Stephen A. Levine, PhD
The biggest conceptual research objections for the patient’s well-being would be the extensively research findings of the association of elevated selenium in patients who later developed diabetes or diabetes-related symptoms. The first such findings were reported by Strange et al in August of 2007.1
An analysis of a randomized, double-blind placebo-controlled trial involved 1,202 patients with skin cancer, excluding melanoma patients. The subjects were chosen from areas where people often had low blood selenium. Participants’ blood was tested for selenium and then patients were supplemented with 200 micrograms of selenium in a baker’s yeast tablet daily, or a placebo (provided by Nutrition 21). Patients were followed for 7.7 years. The cumulative incidence of type 2 diabetes was higher among those receiving selenium than for those receiving placebo. A significant increased risk for type 2 diabetes was observed in the top tertial (top grouping highest in selenium).
It was a small study and subject to uncertainty, as with other small studies. A few more positive cases of diabetes in the placebo group would have led to a nonsignificant result.
This was enough of a finding, considering that millions of people are consuming this amount or similar amounts of selenium daily, to launch an avalanche of selenium/diabetes-related research, which is ongoing.
In extensive studies, even moderate increases of selenium consumption and increases in blood plasma or blood serum or whole blood selenium in humans often led to findings of symptoms of type 2 diabetes in just a few years and much longer. Those living in areas where the soil was rich in selenium were tested. The morbidities tested for included fasting blood sugar elevation, metabolic syndrome, obesity, and nonalcoholic fatty liver disease.
Many millions of dollars have been spent studying the association of selenium and symptoms of diabetes and on analysis, leading to a large body of research both in humans and animals. Numerous findings agree with the positive association between selenium consumption and serum blood, blood plasma, and/or whole blood levels of selenium. However, with closer investigation there are both conflicting and even contrary findings in other studies.
This association of selenium and diabetic symptomatology exists today. Pertinent research is summarized and interpreted in an insightful review published in 2022 in Redox Bio.2 It is one of the only papers that I’ve seen where an in-depth discussion on the interplay between the redox chemistry of selenium and the redox requirements of diabetes are considered. The conclusions reached in this paper deserve special consideration.
“The role of selenium in type-2 diabetes mellitus and its metabolic comorbidities” (Redox Bio. 2022 Jan 24)2
“In this review of type 2 diabetes mellitus (T2DM) and associated disorders, we discuss the dysregulation of fuel metabolism together with epidemiological findings and studies on potential molecular mechanisms that may help to illuminate the inconsistent results in this area of research.”2
“We explore the dysregulated fuel metabolism in T2DM and its co-morbidities, emphasizing the relevance of inflammation and oxidative stress. We describe the epidemiology of observational and experimental studies of selenium in diabetes and related conditions, explaining that the interaction between selenium status and glucose control is not limited to hyperglycemia but extends to hypoglycemia….”2
“While animal studies have revealed potential molecular mechanisms underlying adverse effects of severe selenium/selenoprotein excess and deficiency in the pathogenesis of insulin resistance and B-cell dysfunction, their translational significance (relevance for humans) is rather limited. Importantly, dietary selenium supplementation does not appear to be a major causal factor for the development of type 2 diabetes in humans though we cannot exclude a small contribution of selenium on top of other risk factors, particularly if ingested at high (supranutritional) doses. Elevated selenium biomarkers that are often measured in T2DM patients are more likely to be a consequence, rather than a cause of diabetes.”2 [emphasis added]
Nail and toenail selenium levels had been accepted as valid and stable markers for selenium in the body. However, some of the studies excluded the nail/toenail data as it was found to be inconsistent with blood levels and other analyses.
“After controlling for potential confounders, toenail Se status was lower among men with diabetes than among healthy controls. A later study followed two separate cohorts of 3,630 women from the Nurses’ Health Study and 3,535 HPFS (Health Professionals Follow up study) (2), and men who were free of prevalent T2DM and heart disease at baseline in 1982-83 and 1986-87 respectfully. Toenail Se concentrations were measured at baseline, and over the subsequent 21-26 years when 780 cases of incident T2DM occurred. After multivariable adjustment, the risk of T2DM was lower across increasing quintiles of Se.”2 [emphasis added]
Other such research described in the review is also contrary to the prevailing hypothesis.
I believe that an association does exist between what appears to be elevated selenium and diabetes, or some of the signs of diabetes as per the statement in the Redox Biology review.2 I believe its elevation is caused by the early-stage disease processes: that incipient diabetes may be the cause of the elevated selenium levels. I suggest that part of the reason selenium may appear to be higher in blood is that there is evidence of some abnormality in transport of the selenium in the body via blood plasma for reasons of preexisting disease, which I will describe.
“Human studies indicate that GPX activity is consistently altered in systemic disease states such as Down’s syndrome, schizophrenia, skin disease and cancer.” This and other recent data demonstrate that glutathione peroxidase and selenium are found to be deficient in serious disease states.
“In Griffin and Lane’s study (10, Table 6-3, page 187) on patients with untreated head and neck cancers (squamous cell carcinoma), red blood cell GPX and selenium levels were significantly decreased, and plasma levels were increased. The investigators reported that plasma levels were further increased in those patients with advanced disease and with significant weight loss.Weight loss in cancer patients has been shown to lead to adverse outcomes.”
“They suggested that their patients might suffer from reduced ability to transport selenium from plasma into the red blood cell for incorporation into the GPX enzyme. Such impairment of selenium transport appears to result from oxidative damage to the transport proteins, which are known to be highly sensitive to oxidants (2). Also, Se liberated into the plasma from damaged subunits of the GPX enzyme, which itself is susceptible to oxidative damage, would contribute to the observed increase in plasma Se levels.“2
“A Swedish study (10, Table 6-4, Page 188) of more than 500 patients with a broad range of skin disorders found GPX enzyme measured in whole blood were markedly reduced in the vast majority including atopic dermatitis, eczema, psoriasis, vasculitis, mycosis, fungoides, and dermatitis. Treatment with selenium and vitamin E for 6 weeks raised red cell glutathione peroxidase levels and markedly had an overall beneficial effect, particularly on the patients with severe protracted seborrheic dermatitis.”2
The vitamin E was quite important to reduce the oxidative stress, so that the body could function to rebuild healthy selenium transport proteins, and the GPX enzyme, which sparked the recovery. More selenium was probably advantageous, as the existing high selenium in the plasma was probably not functional and could be bound up with other molecules, prohibiting its appropriate use. Additional selenium could further allow progress in overall healing.
This research is internally consistent with my understanding of how oxidative stress can function in the body. The elevated selenium in plasma was a consequence, not a cause of illness, and vitamin E and selenium were shown to be a major part of the remedy.
Much of the research focused on the role of selenium in causing diabetes uses plasma and serum sources of selenium data. We now have reason to question any data on selenium levels based upon elevated plasma content of selenium. More research should be done to confirm and expand this understanding, and thereby potentially resolve internal inconsistences that exist in this body of research relating to selenium and diabetes.
Notice that often the toe/toenail selenium does not seem to be subject to elevated levels and does not support the prevailing belief.
Another study cited in the article2 is the National Health and Nutrition Experimental Survey (USA NHANES), which showed that an increase of selenium of 10 ug/L in the blood was associated with increased occurrence of diabetes symptoms by 12%. This study involved almost 19,000 people. However, in this, like other concordant studies, there is another important point to consider.
“Comparing the top with the bottom quartiles (four groups) of selenium intake, the OR (odds ratio) for diabetes was 1.44. However, for all-cause mortality, comparing the highest to the lowest quartiles of Se intake have a hazards ratio for all-cause mortality of .77, suggesting that Se status was a bonus overall.”2
This finding that selenium decreases all-cause mortality and cancer-associated mortality is seen in numerous other selenium studies. So, this needs to be integrated into the understanding of selenium’s potential for increasing the risk for diabetes.
Selenium’s protection against cancer and lowering of all-cause mortality, as well as the breadth and magnitude of selenium deficiency in illnesses of varying severity emphasizes how important selenium can be for our health. The GPX4 enzyme is a membrane-bound glutathione peroxidase that is essential for life. Selenium is found to be deficient in cancer patients due to dietary restrictions, weight loss from disease, and disease treatment.
“Selenium in Cancer Rehabilitation – A Retrospective Study from a Specialized Clinic (in Germany)” (Nutrients, 2023 Sept 1; 2023)3
“Micronutrient deficiencies are common at the time of cancer diagnosis and are associated with worse prognosis. In this study a patient quality of life questionnaire (EORTC QLQ -C-30) was used to evaluate patients before and after cancer rehabilitation, and additionally three months after patients were discharged from rehabilitation. Coordinately, zinc and selenium were measured in blood at these times.”3
271 patients with breast, colon, and pancreatic cancer were included. Selenium deficiency varied with the cancer type, (breast <colorectal< pancreatic) from 34% to 90%. The average prevalence of selenium deficiencies in the patient population was 72%. Of the breast cancer patients 34%, colorectal patients 74%, and pancreatic patients 90% were selenium deficient. This could be due to the increased use of chemotherapies for pancreatic cancer and for colorectal cancers and less for breast cancer, or due to the severity of the disease itself, or both. Zinc deficiencies were rare. Supplementation of selenium for three weeks before and for three months during and after rehabilitation at 600 ug of sodium selenite per day was more efficient to correct selenium deficiency compared to 300 ug per day.
“Rehabilitation and increasing selenium status after rehabilitation were associated with improved global quality of life, physical and emotional functioning, and fatigue.”3
Their conclusion was that selenium deficiency is common in cancer patients admitted to a cancer rehabilitation clinic. “Selenium supplementation during rehabilitation effectively corrected selenium deficiency in most cases.”
“The improvement of global quality of life during rehabilitation was also significant in pancreatic cancer patients in both selenium groups. As in colon cancer patient response after three months, scores decreased in the second group (300 ug daily selenite). Global quality of life was significantly better in group 1, (600 ug/d) with increasing selenium status three months after rehabilitation compared to group 2 (300 ug/day) with decreasing selenium levels.” 3
The use of the sodium selenite form of selenium to reverse widespread and profound deficiencies in cancer patients warrants further discussion. In short, selenite would be expected to have numerous benefits as we have discussed beyond the replacement value of selenium. The patients could feel the difference in measurements of well-being, especially with the higher replacement dose.
Many cancer patents generally have unneeded weight loss due to malnutrition, nausea, pain, G.I. disorders, as well as from reaction to the chemotherapy and radiation treatments. This paper briefly reviews other related studies, showing malnutrition at diagnosis and due to chemo and radiation therapy. Decreased selenium status is reported to affect survival. Weight loss due to traditional oxidative therapy has had a significant negative effect on 5-year survival.
“High Dose Selenium Induces Ferroptotic Cell Death in Ovarian Cancer: (Int J Mol Sci. 2023 Jan 18)4
“Sodium selenite (SS) significantly decreased the proliferation and increased the death of ovarian cancer cells, mediated by an increased generation of reactive oxygen species. Notably, high-dose SS decreased the levels of glutathione peroxidase (GPx4) in the cancer cells, without altering other selenoproteins. Furthermore, high-dose SS triggered lipid peroxidation and ferroptosis, a type of iron-dependent cell death, due to dysregulated GPx4 pathways. We demonstrated that intravenous high-dose SS significantly reduced the tumor growth and weight of ovarian cancer cells. Consistent with our in vitro results, mice bearing SKOV3 ( cancer cells) treated with high dose SS (I.V.) showed decreased GPX4 expression in tumors.”4
“Glutathione depletion and ROS generation are all effects of selenite and are promising strategy for cancer therapy.”4
This is presumably due to the oxidative destruction of reduced glutathione, which is a cosubstrate of the glutathione peroxidase enzyme and potentially destruction of the enzyme itself, along with other cellular proteins, by free radical oxidative cascade.
“High dose SS mediated ferroptosis therapy and thus the combination In healthy cells, GPx4 functions to reduce (add electrons) and thereby detoxify lipid peroxides. Loss of GPX 4 in cancer cells makes them critically vulnerable to ROS, which can lead to an oxidative cascade that weakens the cancer cells further and leads to a better response to chemotherapy and or radiation, and possibly, for its use as a solo therapy.
A surprisingly odd statement is found in this paper.
“Importantly, SKOV3 (the ovarian cancer cell line) bearing BALB/C mice showed selenium deficiency compared to non-SKOV3-bearing mice (figure 5D) (selenium levels) Control 34.0 +/- 1.9 Umol/ml; vs SKOV3- bearing mice, 24±1.5 Umol/ml.”4
“The low probability (p <.005) of this as a spontaneous event emphasizes that there was a dramatic reduction in selenium levels from pre to post inoculation of the mice, with ovarian cancer cells. “These phenomena were reversed by treatment with SS suggesting that high-dose SS has the potential as an anti-cancer drug for ovarian cancer.”4
This BALB/C mice line from well-known experimental strains used in laboratories, as expected, the had normal selenium blood levels. After ovarian cancer cells were administered via I.V., at some point blood selenium was tested again in the mice and found to be 29.5% lower into a notably deficient state. The injection of cancer cells into these animals caused them to have cancer and overt selenium deficiency. One might ask, which came first. This is a provocative finding and raises questions about the potentially intimate relationship of selenium deficiency to certain cancers.
“Pre and post chemotherapy evaluation of breast cancer patients; Biochemical approaches of serum selenium and antioxidant enzymes” (Caspian J. Interm Med 2020 Fall)5
This study was done in Iran, where 1 in 15 women have breast cancer. The activity of 4 serum antioxidant enzymes and Se were determined after the use of Adriamycin/Cytoxan (AC) chemotherapy. Fifty breast cancer patients were treated with Adriamycin 60/mg/m2 and Cytoxan 600 mg/m2. After 3 courses of chemotherapy, a significant decrease was seen in each of four antioxidant enzymes and for Se. These were found to be highly deficient at a p value of less than one in one thousand (p<.001) for each of 4 protective antioxidant enzymes and for selenium. This combination of gross deficiency of these four enzymes and selenium suggests that the patient’s antioxidant defense systems, which is tied into immune function, were heavily burdened and compromised. This is further confirmed by the high malonaldehyde levels in the mice.
“These changes are not necessarily dependent on the age and disease stage…We showed that the higher stages of breast cancer are associated with significant increases in malondialdehyde which is a lipid peroxide marker for oxidative stress. So, these patients are experiencing substantial oxidative stress.”5
“Selenium is one of the most essential trace elements due to its important role in prevention of cancer, its antioxidant activities and ( its profound function) for the immune system enhancement. It is proposed that the administration of Se 100200- ug/day can prevent genetic damages and cancer progression in human.“ 5
According to the first study, 300 ug was not enough where 600 ug yielded better results in severely deficient patients.3
“Prediagnostic serum selenium levels in relationship to breast cancer survival and tumor characteristics” (Int J Cancer. May 06 2020)6
“The study was conducted to test whether Se is associated with the aggressiveness of breast cancer tumors. 17035 women were recruited between 1991 and 1996. Inclusion criteria were incident breast cancer. These were compared to controls regarding their pre-diagnostic selenium levels and risk of having a certain tumor characteristic or subtype.”6
“Lower all-cause mortality was found among women in the highest Se quartile compared to the lowest with hazard ratio of .63 at 95% confidence level. Similar results were seen for breast cancer specific mortality hazards ratio .60. …Results of our study support that Se is associated with a lower mortality in breast cancer, not related to established prognostic factors.”6
Though the authors studied prediagnostic selenium levels and breast cancer aggressiveness, they found “better breast cancer specific and overall survival among woman with higher prediagnostic selenium levels, ( p< .05 ), however, no correlation between selenium status and specific breast cancer characteristics. Our results from a previous study, and recent Cochrane systemic review, suggest that it is unlikely that Se is associated with overall risk of breast cancer. However, two studies have reported increased breast cancer mortality among women with the lowest quartile of serum Se. Thus, a potential protective effect of Se seen is seen in outcome rather than incidence.”6
“The mean serum Se level was 91.3 ng/mL among controls, 91.2ng/mL among breast cancer cases with invasive tumors and 92.2 ng/mL among the rest of the cases. Charabopoulos et. al. found that serum Se levels were lower among breast cancer cases compared to aged, matched controls, and Se levels were more than 2-fold higher in the neoplastic breast tissues comparted to healthy breast tissue…… We also found the highest overall mortality among the controls had the lowest Se values in our study….[Other studies with somewhat similar findings are discussed.]”6
“Altogether, the findings suggest that selenium is a prognostic factor for mortality in breast cancer patients.”6
“Selenium status is associated with colorectal cancer risk in European prospective investigation of cancer and nutrition cohort” (Int J Cancer. 2015 March 1)7
“In Europe, Colorectal cancer (CRC) is the second leading cause of cancer related death. There is debate as to whether Se influences CRC or its precursor colorectal adenoma lesions.”7
The study shows that Se status is suboptimal by measuring SePP (selenium protein P) saturation in many Western Europeans.
“Higher SePP concentrations were inversely associated with CRC risk (Ptrend=.009) RR -.89 in men not stastically significant, and more apparent in women (ptrend=.004) IRR =.82, …. The findings indicate that Se status is suboptimal in many Europeans and suggest an inverse association between CRC risk and higher serum Se status is more evident in woman.”7
“The authors find that the selenium status in many Western Europeans is suboptimal. Higher selenium levels were inversely associated with the risk to develop colorectal carcinoma. Populations where selenium status is suboptimal, increasing selenium intake may reduce colorectal carcinoma risk.”7
“Selenium Supplementation in the critically ill” (Nutr Clin Pract. 2012 Feb. 27)8
“Critical illness and systemic inflammatory response syndrome (SIRS) is characterized by selenium depletion and high morbidity and mortality. Se status correlates well with clinical outcome in SIRS and may be useful as an early indicator of survival. Several investigators have evaluated the benefits of Se supplementation for the critically ill, either as a monotherapy or in an antioxidant micronutrient combination. Pharmaconutrition, with high doses Se (from 500 ug- 1600-ug/d) involving an initial loading bolus, followed by continuous infusion, appears to be safe and efficacious with evidence that it can improve clinical outcome by reducing illness severity, infectious complications, and decreasing mortality in the intensive care unit. We now have a clearer understanding of the pharmacokinetics of the initial transient prooxidant effect of I.V. bolus of SS and the antioxidant effects of continuous infusion. Sufficient evidence is available to consider initiating high dose I.V. Se therapy routinely in critically ill patients immediately on admission to ICU.”8
Other related studies suggest Se life-saving effects on critical illness and SIRS can be found. Once again, we are seeing the evidence of SS profound application in life-threatening circumstances.
“Application of Sodium Selenite in the Prevention and Treatment of Cancers” (Cells. 2017 Dec)9
This is an excellent review focusing on sodium selenite’s role in cancer. “There are several hypotheses concerning the anticancer activity of SS, (and how it is able to enter and destroy cancer cells).”9
“In the case sodium fibrinogen, sodium selenite, but not selenate, inhibits disulfide exchange reactions, preventing the formation of a hydrophobic polymer, termed parafibrin, the circulatory accumulations of which is associated with numerous degenerative diseases. Parafibrin can specifically form a protein coat, around tumor cells, that is completely resistant to degradation induced by lymphocyte proteases. In this way cancer cells become protected against destruction by the organism’s immune system.”9
This would be the first action for selenite to get access to cancer cells. As SS damages the formation of parafibrin it then becomes selectively absorbed into cancer cells, where it goes to work as a profound therapeutic chemotherapy. The selective absorption into the cancers by more than twice its entrance into healthy cells, provides more medicine where it is needed and less of a burden on the patient.
Glutathione is then oxidized in the cancer cells which disables the GPX enzyme, as it is required for the enzyme’s function. GPX enzymes are often considered life essential for both healthy and cancer cells.
The article goes on to explain that cancer cells are often under oxidative stress, more so than healthy cells. They are often deficient in antioxidant enzymes, and thereby more vulnerable to many oxidizing chemo therapies and radiation and SS which is in fact, a natural chemotherapy. This difference regarding the extra oxidative stress in cancer cells is that SS itself a multi-faceted oxidant, can be targeted selectively to great advantage, and with low toxicity.
“The experimental data presented by Sinha and El-Bayoumy, demonstrated that selenium may affect the inductance of apoptosis process in various types of cancer cells including prostate, colon cancer, liver cancer, leukemia, and lymphoma. Selenium compounds, those exhibiting redox properties, can produce a certain amount of reactive oxygen species (ROS), which have a prooxidative effect on cancer cell apoptosis.”9
This oxidative mechanism may explain partially the wide spreading findings of selenium’s protective role from cancer development. SS is an inorganic, highly oxidizing compound, and is generally consumed from water via streams, rivers, and lakes. Once it enters the food chain, it temporarily retains its oxidative character from which is can be utilized in cancer treatment. Eventually some of SS will be converted to organic forms by plants, animals and other living forms. SS is somewhat unique, in its varied therapeutic value on many biological targets, as an agile oxidant, well before it functions with proteins.
“It should be emphasized that the use of high doses of SS exhibits promising anticancer effects as described in numerous preclinical studies. Not all forms of organic selenium are equally effective, only those with oxidant activities can have anti-cancer properties….Although the exact mechanisms of oxidative imbalance in cancer are not completely understood the current state of knowledge indicates that sodium selenite may be an ultimate remedy in the treatment of cancer.”9 [emphasis added]
Final Words on the Research Incriminating Selenium in the Diet as Causing Diabetes Years Later
We know there are major conflicts in the data, with some studies showing no difference in diabetes incidence even at higher levels selenium. Other studies find lower levels of selenium in the diabetic patient. Often the nail/toenails samples produce opposite findings.
The reason I described for higher levels of selenium in plasma may well account for most of these inconsistencies. I have shown preliminary but physiologically sound data that that elevated selenium in blood plasma is more likely a consequence of oxidative free radical stress on critical selenoproteins and GPX itself. The high selenium in plasma is liberated from selenoprotein transporters and enzymes and will likely not be bioactive until the enzyme systems are repaired and repartnered with selenium. The first therapeutic step should be to stop the damaging oxidative stress on the patient with other antioxidants, including nutrient antioxidants, allowing the system to recover, as we see with the recovery of skin conditions in patients and of their red blood cell GPX via supplementing with vitamin E and selenium. Yes, more selenium rather than less.
We are not yet able to totally discount this possibility of selenium’s causative action leading to some increased risk of diabetes. However, consider that selenium is found to reduce, sometimes very substantially, cancer and all-cause mortality even at very moderate increased doses. All-cause mortality would include cardiovascular and diabetes, cancer, and infections, as these are the major causes of death in our society. And there is an overlap as diabetes bleeds into cardiovascular disease, and into cancer, obesity, infection and so on. Also I.V. doses of SS have been shown to treat SIDS and other urgent care emergencies with dramatic lifesaving results.
I have briefly highlighted several studies in my literature review. These studies point to selenium’s profound importance, which stems from both redox and immune functions, and its obvious anticancer effects. The findings that selenium causes diabetes, appears to run contrary to uncontested and well supported data which indicates selenium often substantially reduces allcause mortality and cancer-related mortality. Therefore, most of these diseases might be affected by selenium’s longevity effects.
The five cancer patients that were presented in part one of this paper, responded quickly and with no significant side effects to 5,000 micrograms of SS. In other cases, doses of 350 ug, of Pico™ ionic selenite were used with excellent results without side effects. We are suggesting that a three- or four-month treatment term may be enough to be followed by lower dosing. Certainly, some more serious research is called for, along with appropriate use in certain patients.
References
- Stranges S, et al. Effects of Long-Term Selenium Supplementation on the Incidence of Type 2 Diabetes. Annals of Internal Medicine. August 21, 2007.
- Steinbrenner H, et al. The role of selenium in type-2 diabetes mellitus and its metabolic comorbidities. Redox Bio. [epub] January 24, 2022.
- Pfister C, Schoenemann J. Selenium in Cancer Rehabilitation – A Retrospective Study from a Specialized Clinic [in Germany]. Nutrients. September 1, 2023.
- Jung-A Choi, et al. High Dose Selenium Induces Ferroptotic Cell Death in Ovarian Cancer. Int J Mol Sci. January 18, 2023.
- Pakmanesh F, et al. Pre and post chemotherapy evaluation of breast cancer patients: Biochemical approaches of serum selenium and antioxidant enzymes. Caspian J. Intern Med. Fall 2020.
- Sandsveden M, et al.Prediagnostic serum selenium levels in relationship to breast cancer survival and tumor characteristics, Int J Cancer. [ePub] May 2020.
- Hughes DJ, et al. Selenium status is associated with colorectal cancer risk in European prospective investigation of cancer and nutrition cohort. Int J Cancer. March 1, 2015.
- Hardy G, et al. Selenium Supplementation in the critically ill. Nutr Clin Pract. February 2012.
- Kieliszek M, et al. Application of Sodium Selenite in the prevention and Treatment of Cancers. Cells. December 2017.
- Levine, SA, Kidd PM 1985; Antioxidant Adaptation, Its Role in Free Radical Pathology; Biocurrents Division, Allergy Research Group
Published May 18, 2024
About the Author
Stephen A. Levine, PhD, is recognized internationally for his classic text on free radical biochemistry – Antioxidant Adaptation: Its Role in Free Radical Pathology (Levine & Kidd, 1985) – and as a leader in the development of research-based nutritional supplementation. He founded Allergy Research Group (ARG) in 1979, and in 1980 he founded the company’s subsidiary, Nutricology.