Vitamin C is excellent for the body during radiation therapy, as it helps protect against oxidative stress. The vitamin C you get from fruits and vegetables will work, but the form of the supplement works even better.
You may be told to take a multivitamin and mineral supplement while you are undergoing cancer radiation therapy. There are many reasons why vitamin C is beneficial to the body during and after cancer radiation therapy:
vitamins for radiation exposure
Some cancer patients frequently experience bone pain or nausea. This is often caused by the side effects of radiation therapy, and it’s easy to miss vitamin C when planning a diet for your loved one.
Radiation is a serious medical emergency. Vitamin C and other antioxidants are known to help protect the body from the harmful effects of radiation.
can you take vitamins during radiation therapy
Antioxidants mitigate radiation-induced lethality when started soon after radiation exposure, a delivery time that may not be practical due to difficulties in distribution and because the oral administration of such agents may require a delay beyond the prodromal stage of the radiation syndrome. We report the unexpected finding that antioxidant supplementation starting 24 h after total-body irradiation resulted in better survival than antioxidant supplementation started soon after the irradiation. The antioxidant dietary supplement was l-selenomethionine, sodium ascorbate, N-acetyl cysteine, α-lipoic acid, α-tocopherol succinate, and co-enzyme Q10. Total-body irradiation with 8 Gy in the absence of antioxidant supplementation was lethal by day 16. When antioxidant supplementation was started soon after irradiation, four of 14 mice survived. In contrast, 14 of 18 mice receiving antioxidant supplementation starting 24 h after irradiation were alive and well 30 days later. The numbers of spleen colonies and blood cells were higher in mice receiving antioxidant supplementation starting 24 h after irradiation than in mice receiving radiation alone. A diet supplemented with antioxidants administered starting 24 h after total-body irradiation improved bone marrow cell survival and mitigated lethality, with a radiation protection factor of approximately 1.18.
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INTRODUCTION
Dietary supplementation with antioxidants has the potential to increase the probability of survival after an otherwise lethal total-body irradiation (TBI). Recently, Wambi et al. demonstrated that an antioxidant diet started 1 week before the radiation exposure improved the percentage of mice that survived TBI compared with groups of mice that received a control diet (1). Furthermore, at 30 days after TBI, the same percentage of mice survived TBI when mice either switched from the antioxidant diet to a control diet hours before TBI or when mice switched to an antioxidant diet from a control diet 2 h after TBI. The commonality for improved survival under each condition appears to be the presence of antioxidants in the diet at about the time of the radiation exposure plus or minus a few hours. An improved survival as a result of an antioxidant diet has been attributed to a reduction in radiation-induced oxidative stress and apoptosis of the bone marrow cell population, minimizing the bone marrow syndrome (1). An antioxidant diet is a readily available and translatable countermeasure for human use. Unfortunately, antioxidant supplements may have limited potential usefulness in a practical situation unless they are effective approximately 1 day after TBI.
The optimum timing of administration of an anti-oxidant diet as a radiation countermeasure has not been determined. To allow for delivery and distribution of a countermeasure agent, it is likely that a minimum of 1 day is needed. Also, after a significant total-body radiation exposure (1 to 7 Gy), individuals may experience nausea, vomiting and diarrhea, preventing effective administration of the diet. After this prodromal phase, symptoms of radiation exposure subside and victims of radiation exposure could be given an antioxidant diet. The current studies were designed to determine whether an antioxidant diet is an efficacious countermeasure when started 24 h after TBI.
The advantages of an antioxidant diet over other countermeasures requiring an injection, such as growth factors and cytokines, are threefold. First, an antioxidant diet can be made readily available without the government stockpiling and distribution that would be needed for growth factors and cytokines. Second, an antioxidant diet can be given orally, unlike injectables that usually require trained personnel for administration. Third, an antioxidant diet is considered safe even with prolonged use, which may not be the case for growth factors and cytokines (2–4).
In this communication we present the previously unreported observation that the survival of mice improves when the beginning of administration of the antioxidant diet is delayed for 24 h after the radiation exposure compared to antioxidant diet supplementation started a few hours after radiation exposure.
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METHODS AND MATERIALS
Animal studies were performed in an AAALAC-accredited facility at Henry Ford Hospital and were reviewed and approved by the IACUC at Henry Ford Hospital. Groups of C57BL/6 mice, 7 to 8 weeks old, were exposed to radiation alone or in combination with antioxidants as described below. Mice were acclimated for 1 week before irradiation, were housed in a temperature-controlled, HEPA-filtered environment, and were offered food and acidified water ad libitum. Food was either AIN-93G rodent chow (Land O’Lakes Purina Feed, Lansing, MI) or the same diet supplemented with antioxidants.
Antioxidant
The antioxidant-supplemented AIN-93G rodent chow was prepared under our direction by Land O’Lakes Purina Feed (Lansing, MI). Antioxidant diet supplementation was started at a fixed time, as indicated, after the radiation exposure. Once started, the diet was continued for the duration of the experiment. The antioxidant supplements per gram of diet were: 0.12 μg l-selenomethionine, 19 μg sodium ascorbate, 51 μg N-acetyl cysteine, 100 μg α-lipoic acid, 8.6 μg α-tocopherol succinate and 51 μg co-enzyme Q10; the antioxidant formula was designed to be identical to the “Diet A” regimen in the study of Guan et al. (5), but some rounding errors occurred in its preparation resulting in minor deviations.
Lethality End Point
Survival was measured in C57BL/6 mice after TBI alone or in combination with the antioxidant diet. The radiation was delivered to unanesthetized mice four at a time using a 5000-Ci (185-TBq) 137Cs source (Mark I, J. L. Shepherd and Associates, San Fernando, CA). Mice were killed humanely 30 days after irradiation because mice that survive 30 days after a TBI have normal blood counts and, if allowed, generally have a normal life span (6). Survival was defined as the time from radiation exposure to the time of euthanasia. Mice that were assessed to be moribund were euthanized based on criteria that relied on changes in weight, behavior and appearance. Mice were weighed at least three times a week with care taken to minimize potential distress (e.g., a slow, even motion was used when transporting mice between the cage and the weighing boat). When two consecutive measurements indicated that mice were losing weight, they were weighed daily. Mice that exhibited a weight loss of 20% or more were scrutinized more closely with respect to their behavior and appearance. Mice were observed for changes in response to external stimuli (e.g., lack of response when the animal was touched gently) and for changes in such nonspecific behaviors as a decrease in the frequency of grooming, eating (assessed from fecal material in cage), and drinking. Changes in appearance indicating a loss of normal body condition included posture changes (e.g. prolonged hunched posture) and sunken eyes and/or skin upon pinching that did not return quickly to the normal position, indicative of advanced dehydration. Mice were observed for weakness and/or inability to obtain food and water (e.g., inability or reluctance to stand), inability to ambulate that prevented the animal’s access to food and/or water, and inability of the animal to maintain itself in an upright position. Using these criteria, the institution’s staff veterinarian made a determination of moribundity, the requirement for euthanasia.
Reactive Oxygen Species (ROS) in Cells
ROS in vitro or in vivo were measured by the oxidation of dihydroethidium (DHE). WI-38 human embryonic fibroblasts obtained from the American Type Culture Collection were maintained in Eagle’s minimum essential medium with 10% fetal bovine serum. Approximately 50% confluent WI-38 cells were γ-irradiated (using the 137Cs source described above) or were sham-irradiated. Immediately after irradiation or sham irradiation, fresh cell culture medium with or without an antioxidant supplement was added and the cells were returned to their incubators until the next day. The antioxidant supplement was 50 μM ascorbic acid, 50 μM α-lipoic acid, 10 μM l-selenomethionine, 10 μg/ml co-enzyme Q10, 50 μM vitamin E succinate, and 0.1% (vol/vol) ethanol (solvent). DHE staining was performed 24 h after irradiation as described below for tissue sections.
ROS in Tissue
The effect of the antioxidant diet on the ROS in skin was assessed in mice that received TBI with or without the diet given starting 24 h later. Two weeks after sham irradiation or irradiation (i.e. after 13 days of the antioxidant diet), mice were injected with DHE (27 mg/kg, i.p.); 4 h later, mice were anesthetized with ketamine (100 mg/kg, i.p.) and xylazine (10 mg/kg, i.p.). Then skin was excised, frozen at –80°C, and cryosectioned for subsequent fluorescence microscopy. DHE powder was dissolved in dimethyl sulfoxide to create a DHE stock solution (10 mg/ml). The DHE injectate (200 ml final, 27 mg/kg) was produced by adding DHE stock solution to PBS maintained at 40uC. Quick and Dugan (7) noted that temperatures lower than 37°C resulted in precipitation of the DHE.
Spleen Colony-Forming Unit (CFU) Assay
The relative number of bone marrow cells surviving TBI was quantified by the endogenous spleen CFU assay as described previously (6). The number of spleen colony-forming units was measured to assess the in vivo effect of the antioxidant diet on bone marrow cell survival. Groups of C57BL/6 mice were exposed to 7.0 or 7.5 Gy alone or in combination with the antioxidant diet (started 24 h after radiation exposure). Twelve days after TBI, the spleens of the mice were excised and immersed in Bouin’s solution for at least 1 day. Then the colonies were counted using a dissecting microscope.
Peripheral Blood Count
At the selected times after TBI, mice were anesthetized with ketamine (100 mg/kg) and xylazine (10 mg/kg) for blood collection. Blood (0.5 ml) obtained by cardiac puncture with a 25 gauge needle was placed into heparinized anticoagulant tubes. Complete blood counts were measured using an Advia 120 hematology analyzer (Siemens Diagnostics) by Antech Diagnostics (Detroit, MI).
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RESULTS
The majority (78% ± 10%) of a group of 18 C57BL/6 mice survived an otherwise lethal dose of radiation when their diet was supplemented with antioxidants. Figure 1 illustrates that the antioxidant diet given starting 24 h after TBI provided significant mitigation from radiation-induced lethality (Kaplan-Meier test, P < 0.005). Similar results were obtained for TBI with a dose of 7.5 Gy (results not shown). Four of eight mice receiving TBI alone at this dose died, while all mice receiving TBI plus the antioxidant diet survived. The benefit of the antioxidants depended strongly on the time of their administration (Fig. 2). All mice died within 30 days of irradiation when they were supplied a diet supplemented with antioxidants started immediately after TBI. The diet given starting 24 h after 8 Gy TBI provided significant mitigation compared with the antioxidant diet started either immediately after TBI, 12 h after TBI, or 48 h after TBI (logrank test, P < 0.005).
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FIG. 1
Antioxidants given starting 24 h after TBI enhanced the survival of C57BL/6 mice. Data are shown for 8.0 Gy with (dashed line) and without antioxidants (solid line).
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FIG. 2
The effectiveness of antioxidants in reducing radiation-induced lethality was greatest when the start of the antioxidant diet followed irradiation by 24 h. Groups of 14–20 mice received 8 Gy TBI and were then started on the antioxidant diet immediately or 12–48 h later.
A quantitative assessment of the magnitude of mitigation was made when the antioxidant diet was started 24 h after irradiation. Figure 3 shows that with increasing radiation dose, survival decreased approximately linearly with dose over the range of 7.0 to 8.0 Gy (correlation coefficients, r2, for radiation alone and radiation plus antioxidant diet were 0.97 and 0.63, respectively). The slope of the line for mice that received radiation alone was found to be significantly (P = 0.02) different from zero with a slope of -74 ± 10 (% survival/Gy), whereas the deviation from zero was not significant (P = 0.2) for the line for the antioxidant diet started 24 h after irradiation, which had a slope of –31 ± 17. Over the range of radiation doses studied, the addition of the antioxidant diet made a significant difference in survival. The radiation protection factor was approximately 1.18, calculated as the ratio of the extrapolated estimate of the LD50 from the curve for radiation plus antioxidant diet and the estimated LD50 for radiation alone.
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FIG. 3
The survival of mice at 30 days (n = 8–18/group) decreased with increasing radiation dose; the slope for mice without antioxidants in their diet (open symbols) was steeper than that for mice receiving the antioxidant diet (solid symbols). Lines were fitted and LD50’s were calculated as described in the text.
The effect of the antioxidant diet given starting 24 h after TBI on bone marrow stem cells was measured using the endogenous S-CFU assay (Fig. 4). Twelve days after sublethal irradiation plus antioxidant diet (started 24 h after irradiation), the numbers of spleen colonies were two- to threefold higher (P < 0.01, Student’s t test) than in the group of mice exposed to either 7.0 Gy or 7.5 Gy radiation alone. Spleen weights were less in mice that received TBI. Spleen weights were significantly greater in mice receiving the antioxidant diet starting 24 h after irradiation, although they were still below the spleen weights of unirradiated control mice (data not shown).
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FIG. 4
Number of endogenous spleen colonies and blood counts in mice that after sublethal TBI. Data are shown for 7.0 and 7.5 Gy with and without antioxidants (n = 4 mice per group; the same mice were used for both blood counts and spleen colony assays). Spleen colonies are actual counts/spleen. WBC counts are 103 per μl of blood. RBC counts are 106 per μl of blood. Platelet counts are 103 per μl of blood.
Peripheral blood counts are shown in Fig. 4 for blood collected 12 days after sublethal TBI alone (7.0 Gy or 7.5 Gy) or TBI followed by antioxidant diet supplementation starting 24 h later. Leukocyte, erythrocyte, platelet and neutrophil counts were all significantly lower in irradiated mice than in unirradiated control mice (n = 4; P < 0.05, Student’s t test). In mice that received the antioxidant diet for 11 days starting 1 day after irradiation, there was a trend toward higher numbers of cells compared with mice that did not receive the antioxidant diet (n = 4 per group); the elevated blood counts reached significance for leukocytes in mice receiving 7.5 Gy (P = 0.05, Student’s t test), erythrocytes in mice that received 7.0 Gy (P = 0.05, Student’s t test), and platelets in mice that received either 7.0 Gy (P < 0.005 Student’s t test) or 7.5 Gy (P < 0.05 Student’s t test). Peripheral neutrophil counts were not changed. Despite the lack of benefit on neutrophil numbers, the overall results indicate that the antioxidant diet mitigated bone marrow radiation injury, increased the number of blood cells, and increased an animal’s chance of survival after a potentially lethal radiation exposure.
In an attempt to confirm that the antioxidants produced their beneficial effect by reducing reactive oxygen species, as proposed by others (8), we measured ROS in cells and mouse skin after irradiation with or without antioxidant supplementation. WI-38 human embryonic lung fibroblasts were exposed to 8 Gy and culture medium was immediately replaced with medium containing or not including an antioxidant supplement. Cells were assessed 24 h later for ROS by DHE fluorescence staining. Figure 5A and B shows that cells treated with antioxidants contained less ROS. The results were confirmed by studies of skin samples from mice previously receiving radiation alone or radiation followed 24 h later by the start of a diet supplemented with antioxidants for about 2 weeks. As with cultured cells, irradiated tissue demonstrated an increase in ROS. The increase in ROS was mitigated by antioxidant diet supplementation starting after irradiation (Fig. 5C–H). Consequently, both in vitro and in vivo, ROS were increased days (in cell culture) to weeks (in animals) after irradiation, and the effect was mitigated by antioxidant supplementation.
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FIG. 5
Radiation-induced reactive oxygen species were reduced by antioxidants in vitro and in vivo. Panel A: WI-38 cells were exposed to 8 Gy and ROS was assayed 24 h later by fluorescence from oxidized dihydroethidium (DHE). Panel B: DHE fluorescence in WI-38 cells treated with antioxidants for 24 h starting immediately after the radiation exposure. Panels C–H: Skin from mice 2 weeks after 8 Gy TBI. Panels C, D and E are light microscope images of skin sections after sham irradiation, 8 Gy TBI alone, and TBI plus antioxidants, respectively. Panels F, G and H are fluorescence images of oxidized DHE in tissue slices adjacent to panels C, D and E, respectively. Original magnifications are shown in individual panels.
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DISCUSSION AND CONCLUSIONS
Ionizing radiation initiates cellular damage directly by ionization and indirectly by producing free radicals. Approximately two-thirds of radiation-induced damage is caused by the free radicals that are generated during exposure. In addition to short-lived free radicals produced during exposure, free radicals are generated after the radiation exposure; ROS and pro-inflammatory cytokines induce a multitude of biological injuries long after the radiation exposure has ended. One of the approaches to counter oxidative stress caused by free radicals and ROS is to use antioxidants such as α-tocopherol succinate, ascorbic acid, β-carotene, vitamin A, α-lipoic acid, N-acetylcysteine, selenium or an SH compound (e.g. amifostine) (9, 10).
The rationale for using a combination of antioxidants is based on a number of observations. Individual antioxidants can act as pro-oxidants when they themselves are oxidized; therefore, individual antioxidants could enhance the progression of postirradiation damage to tissues and organs. In addition, humans have a pool of antioxidants, both endogenous antioxidants that are constitutively synthesized by cells and antioxidants that are consumed in the diet. Individual antioxidants function by different mechanisms and have different affinities for various free radicals. For example, α-tocopherol is more effective as a quencher of free radicals in a reduced oxygen environment, vitamin E has little effect on oxidants derived from nitric oxide, and vitamin A is most effective under higher atmospheric pressures. Ascorbic acid is needed to protect cellular components in aqueous environments, whereas carotenoids, vitamins A and E protect cellular components in non-aqueous environments. Vitamin C recycles oxidized vitamin E to an active form (11). Vitamins E and C combined inhibit apoptosis in human endothelial cells more effectively than each alone, increasing Bcl-2 and down-regulating the pro-apoptotic Bax (12).
Other observations affected our choice of antioxidant mixture. The form and type of vitamin E are important in determining its functional abilities. For example, various organs of rats selectively absorb the natural form of vitamin E and α-tocopherol succinate, the most effective form of vitamin E, for inhibiting cancer growth and a potent radioprotector when given prior to TBI (13). Selenium is a co-factor of glutathione peroxidase, and Se-glutathione peroxidase acts as an antioxidant. Glutathione cannot be used orally to increase intracellular levels of glutathione, because it is completely hydrolyzed in the gut. In contrast, an oral administration of N-acetylcysteine (NAC) and α-lipoic acid, another endogenous antioxidant, can increase the intracellular levels of glutathione by different mechanisms and can be used in place of oral glutathione to reduce the radiation injury. Co-enzyme Q10, a weak endogenous antioxidant, scavenges peroxy radicals at a faster rate than α-tocopherol and, like vitamin C, can regenerate vitamin E in a redox cycle. The foregoing discussion suggests that a combination of antioxidants may be more effective in reducing the radiation-induced injury than any individual antioxidant alone. Guan et al. showed that diet supplement with a combination of antioxidants completely prevented the reduction in the plasma levels of total antioxidant status in mice and rats exposed to proton or HZE-particle radiation (5). Recent studies with 225 kVp X rays demonstrated marked protection from radiation injury, but generally it is believed that antioxidants need to be present during the irradiation or up to 2 h after irradiation to have a significant protecting effect (1).
The data presented here show that an antioxidant-supplemented diet started 24 h after an otherwise lethal radiation exposure effectively mitigated death (Fig. 1) mediated by a sparing of bone marrow cells (Fig. 4), perhaps due to a reduction in reactive oxygen species (Fig. 5). The effect of 8 Gy on the gastrointestinal system warrants discussion. Recent evidence suggests that the mechanisms governing the bone marrow syndrome and the gastrointestinal syndrome after TBI evolve concomitantly (14). Consequently, the possible implications of radiation damage for the uptake of antioxidants need be considered. One might expect an even greater mitigating effect if the biodistribution of antioxidants were compromised by gastrointestinal injury.
The connection between ROS and hematopoiesis is being elucidated on a molecular level. Growth factors that stimulate hematopoiesis such as IL3 and GM-CSF have been shown to cause an increase in intracellular ROS levels (15, 16). The generation of ROS in response to hematopoietic growth factors contributes to downstream signaling events involving tyrosine phosphorylation such as cell proliferation (15) and apoptosis (17). Iiyama et al. (17) implicated ROS in hematopoietic cytokine-induced cell cycle progression from G1 to S phase through inducing expression of c-Myc, cyclin D2 and cyclin E and reducing expression of p27. Iiyama et al. (16) also showed that ROS play a role in cytokine activation of Jak2 with downstream signaling of proapoptosis pathways including MEK/ERK. Treatment with antioxidants inhibits the increase in ROS, reduces tyrosine phosphorylation, reduces proliferation induced by GM-CSF (15, 16), and reduces apoptosis (1).
Our data are the first to show that a delay in antioxidant administration after cellular stress can be beneficial to cell and animal survival. The kinetics of ROS generation by hematopoietic cytokines as well as the mechanisms by which ROS are involved in cytokine receptor signaling to regulate proliferation and apoptosis of hematopoietic cells was studied by Iiyama et al. (16). They demonstrated that hematopoietic cytokines IL3 and Epo induce a rapid and transient increase in ROS that peaked at 30 min followed by a slow progressive increase in ROS 24 h after the cytokine administration. It would appear that ROS pathways controlling proliferation and apoptosis of hematopoietic cells involve two separate increases in ROS, a transient increase at 30 min and a prolonged increase that continues for at least 24 h.
Mitigation of radiation lethality by antioxidants administered soon after radiation exposure has been attributed to a reduction in apoptosis (1). Our experience with C57BL/6 mice is not inconsistent with these results, as shown in Fig. 2, which also illustrates the added benefit of waiting to start administering a diet supplemented with antioxidants until 24 h after irradiation. It would appear that the first transient wave of ROS has some beneficial effect on survival since minimizing ROS early has a detrimental effect on bone marrow cell survival.
In addition to inhibiting apoptosis, reducing ROS by antioxidants soon after the radiation exposure inhibits the progression of cells from G1 to S (18), the phase of the cell cycle in which repair of DNA damage is most efficient (19). Repair of DNA damage has a half-time of 1 to 2 h (20, 21). Consequently arresting cells before S phase too soon after a radiation exposure may decrease the ability of the cells to completely repair the damaged DNA. One explanation for the increased animal survival when the antioxidant diet is given starting 24 h after irradiation is that delaying the start of the antioxidant diet allows for the most efficient repair of radiation injury and the largest increase in the survival of bone marrow cells. Further studies are needed to confirm or refute this hypothesis.
In conclusion, our results extend the work of others to show that a diet supplemented with antioxidants is effective at mitigating radiation lethality when it is started 24 h after the radiation exposure and is more effective than if given soon after the exposure. Our results support the value of antioxidants as countermeasures against radiological terrorism, especially in the practical scenario of starting a diet supplemented with antioxidants 24 h after the exposure.
At the time of this writing, three nuclear reactors in Japan were crippled, releasing radioactive particles into the air, sea, and groundwater. A potential medical crisis has been generated—one that Life Extension® members were warned about long ago.1,2
Just days after the devastating tsunami struck Japan’s nuclear reactors—suppliers of the radioprotective compound potassium iodide had no inventory left.3
The reason potassium iodide needs to be available for a nuclear emergency is that the most carcinogenic of the radioactive isotopes of iodine (iodine-131) can destroy thyroid tissue and cause cancer. If potassium iodide is taken in time, it saturates the thyroid gland with iodine so the radioactive iodine cannot easily enter.
Potassium iodide is the most important primary intervention to protect against thyroid cancer. It has long been approved by the FDA for this purpose.4
Based on our warnings dating back to 2002, most of our members had already stocked up and were prepared in case of emergency.
Not everyone heeded our prior advice. Had there been a nuclear emergency in the United States, those without immediate access to potassium iodide could have been exposed to lethal amounts of radioactive iodine.
Radioactive particles damage far more than the thyroid gland, as leukemia and other cancers are elevated in those exposed to radiation. We know that radiation inflicts free radical damage to our cells. Fortunately, supportive data reveals many of the nutrients already taken by Life Extension members may optimize one’s defenses against radiation exposure.
What Are the Real Risks Americans Face from Japan?
In the May 2002 issue of Life Extension Magazine®, we published an article titled “Vindication for Linus Pauling.”5
This article (re-published with this month’s issue), described a belated report from our Federal government whereby they admitted that above-ground nuclear testing that took place between 1951 and 1962 directly caused at least 15,000 cancer deaths in the United States.6,7
What Are the Real Risks Americans Face from Japan?
If it were not for Linus Pauling, above-ground nuclear testing would have continued, killing thousands more Americans from what the Federal government initially claimed was “harmless” radioactive ash.5,7,8
At the time that Linus Pauling was warning about the lethal dangers of radioactive fallout, our Federal government was devising ways to have him (and others) incarcerated on pretenses that they were enemies of the state.
But it was not only above-ground testing in the United States that was causing these cancers. Above-ground nuclear testing in the former Soviet Union and on Pacific Islands used by the US and its allies was also generating radioactive particles that reached the United States.7,9,10
We know today that small amounts of radiation from the crippled Japanese reactors are being detected in the United States.11,12 Government officials state there is no danger. The track record of our government when it comes to recognizing the long-term consequences of radiation exposure, however, is quite dismal.
Since most Life Extension members recognize the dangers that free radicals pose to healthy tissues, they are already obtaining some degree of protection by taking nutrients that boost natural protection against radiation.
In the event that radiation levels in the United States spike, it would appear prudent to increase one’s ingestion of the specific nutrients that are described in this article.
A Bacterium That Thrives Inside Nuclear Reactors!
Most people think radiation is toxic to all living organisms.
Not so with a bacterium called D. radiodurans,13 whose ultra-high levels of antioxidants superoxide dismutase (SOD) and catalase enable it to thrive inside nuclear reactors.14
Radiation acutely kills by inflicting free radical damage to life-sustaining cells. Due to its naturally high antioxidant status, D. radiodurans can withstand a radiation dose that is 3,000 times greater than what would kill a human.15,16
Delicate cellular structures are oxidized in the presence of high levels of radiation.17 Intriguing data suggests that maintaining high levels of antioxidants confers at least partial protection against radiation-induced free radicals.18
So while it is important to have potassium iodide on hand to protect the thyroid gland in case of a nuclear emergency,19 maintaining high cellular antioxidant levels could add an additional layer of protection to cells throughout the body.20,21
This article first explains how potassium iodide protects the thyroid gland and then more importantly, describes the specific antioxidants and other nutrients that have demonstrated radiation-protective effects in peer-reviewed published studies.
Potassium Iodide: First Line Defense
Thyroid cancer is the most common malignancy caused by exposure to materials released from damaged nuclear power plants.22 Reactor accidents release a number of radioactive elements, the most common of which is called iodine-131.22,23 Radioactive iodine is readily absorbed into the body primarily by inhalation of contaminated air and also by ingestion of contaminated vegetation, dairy, and meat. It is rapidly taken up into the thyroid gland.24 In the thyroid, ionizing radiation given off by the isotope damages DNA and causes cancer.
You can block absorption of radioactive iodine into the thyroid gland by taking a 130 mg dose of potassium iodide not later than 2 hours after possible inhalation or ingestion of radioactive iodine. (Note that 130 mg is the adult dosage. The dose for children ages 3-18 years old is 65 mg; the dose for children 1 month-3 years is 32 mg, and the dose for infants up to 1 month old is 16 mg.)23-26
The thyroid gland absorbs all forms of iodine equally; supplying the body with optimal amounts of iodine in the form of potassium iodide prevents radioactive iodine from reaching vulnerable thyroid tissue in appreciable amounts. A dose of potassium iodide taken appropriately can reduce the risk of thyroid cancer by a factor of 3 and is the single most effective means of preventing thyroid cancer following a nuclear disaster.23,24
Keep potassium iodide tablets readily available in your home, office, and any vehicle—there is not yet sufficient supply nor production capacity to obtain them during an actual event. (Despite the Congressional legislation mandating it be available, only the state of Vermont has implemented a program for distributing potassium iodide to its citizens living within 10 miles of the state’s nuclear facilities.)27
Potassium iodide, however, should not be taken on a regular basis as general protection. There are other nutrients, however, that have been shown to confer a multitargeted radioprotective benefit. They may help to maximize your body’s ability to withstand the effects of ionizing radiation, the source of free radical damage that ultimately leads to radiation-induced cancer.28-34
Polyphenols
Polyphenols are versatile molecules found in plants. They act across a range of biomolecular pathways in the body, including favorable modification of gene expression that protects tissues from ionizing radiation.35,36
Resveratrol, quercetin, and green tea polyphenols rank among the best-studied and most potent radioprotectants in this class. Resveratrol is both a radioprotector in healthy tissue and also has antitumor activity.37,38 In animal models, resveratrol has been shown to protect chromosomes from radiation-induced damage.39 Its antioxidant properties prevent radiation toxicity to animal liver and small intestines, two tissues most immediately sensitive to radiation’s ill effects.40
Quercetin and its related compounds protect lipids and proteins from otherwise-lethal doses of gamma radiation, again largely through their antioxidant properties.41 Quercetin and other polyphenols not only provide chromosomal radioprotection, but also shield mitochondrial DNA from radiation-induced oxidant damage.42 Quercetin also ameliorates biochemical changes in human white blood cells following radiation exposure.43
The polyphenol epigallocatechin gallate (EGCG), derived from green tea, also protects animals from whole-body radiation, blocking lipid oxidation and prolonging life span.44 Green tea extracts can protect rapidly reproducing cells in the intestine and hair follicles from the damaging effects of radiation therapy, a form of radiation exposure far more intense than typical computed tomography (CT) doses—and one that more closely resembles the immediate effects of exposure to a nuclear plant disaster.45,46
WHAT YOU NEED TO KNOW: OPTIMIZE YOUR INTERNAL DEFENSES AGAINST RADIATION
Optimize Your Internal Defenses Against Radiation
Potassium iodide is the single most important intervention to prevent lethal damage from radiation exposure.
For nearly a decade, Life Extension® has warned of the critical need for individuals to maintain their own supply of potassium iodide in case of a nuclear event.
Egregious government neglect and an unenlightened public led to a worldwide potassium iodide shortage amidst Japan’s ongoing nuclear disaster, creating the potential for many preventable deaths from radiation exposure.
In addition to keeping adequate supplies of potassium iodide on hand for short-term radioprotection, resveratrol, green tea polyphenols, the soy-derived compound genistein, and trace minerals and antioxidants may afford long-term protection from deadly radiation exposure.
Soy
Soybeans contain a wealth of health-promoting substances, among them several with remarkable radioprotective effects. Genistein, an isoflavone, can protect mice from ionizing radiation injury after a single dose.51 One mechanism is its protection against radiation-induced lipid peroxidation, which when unchecked disrupts cell membranes and structures.52 Genistein also stimulates production of red and white blood cells following whole-body radiation, again after as little as a single dose.53,54 (Blood stem cells in bone marrow are among the most vulnerable to radiation’s deadly effects.) Because of its powerful induction of cytokines that stimulate new blood cell formation, genistein is under intensive study as a way to protect military and civilian personnel against a potential nuclear threat.55
Soybeans also contain a radioprotective enzyme inhibitor known as the Bowman-Birk inhibitor (BBI).56 BBI activates genes involved in DNA repair, making it among the most valuable compounds for preventing or mitigating the effects of radiation toxicity.57,58 BBI also stabilizes enzymes that would otherwise produce radiation-induced arrest of skin cell growth.59 Remarkably, BBI enhances survival of healthy cells, but not diseased cells, following radiation exposure.60,61 BBI survives processing in commercial soybean products (e.g., soy milk, soybean concentrate, and soy protein isolates), making it a highly accessible radioprotectant.62,63
Curcumin and Other Plant Extracts
Compelling scientific evidence suggests that many plant extracts have valuable gene expression-modifying effects that are relevant in protecting our bodies from radiation exposure.
NUCLEAR POWER STATIONS IN 2011
Total Nuclear Power Reactors, Global
44247
Percent of World’s Electricity
15%48
Largest Producer of Nuclear Energy
USA49,50
Number of Nuclear Plants in the USA
10449
Percent of US Power from Nuclear Reactors
20%49,50
Curcumin, derived from the curry spice turmeric, exerts powerful radioprotective effects as a result of its antioxidant and detoxifying characteristics.64 Curcumin supplements reduce DNA damage and tumor formation in rats; they reduce both DNA damage and lipid peroxidation in cultured human white blood cells.65,66 Curcumin has “dual action.” Its antioxidant effects protect normal tissue from radiation. But it also upregulates genes responsible for cell death in cancers, enhancing tumor destruction by radiation.67 The result is increased survival in animals exposed to high-dose radiation.68
Together, garlic and ginger also afford significant radioprotection. Garlic’s high sulfur content supports natural antioxidant systems.69 Garlic extracts protect red blood cells from radiation damage by a glutathione-related mechanism.70 In mice, garlic extracts have been shown to prevent radiation damage to chromosomes in vulnerable bone marrow cells.71 Via a discrete physiological mechanism, garlic extracts downregulate X-ray-mediated increases in the inflammatory nuclear factor-kappaB (NF-kB) system.72 Ginger extracts boost glutathione activity and reduce lipid peroxidation by a separate and complementary mechanism.73 These extracts directly scavenge a host of free oxygen and nitrogen radicals immediately following their formation by radiation.74-76
Lab studies show that extracts of ginkgo biloba reduce the effects of clastogenic factors—external materials (including plutonium and other radioactive substances) that fragment or delete DNA and inflict chromosomal damage, leading to mutation and cancer proliferation.77,78 This effect is so powerful that it proved useful in treating workers at the Chernobyl nuclear plant long after their exposure.79 More recently, ginkgo extracts proved to protect animals’ organs from direct radiation-induced damage.80 Ginkgo also protected humans from cell damage following radioactive iodine treatment for hyperthyroid Grave’s disease.81
Ginseng is another plant important in traditional medicine that confers substantive radioprotective effects.82,83 A variety of ginseng extracts have been shown to protect against radiation-induced DNA damage.84-86 It protects hair follicles and other rapidly reproducing (but healthy) tissues from damage by radiation.87,88 Its antioxidant effects have resulted in protection of a variety of radiation-sensitive tissues, including cells in bone marrow, spleen, and testicles.82,89 Ginseng’s immunomodulatory effects make it especially useful in defending our bodies against the ravages of radiation injury.90 A North American ginseng extract was recently found to protect human white blood cells from DNA damage even up to 90 minutes following radiation exposure.91 That makes it of great interest to defense and national security researchers—and to the general public in an era of concern about nuclear plant safety.91
Silymarin, an active compound found in milk thistle, is well known for its ability to protect liver cells from alcohol and various chemical toxins. Less well known is its power to protect liver tissue from radiation damage as well.92,93 It reduces DNA damage and extends survival in animals exposed to dangerous levels of radiation.94 Silymarin’s free radical-scavenging and direct antioxidant effects are credited with producing these results.95
NUCLEAR POWER AND RADIATION RISKS
Curcumin and Other Plant Extracts
It has been known since the 1940s that so-called ionizing radiation damages human DNA, causing many different kinds of cancers, most notably thyroid cancer and leukemias.22,142,143 Ionizing radiation also causes immediate, catastrophic radiation sickness following short-term, high-dose exposure. Recent events at Japan’s Fukushima Daiichi Nuclear Power Station serve as a grave reminder that these threats are neither futuristic nor theoretical.
There have been eight nuclear power plant accidents, each causing more than $300 million in property damage, since 1975.144-146 While the costs in human lives and long-term health from the Fukushima tragedy remain unknown, we can expect them to be substantial. The worst previous nuclear disaster, in Chernobyl in 1986, resulted in 237 cases of acute radiation sickness with 31 immediate deaths, and more than 5,400 cases of thyroid cancer in the 22 years following the accident.22,142,147-149 The risk of thyroid cancer following that accident was determined to be increased by 4.5-fold in adults, 12.7-fold in adolescents, and 87.8-fold in children.142
N-Acetyl Cysteine
N-acetyl cysteine or NAC is a sulfur-containing compound that supports natural intracellular antioxidant systems, particularly glutathione, rendering it an effective radioprotective agent.96 NAC minimizes liver damage from radiation in mouse models, reducing oxidative damage and resultant DNA damage—both before and after radiation exposure.97,98 By a separate underlying mechanism of action, NAC stimulates release of cytokines known to protect bone marrow against radiation injury.99 NAC also protects bone marrow cells from radiation, largely by preventing DNA damage.100,101 A multi-compound mixture including vitamins C and E plus NAC significantly increased 30-day survival of mice exposed to a potentially lethal dose of X-rays.102 Remarkably, the effect was the same whether the supplement was given before or after the exposure.
Soy
S-adenosylmethionine (SAMe)
Like NAC, S-adenosylmethionine (SAMe) is a powerful compound essential for maintaining cellular levels of glutathione.103,104 Enzymes vital for DNA repair (and hence cancer protection) can’t function properly in the absence of methyl donors such as SAMe.105 In early 2010 we learned that ionizing radiation suppresses SAMe levels in animal models.106 Increasing the animals’ SAMe levels, on the other hand, minimized DNA damage from ionizing radiation.106
Antioxidant Vitamins
The “ACE” vitamins (A, C, and E) offer proven antioxidant protection as a result of their molecular structures. High intakes of these vitamins and other antioxidants have been shown to protect airline pilots from radiation-induced chromosomal damage,107 an occupational hazard for those who work at high altitudes. ACE supplements have been proposed as “space foods” to protect astronauts from high radiation levels.108
Beta-carotene, the precursor of vitamin A, was first used clinically in the wake of the Chernobyl nuclear accident as a first-line treatment for children from the region. Supplementation reduced the amount of radiation-induced oxidized lipids.109 More controlled animal studies showed that vitamin A could reverse radiation-induced gene expression abnormalities that could lead to cancer.110-112 Other studies show that vitamin A ameliorates other radiation effects and enhances death of cancerous cells.113 Still other studies reveal that vitamin A can actually prevent radiation-induced death of healthy cells.114
Vitamin C, together with natural antioxidant systems such as glutathione, helps protect DNA and chromosomes from oxidative damage.115-117 Vitamin C also inhibits radiation-induced death of human blood cells through modulation of protective gene expression.118 Remarkably, vitamin C can counteract radiation-induced “long-lived radicals” (LLRs) that destabilize chromosomes and induce cancerous mutations.119 The ability to counter both classical radicals and LLRs may be vital in preventing genetic damage from radiation.119
Like vitamin C, vitamin E quenches free radicals once they form, reducing their toxicity, an effect vital in radioprotection.28 Importantly, vitamin E enhances the growth-inhibiting effect of radiation on cancer tissue while simultaneously protecting normal cells.120 Animal studies show that vitamin E significantly protects mice from dying after exposure to otherwise lethal levels of gamma rays.121 Intriguingly, this effect is the result of modulation of cytokines; it is accompanied by valuable increases in new blood cell formation suppressed by radiation.121,122
A remarkable study among X-ray technicians reveals just how powerful antioxidant vitamins can be. Radiology technicians are nominally protected by elaborate shielding, but they’re still exposed to unnaturally high levels of radiation over the course of a lifetime. As a result, they tend to have higher levels of tissue oxidation. But when a group of techs was supplemented with vitamins C (500 mg) and E (150 mg) daily for 15 weeks, their markers of tissue oxidation plummeted, and their levels of natural antioxidants (such as glutathione and glutathione peroxidase in red blood cells) rose significantly.123
Ginseng
Lipoic Acid
Lipoic acid is often referred to as the “universal antioxidant” because it quenches free radicals in both aqueous and lipid-soluble environments, such as cellular membranes.124 Lipoic acid exists in two mirror-image forms: R-lipoic acid and S-lipoic acid. While most commercially available products contain a 50:50 mixture of the two forms, only R-lipoic acid is produced by life processes and is thus likely to be the more potent of the two.125,126 Compelling evidence suggests that lipoic acid may offer important protection against the threats posed by various types of radiation exposures.
When used in combination with other antioxidants including selenium, vitamin C, vitamin E, N-acetyl cysteine, and coenzyme Q10, lipoic acid helped improve survival of mice following total-body irradiation. This study was particularly noteworthy because the antioxidant combination was effective even when administered 24 hours after a dose of radiation exposure that is often lethal.127
Lipoic acid shows benefits for supporting the immune health of individuals who were involved in the clean-up of the Chernobyl nuclear accident, even years after the event. Eleven to twelve years after the Chernobyl clean-up, study participants received 600 mg of lipoic acid daily for two months. Signs of general immune health improved, and white blood cells called neutrophils demonstrated an improved ability to ingest invading cells and cellular debris.128
Radiation therapy as a component of cancer treatment frequently causes adverse effects on skin health such as swelling and a sunburned appearance. When animal skin cells were incubated with lipoic acid, they experienced less cell injury, compared with skin cells that received radiation but no lipoic acid. These promising findings suggest that lipoic acid may have important applications in preserving skin health in individuals who must undergo cancer radiation therapy.129
Other Potent Radioprotective Nutrients
Trace Minerals
Your body’s internal antioxidant defenses, including superoxide dismutase, catalase, and glutathione peroxidase all depend on trace minerals as cofactors for their function. Zinc and manganese are of particular importance for sustaining whole-body resistance to ionizing radiation. Zinc supplements have been shown to protect rats from oxidative damage to their red blood cells induced by radioactive iodine.130,131 And a zinc supplement protected bone marrow, but not tumor cells, from radiation-induced damage.132 Since mitochondria produce huge amounts of free radicals, they are especially susceptible to radiation damage. Both zinc and manganese provide powerful mitochondria-specific radioprotection in animal studies.133
Other Potent Radioprotective Nutrients
Most nutrients with powerful antioxidant activity can be expected to protect you against radiation exposure from medical tests and from temporary increases in radiation in the environment.134 In addition to those already examined, there’s good evidence for radioprotection by spirulina extracts, which protect bone marrow cells from DNA damage.135 Melatonin also protects dividing cells and circulating blood cells from chromosomal injury by radiation.136,137 Licorice extracts block DNA damage and protect cellular organelles from radiation.138 The Indian gooseberry (Emblica officianalis) increases survival time and reduces mortality of mice exposed to whole-body radiation.139 Effects include protection against lipid peroxidation and protection of rapidly-dividing cells in the intestine.140 Carnosic acid and other rosemary extracts protect against DNA damage through their antioxidant activity, both before and after radiation exposure.141
Trace Minerals
Summary
Potassium iodide is the single most important intervention to prevent lethal damage from radiation exposure. Life Extension® long ago warned the American public to keep supplies of potassium iodide on hand in the event of a nuclear catastrophe. Not everyone heeded our warning.
As we predicted, the world’s leading potassium iodide makers failed to maintain adequate supplies and ran out amidst Japan’s ongoing nuclear disaster. In addition to keeping adequate supplies of potassium iodide on hand for short-term radioprotection, there exists a broad array of scientifically-validated nutrients that may optimize your body’s natural defenses against radiation exposure.