014).

Under normal conditions, vascular smooth muscle tone is regulated by NO derived from eNOS; the complex regulation of eNOS has been recently reviewed (Shu et al., 2015). NO activates guanylyl cyclase in the vascular smooth muscle cell, raising cGMP and cAMP and relaxing the vessel. Superoxides produced during sepsis react with inflammatory (iNOS derived) NO to produce peroxynitrites that inactivate endothelial prostacyclin (PGI₂) synthase and limit PGI₂ production from membrane arachidonic acid. Ascorbate reduces superoxide and peroxy radical production by inhibiting inducible iNOS, and prevents activation of the Jak2/Stat1/IRF1 signaling pathway, blocking superoxide production via NADPH oxidase (Wu et al., 2007). Ascorbate can also reduce physiologically relevant circulating radicals, including urate and glutathione radicals (Lykkesfeldt et al., 2014) restoring their activity.

Vascular changes that accompany sepsis include reduced density of perfused capillaries, increased vascular permeability, and reduced arteriolar responsiveness. While these changes, if localized, facilitate healing, if they occur system-wide, they can induce tissue hypoxia, mitochondrial dysfunction, ATP depletion, and organ failure, despite adequate fluid resuscitation and blood oxygen. Persuasive evidence (Wilson, 2009) suggests that ascorbate protects against vascular changes by multiple mechanisms. Ascorbate reduces endothelial dysfunction by inhibiting oxidation of tetrahydrobiopterin (BH4), thus preventing eNOS uncoupling and reducing superoxide formation (refer to Chapter 6: Atherosclerosis and Arterial Calcification). Ascorbate maintains vascular tight junctions by inhibiting PP2A activation, which dephosphorylates occludin (refer to Essentials IV: Diet, Microbial Diversity, and Gut Integrity) (Han et al., 2010; Zhou et al., 2012). Ascorbate also inhibits microcirculatory flow impairment by inhibiting TNFα-induced ICAM expression, which triggers leukocyte stickiness and sludging. It should be noted that many of these studies were done in animal models, only some of which had the l-gulonolactone oxidase gene inactivated to model ascorbate-deficient human physiology (Fig. 2.11).

A recent study tested whether vitamin C restores endotoxemia-compromised blood flow in humans. LPS was administered to healthy human subjects to produce acute endotoxemia and forearm blood flow (FBF) was measured following provision of placebo and two levels of intravenous vitamin C. As expected, LPS decreased plasma vitamin C concentrations and reduced the acetylcholine (ACh)-dependent increase in FBF by up to 76%. Vitamin C supplementation raised the mean plasma ascorbate concentration to 3.2 or 4.9 mmol/L in the two treatment groups and restored the FBF to baseline (Aschauer et al., 2014).

Host defense requires a competent innate and adaptive immune response. Inflammatory cells concentrate ascorbate at levels as great as 100-fold across the membrane (Bergsten et al., 1990), suggesting that the nutrient is essential for function. Upon mediator stimulation, PMNs are recruited on a chemotactic gradient and peak at the infected site within 24–48 hours. PMNs have short half-lives and rapidly undergo apoptosis. PMNs from scorbutic guinea pigs contained 16-fold less ascorbate than normal, were morphologically distorted, killed only 12% of phagocytosed bacteria, and displayed no chemotactic responses in vitro (Goldschmidt, 1991). PMN from ascorbate-deficient mice lacking the functional gene for l-gulonolactone oxidase (Gulo), while morphologically normal, had limited phagocytic capacity and failed to undergo normal apoptosis, dying in a few days in necrosis, the debris providing chemotactic inflammatory signals. Ascorbate-deficient PMNs from these mice also had elevated levels of hypoxia-inducible factor α (HIFα) (refer to Essentials I: Life in an Aerobic World. Ascorbate), previously shown by the authors to inhibit PMN apoptosis under hypoxic conditions (Vissers and Wilkie, 2007). These findings were confirmed ex vivo in macrophages from Gulo-deficient mice subjected to sterile inflammation. Increased expression of inflammatory mediators (IL-1β, TNFα, and MCP-1) and decreased antiinflammatory mediator expression were observed in macrophages from ascorbate-deficient mice. Gulo-deficient mice exposed to an intraperitoneal infusion of a fecal stream solution (fecal stream solution was prepared by rehydrating mouse fecal pellets; supernate was used as to induce peritonitis) suffered multiple organ damage and coagulation abnormalities; ascorbic acid infusion (200 mg/kg) attenuated the damage (Fisher et al., 2013). Of great interest was the ability of ascorbate to regulate neutrophil extracellular trap (NET) formation. Neutrophils have the ability to extrude antimicrobial material including DNA, trapping and killing pathogens; excessive NET in sepsis can damage organs and tissues (Mohammed et al., 2013). Additionally, ascorbate enhanced facilitation of efferocytosis, removal of dead/dying cells, allowing suppression of inflammation with resolution (Ravichandran and Lorenz, 2007; Divangahi, 2015), thus dampening proinflammatory responses.

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Vitamin and Mineral Basics: The ABCs of Healthy Foods and Beverages, Including Phytonutrients and Functional Foods

Jacqueline B. Marcus MS, RD, LD, CNS, FADA , in Culinary Nutrition, 2013

Vitamin C (Ascorbic Acid, Ascorbate)

In contrast to other mammals, humans cannot make their own vitamin C, so it must be obtained by the diet. Vitamin C is responsible for producing and maintaining collagen , the protein that is found in bones, connective tissues, skin, teeth and tendons. Vitamin C also functions as an antioxidant; it protects the human body from oxidative damage due to factors such as environmental pollutants, ozone, radiation and ultraviolet light.

Vitamin C is essential in the immune process; it fights infections and illnesses from the common cold to certain cancers and cardiovascular disease. While vitamin C may not prevent colds, it may help to decrease their severity and duration—especially if it is started at the onset of symptoms.

Vitamin C may also help the human body rebound from physical stress, such as from strenuous physical exertion or extreme temperatures. Vitamin C studies, which assess its relationship to cancers, cardiovascular disease, diabetes, hypertension, and other stressful conditions, are ongoing.

Vitamin C is abundant in fruits and vegetables, particularly bell peppers, broccoli, cantaloupe, grapefruit, kiwifruit, oranges and papaya. These foods and their juices contain many other health-enhancing phytonutrients beside antioxidants.

A vitamin C deficiency may develop in people who do not consume enough fruits or vegetables. A classic example of vitamin C deficiency occurred in the 1700s when British sailors developed scurvy , a potentially fatal disease that is characterized by bleeding, bruising, hair and tooth loss, joint pain and swelling. These symptoms are related to weakened blood vessels, bones and connective tissues, since the disease affects collagen formation. While scurvy is rare today in developed countries, cases of scurvy in undeveloped countries and in some children and the elderly who follow very restricted diets have been reported. Taken in excess in supplements, vitamin C may cause gastrointestinal distress.

Sources of vitamin C: berries, citrus fruits, cruciferous vegetables, dark green leafy vegetables, melons, potatoes, tomatoes, tropical fruits

Roles in body: antioxidant, collagen formation, immunity, promotes iron absorption, wound healing

Deficiency: anemia, bleeding gums, bone weakening, depression, hemorrhages, infections, poor wound healing, scurvy, muscle wasting

Toxicity: abdominal pain, diarrhea, kidney stones, nausea

Cooking Foods with Vitamin C

Vitamin C is very sensitive to air, temperature and water. The longer the time that fruits and vegetables are exposed to any of these factors, the greater the potential loss of vitamin C. Vitamin C can also decrease during blanching, freezing and/or unthawing.

To preserve vitamin C, store raw, cut fruits and vegetables in airtight containers and refrigerate. Do not soak or store fruits and vegetables in water for extended periods of time. Refrigerate juices, and then store them only 2 to 3 days. Simmer or steam foods in a very small amount of water, or microwave for a short time. Cook potatoes in their skins.

The RDA for vitamin C is 75 milligrams (mg) daily for females and 90 milligrams (mg) for males aged 19 years and older. The RDA for smokers is 110 milligrams of vitamin C for woman and 125 milligrams of vitamin C for men aged 19 years and older [22–24].

Sources of Vitamin C	Amount (milligrams)
1 cup whole strawberries	85 mg
1 orange	70
½ cup sweet bell pepper	65
½ cup cooked broccoli	51
½ medium grapefruit	38
1 medium tomato	16

Food Byte

Limes are tarter than lemons. Limes come in two varieties: the larger, greener Persian lime and the smaller, yellow key or Mexican lime. "Key lime" is an American creation. Limes are valued in Mexican, southwestern United States, and Thai cuisines for their acidity and zest. Common culinary uses of limes include key lime pie, a traditional Floridian dessert; limeade, a refreshing citrus beverage; and ceviche, a raw seafood dish that relies on acidic ingredients, such as lime juice, to break down the protein fibers. The leaves of the Kaffir lime are used in Southeast Asian cooking. Dried limes are used as flavoring in Persian cuisine. The tartness of limes can be tempered by a little bitters, cream, salt or sugar.

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Nutrition in the Second Half of Life

R. Chernoff , in Reference Module in Biomedical Sciences, 2014

Vitamin C

The vitamin C deficiency disease, scurvy is rare. However, as new metabolic properties of vitamin C (ascorbic acid) are identified, an adequate intake of vitamin C-rich foods remains a key for health maintenance, especially in older adults (Levine and Padayatty, 2012). There are no age-related changes in absorption and metabolism at median vitamin C intakes; therefore it can be assumed that any deficiency is related to poor intake. Dietary vitamin C intakes vary mainly as a function of the presence of illness associated with overall poor nutrient intake, institutionalization, and age (Lowik et al., 1993).

The intake of different dietary supplements, especially vitamin C supplements, has increased and contributes considerably to the nutrient intake of large segments of the elderly population (Suter, 2014). Institutionalization, hospitalization, and illness lead to a decrease in vitamin C intakes contributing to low plasma levels (Schmuck et al., 1996).

It has been reported that lower ascorbic acid levels are seen more frequently in elderly men than in elderly women; sex differences in plasma ascorbic acid concentration might be caused by a lower tubular reabsorption of vitamin C in elderly men (Schleicher et al., 2009). Healthy centenarians had significantly lower vitamin C plasma concentrations because of lower intakes (Mecocci et al., 2000).

The presence of pressure sores is also associated with lower vitamin C serum concentrations (Selvaag et al., 2002). It may be that any disease state has a high probability of leading to an impairment of vitamin C status and that this should be corrected by dietary means or short-term supplementation. Higher serum concentrations of vitamin C are desirable, especially in elderly people. Elderly men had to ingest approximately 150 mg day⁻¹ and the elderly women, approximately 80 mg day⁻¹, to maintain saturated ascorbic acid pools; data suggest that some elderly people might need even higher vitamin C intakes to maintain adequate vitamin C status (Suter, 2014).

Low levels of vitamin C in healthy elderly people can be corrected easily by the administration of oral ascorbic acid supplements, but when stopped, there may be a rapid decrease in the blood levels (Bendich and Langseth, 1995). Elderly people with low vitamin C levels do not necessarily show clinical symptoms, so it has been concluded that there is no real need to raise the ascorbic acid levels in the blood through supplementation. Because of the functions of vitamin C, this conclusion might be incorrect. In view of what is known or not yet known about the significance of low plasma levels, a continuous, adequate daily intake should be ensured.

Ascorbic acid can be important in the pathogenesis of chronic diseases of aging (Smith, 2010). Ascorbic acid has been found to be potentially important in the prevention of atherosclerosis, cancer, senile cataract, lung diseases, cognitive function, and degenerative diseases of miscellaneous organs (Institute of Medicine, 2000). Vitamin C supplements are promoted to decrease lipid levels, thereby reducing the risk of atherosclerosis. However, a 5-year vitamin C supplementation trial had no markedly favorable effects on the serum lipid and lipoprotein profile in an adult population (Kim et al., 2004).

Vitamin C supplements do not prevent any of the chronic diseases of aging. This does not mean that vitamin C does not play a role in the pathogenesis of disease, but pharmacological doses of vitamin C do not have a protective effect (Suter, 2014). The current recommendation for ascorbic acid seems to be adequate for older adults, although some individuals might find it difficult to achieve this intake level from diet alone. Nevertheless, intake should be optimized in elderly individuals who are institutionalized, ill, or of lower socioeconomic status. An increased consumption of fresh fruits and vegetables should be encouraged in elderly people.

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What Happens With Vitamin C Deficiency

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What Happens With Vitamin C Deficiency

Dennis Desember 03, 2021