Posts

Breast Cancer Prevention

hope-for-a-cureThe natural, alternative approach to cancer treatment and prevention can’t make money for an entity because natural substances cannot be patented.  Therefore, little interest in their exploration and development has emerged.  Without funding, classic studies can’t be performed on a large scale.  Yet, there are a few brave souls who delve into the bright possibilities (hope) of promoting natural substances to heal disease, whether they come directly from foods or indirectly via sensible supplementation.   All the while, common elements that traditional and integrative medicine share are the promotion of health by altering one’s lifestyle and using known factors to predict risk of disease.

There are so many components tied to the onset of cancer that it’s hard to tell which have the strongest influence on prevention or promotion.  In 2009, scientists at the California Pacific Medical Center Research Institute examined a few of these factors and concluded that screening for breast cancer has a positive influence on outcomes, while certain lifestyle interventions may enhance the potential to prevent it.  Estimating breast cancer risk is not a cut and dry matter, but breast density and estradiol levels are strongly associated with disease.  (Cummings. 2009)  Exercise, weight reduction, low-fat diet, and reduced alcohol use are matters to consider because all are associated with reduced risk.  Post-menopausal women appear to fare poorly from breast density factors and are urged to consider chemoprevention if found to be at high risk after all parameters are evaluated.  (Ibid.)  Mammography and self-examination reduce breast cancer mortality by a significant amount, especially among women between ages forty and seventy-four.  (Humphrey. 2002)  Tamoxifen and raloxifene, used for chemoprevention, are not without their side effects, ranging from vision changes to chest pain to hot flashes.  What about alternatives?

Prevention of obesity, or losing weight if already a problem, is essential to addressing breast cancer, both as a risk and as an established disease.  The relationship is complicated, but the association is there.  Body mass index, weight, weight gain, and waist-to-hip ratio have all been positively tied to breast cancer risk in post-menopausal women, though the tie-in is not so strong among pre-menopausal women.  (Carmichael. 2006)  Nonetheless, obesity at the time of diagnosis is significant as a poor prognostic factor.  Weight management as preventive cannot be stressed strongly enough.  Poor dietary choices are the main cause of weight gain, either eating the wrong foods or too much of the right ones.  Eating more plant-based protein and lots of fruits and vegetables, being adequately hydrated, eliminating or limiting simple carbohydrates and sugars, avoiding food preservatives and artificial colors where practicable, and enjoying nuts and seeds are strongly recommended practices.  Look at this as an abundance model rather than a deprivation model.

Certain enzymes are entailed in the incidence and progress of cancer, including breast and other soft tissues.  Their names include aromatase, telomerase, and one simply named AKT.  Inhibition of these substances is one of the goals of cancer researchers, some of whom have found that a food component termed indole-3-carbinol (I3C) is such an inhibitor.  Produced by the Brassica family of vegetables—including Brussels sprouts, cabbages, broccoli, etc.—I3C inhibits cell proliferation and induces cell death (apoptosis) in abnormal breast, prostate, and colon tissues.  What’s more, laboratory-enhanced analogues of I3C were found to be more potent at downregulating AKT in particular and other enzymes in general.  (Kim. 2011)  Additional findings indicated that cell cycle arrest of estrogen-responsive breast cancer lines was initiated by cruciferous vegetable constituents.  (Marconett. 2011)  Under acidic conditions, such as exist in the stomach, I3C is potentiated to its most active metabolite, di-indolylmethane (DIM), the main factor responsible for biological effects inside the body and resulting suppression of cancer cell proliferation.  (Aggarwal.  2005)  I3C supplements are available.

When cells are overstressed and their innate anti-oxidant capabilities are taxed, carcinogenesis may occur.  Several phytochemicals, derived from plants that include herbs and spices and not just fruits and vegetables, have demonstrated excellent chemoprotective characteristics.  Besides the crucifers cited, the simple herb cardamom, a member of the ginger family, shows promise as a provider of DIM to be applied to prophylaxis and treatment not only in carcinogenesis, but also in atherosclerosis and HPV infection.  (Acharya. 2010)  Another Brassica component with breast cancer protection properties is benzyl-isothiocyanate, a material that has exhibited anti-proliferation capability in both breast and pulmonary tissue.  (Kim.  2011)

One of the nutrients in sore supply in humans is iodine, a mineral that has been taken for granted since it appeared as a salt additive years ago.  Iodine deficiency affects almost two billion people on earth and is the number one preventable cause of mental handicap.  With the advent of other salts for culinary use, iodine has been relegated to the back burner.  The consumption of iodine-rich foods, as exemplified by those who eat seaweed as part of their traditional cuisine, does not appear to cause toxicity, but instead may reveal itself as an important element in maintaining breast tissue architecture and function.    (Patrick.  2008)  Seaweed as a dietary preference in Japan, for example, may be associated with the very low incidence of malignant and benign breast disease.  Therapeutic administration of iodine in the presence of selenium has shown anti-oxidant as well as anti-proliferative character.  (Cann.  2000)  Mexican investigators have discovered iodine to be useful as adjuvant treatment in breast cancer therapy, contributing to the integrity of normal mammary tissue.  (Aceves.  2005)  Kelp, yogurt, eggs, strawberries, and seafoods are good food sources.  Revisiting iodized salt is a prudent option.

In active disease, cancer cells may exhibit resistance to radiation.  It is this feature that has led researchers to find a way to make these stubborn cells less so.  Vitamin K, as a newly-synthesized form of K2 (VK2), not only restored radiation sensitivity, but also inhibited growth of cancer cells.  But not just in breast cancer lines.  Lung and colon cancers also responded.  The formation of selective reactive oxygen species, affecting only the cancerous but not the healthy cells, seems to be the driving mechanism.  (Amalia.  2010)   Vitamin K3, a synthetic form also called menadione, is not generally used to make supplements due to its toxic nature, but has been used successfully to alter the course of breast cancer treatment.  (Akiyoshi.  2009)

We don’t think of rest as being part of the armamentarium in treating sickness, but a relationship between sleep and interruption of the circadian clock has been found to have a decided impact on cancer genesis.  When jobs and entertainment interfere with the body’s response to night-time chemical manufacture, maybe we shouldn’t be too surprised that metabolic upset occurs.  Back in the 80’s it was proposed that the increasing use of electricity to light the night could account for the global rise in breast cancer risk.  It was theorized that blindness and long sleep duration reduce risk, and shift work increases risk.

This has spawned an interest in exploring the function of circadian genes, thinking that epigenetic alterations might be causative.  Studies indicate that certain urine melatonin compounds, concentrations of luteinizing hormones, follicle stimulating hormone, and estradiol are indicators of breast cancer risk.  Though not definitive, the implications are not to be ignored.  (Stevens.  2009)  (Davis.  2006)  Getting by on four hours of sleep does a body no good.

Nutrient intake unbalances the scale in favor of breast cancer prevention.  Among the nutrients studied are vitamins B2, B3, B6, B12, folate, and the amino acid methionine.  A study of Chinese women conducted by Vanderbilt University indicates that high folate intake may reduce breast cancer risk and that the association depends on estrogen and progesterone receptor status, particularly as related to pre-menopausal women. (Shrubsole.  2011)   Earlier probes likewise found folate to be preventive in light of hormone conditions, but even more so when combined with vitamin B12.  (Wu.  1999)
(Larsson.  2008)  (Lajous.  2006)  A synergy was discovered when the beneficial effect of folate was accentuated by dietary intake of methionine, vitamin B12, and B6.  (Shrubsole.  2001)  Folinic acid is a form of folate that has vitamin function equivalent to folic acid, but requires no enzymatic conversion.  Folinic acid encourages normal DNA replication and RNA transcription, and has the unique ability to reinforce drug treatment for active disease.

Xanthophylls are pigments that accompany chlorophyll in green plants, and are often identified with lutein.  Being yellow, their color is masked by chlorophyll in mature leaves.  Their job is to absorb certain wavelengths of light not gathered by chlorophyll, then to transfer that energy to the chlorophyll by ramping up electrons.  They are similar to, but not exactly like, carotenes.   Foods that contain xanthophylls have demonstrated protection against the onset of breast and lung cancers, although their claim to fame is protecting vision against both cataracts and age-related macular degeneration.  Research in this arena is somewhat limited, but recommendations for intake align with current dietary guidelines.  (Judy.  2004)  All leafy greens are sources.

Undergoing serious examination as preventive of breast cancer is curcumin, the active ingredient of turmeric.  Cancer cells treated with this polyphenol fail to proliferate and invade at normal rate by virtue of protein disruption (Zong.  2011).  Curcumin’s cytotoxicity as an anti-oxidant is dose-dependent, but its presence in the breast cancer war can’t be overlooked.  (Quiroga.  2010)

It’s been estimated that 30%-40% of all cancers can be prevented by lifestyle and dietary measures alone.  The protective elements in a cancer prevention diet may reduce likelihood of disease by more than 60%, and would favor recovery from disease as well.  (Donaldson.  2004)

References

Aceves C, Anguiano B, Delgado G.
Is iodine a gatekeeper of the integrity of the mammary gland?
J Mammary Gland Biol Neoplasia. 2005 Apr;10(2):189-96.

Acharya A, Das I, Singh S, Saha T
Chemopreventive properties of indole-3-carbinol, diindolylmethane and other constituents of cardamom against carcinogenesis.
Recent Pat Food Nutr Agric. 2010 Jun;2(2):166-77.

Aggarwal BB, Ichikawa H.
Molecular targets and anticancer potential of indole-3-carbinol and its derivatives.
Cell Cycle. 2005 Sep;4(9):1201-15.

Akiyoshi T, Matzno S, Sakai M, Okamura N, Matsuyama K.
The potential of vitamin K3 as an anticancer agent against breast cancer that acts via the mitochondria-related apoptotic pathway.
Cancer Chemother Pharmacol. 2009 Dec;65(1):143-50.

Amalia H, Sasaki R, Suzuki Y, Demizu Y, Bito T, Nishimura H, Okamoto Y, Yoshida K, Miyawaki D, Kawabe T, Mizushina Y, Sugimura K.
Vitamin K2-derived compounds induce growth inhibition in radioresistant cancer cells.
Kobe J Med Sci. 2010 Sep 28;56(2):E38-49.

Cann SA, van Netten JP, van Netten C.
Hypothesis: iodine, selenium and the development of breast cancer.
Cancer Causes Control. 2000 Feb;11(2):121-7.

Carmichael AR.
Obesity and prognosis of breast cancer.
Obes Rev. 2006 Nov;7(4):333-40.

Cummings SR, Tice JA, Bauer S, Browner WS, Cuzick J, Ziv E, Vogel V, Shepherd J, Vachon C, Smith-
Bindman R, Kerlikowske K.
Prevention of breast cancer in postmenopausal women: approaches to estimating and reducing risk.
J Natl Cancer Inst. 2009 Mar 18;101(6):384-98.

Davis S, Mirick DK.
Circadian disruption, shift work and the risk of cancer: a summary of the evidence and studies in Seattle.
Cancer Causes Control. 2006 May;17(4):539-45.

Michael S Donaldson
Nutrition and cancer: A review of the evidence for an anti-cancer diet
Nutrition Journal 2004, 3:19

Francini G, Petrioli R, Aquino A, Gonnelli S.
Advanced breast cancer treatment with folinic acid, 5-fluorouracil, and mitomycin C.
Cancer Chemother Pharmacol. 1993;32(5):359-64.

Humphrey LL, Helfand M, Chan BK, Woolf SH.
Breast cancer screening: a summary of the evidence for the U.S. Preventive Services Task Force.
Ann Intern Med. 2002 Sep 3;137(5 Part 1):347-60.

Kim EJ, Hong JE, Eom SJ, Lee JY, Park JH.
Oral administration of benzyl-isothiocyanate inhibits solid tumor growth and lung metastasis of 4T1 murine mammary carcinoma cells in BALB/c mice.
Breast Cancer Res Treat. 2011 Nov;130(1):61-71.

Judy D. Ribaya-Mercado, ScD and Jeffrey B. Blumberg, PhD, FACN
Lutein and Zeaxanthin and Their Potential Roles in Disease Prevention
J Am Coll Nutr December 2004 vol. 23 no. suppl 6 567S-587S

Kim DJ, Reddy K, Kim MO, Li Y, Nadas J, Cho YY, Kim JE, Shim J, Song NR, Carper A, Lubet RA, Bode AM, Dong Z.
(3-Chloroacetyl)-indole, a novel allosteric AKT inhibitor suppresses colon cancer growth in vitro and in vivo
Cancer Prev Res (Phila). 2011 Sep 1.

Lajous M, Lazcano-Ponce E, Hernandez-Avila M, Willett W, Romieu I.
Folate, vitamin B(6), and vitamin B(12) intake and the risk of breast cancer among Mexican women.
Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):443-8.

Lajous M, Romieu I, Sabia S, Boutron-Ruault MC, Clavel-Chapelon F.
Folate, vitamin B12 and postmenopausal breast cancer in a prospective study of French women.
Cancer Causes Control. 2006 Nov;17(9):1209-13.

Larsson SC, Bergkvist L, Wolk A.
Folate intake and risk of breast cancer by estrogen and progesterone receptor status in a Swedish cohort.
Cancer Epidemiol Biomarkers Prev. 2008 Dec;17(12):3444-9.

Marconett CN, Sundar SN, Tseng M, Tin AS, Tran KQ, Mahuron KM, Bjeldanes LF, Firestone GL.
Indole-3-carbinol downregulation of telomerase gene expression requires the inhibition of estrogen receptor-alpha and Sp1 transcription factor interactions within the hTERT promoter and mediates the G1 cell cycle arrest of human breast cancer cells.
Carcinogenesis. 2011 Sep;32(9):1315-23

Patrick L.
Iodine: deficiency and therapeutic considerations.
Altern Med Rev. 2008 Jun;13(2):116-27.

Quiroga A, Quiroga PL, Martínez E, Soria EA, Valentich MA.
Anti-breast cancer activity of curcumin on the human oxidation-resistant cells ZR-75-1 with gamma-glutamyltranspeptidase inhibition.
J Exp Ther Oncol. 2010;8(3):261-6.

Shrubsole MJ, Jin F, Dai Q, Shu XO, Potter JD, Hebert JR, Gao YT, Zheng W.
Dietary folate intake and breast cancer risk: results from the Shanghai Breast Cancer Study.
Cancer Res. 2001 Oct 1;61(19):7136-41.

Shrubsole MJ, Shu XO, Li HL, Cai H, Yang G, Gao YT, Gao J, Zheng W.
Dietary B vitamin and methionine intakes and breast cancer risk among Chinese women.
Am J Epidemiol. 2011 May 15;173(10):1171-82.

Stadel BV.
Dietary iodine and risk of breast, endometrial, and ovarian cancer.
Lancet. 1976 Apr 24;1(7965):890-1.

Stevens RG.
Working against our endogenous circadian clock: Breast cancer and electric lighting in the modern world.
Mutat Res. 2009 Nov-Dec;680(1-2):106-8.

Wu K, Helzlsouer KJ, Comstock GW, Hoffman SC, Nadeau MR, Selhub J.
A prospective study on folate, B12, and pyridoxal 5′-phosphate (B6) and breast cancer.
Cancer Epidemiol Biomarkers Prev. 1999 Mar;8(3):209-17.

A. Zaniboni, F. Meriggi, G. Arcangeli, P. Marpicati, E. Montini, E. Simoncini and
G. Marini
L-folinic acid and 5-fluorouracil in the treatment of advanced breast cancer: A phase II study
Ann Oncol (1993) 4 (suppl 2): S41-S43.

Zong H, Wang F, Fan QX, Wang LX.
Curcumin inhibits metastatic progression of breast cancer cell through suppression of urokinase-type plasminogen activator by NF-kappa B signaling pathways.
Mol Biol Rep. 2011 Sep 24. [Epub ahead of print]

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Exercise And The Common Cold

winter-runningSome things never come our way, no matter how hard we try. Wouldn’t it be really cool if you could win the trillion dollar lottery at least once? Or maybe twice? On the other hand, some things do come to us without trying, like the in-laws at holiday time, the IRS in April, and the common cold, also known as coryza. If you’re an adult—and if you’re reading this you probably are—you’ll get about two to four such viral infections a year. Your kids will get more than a half dozen. Then, again, you might be one of the fortunate few who get none. Collectively, colds, the flu and other upper respiratory infections are classed as influenza-like illnesses.

Some science people hold that viruses are not actually living things because they cannot reproduce on their own. They can’t go through cell division because they are acellular, not made of cells. That means they have to use your cellular material to make copies of themselves, and that means they have to get inside one of your cells, where they disguise themselves as part of the gang.  That’s when they start to sneak around, fooling other cells to accept them as friends, and then cloning themselves repeatedly. If your immune system is awake and on the job, it’ll recognize this fraud and take steps to halt it.  If it isn’t, you’ll get sick for as long a time as it takes to recoup your resources.

The rhinovirus is the most studied of the pathogens that cause upper respiratory infections (URI).  There are more than a hundred, and are most infectious in the first three days after the onset of symptoms. One of the things that separate a cold from the flu is that cold symptoms show up a couple of days after infection; with the flu, it’ll be sudden onset with extreme fatigue.  (Eccles. 2005)  Exposure to the cold weather has little to do with catching a cold, although it might compromise the immune system. Staying indoors and being in close proximity to other people is a more likely cause. All you have to do is to touch a doorknob turned by a sneeze-covered hand, or to breathe in the particles that already erupted from somebody’s nose or throat, and bingo, you’ve got it. Makes you want to stay home, doesn’t it?

There is not one thing on the market that can get rid of a cold. Nada. Nothing. Zip. You might be able to control symptoms, though, and for most of us, that’s enough. Vapor rubs for the chest, antihistamines for the runny nose, analgesics for physical discomfort, and chicken soup for the soul, which, by the way, might just be the last word in cold medicine. It’s kind of frustrating to find out that medical books don’t really address colds (at more than a few hundred dollars each), but that granny does. (Ibid.)

Whatever you do, don’t ask for an antibiotic. You can’t kill things that aren’t alive in the first place, but you can disrupt the whole immune system machinery and get the nasty side effects.  If you really and truly want to do something about your cold, exercise it away. Sounds goofy, especially because you don’t feel like it.

People who exercise seem to have fewer and milder colds, says a report from the Appalachian State University in North Carolina. Dr. David Nieman and colleagues collected data from more than a thousand subjects, ages 18 to 85, and tracked the number of URI’s they suffered.  Among the data were reports of the kinds and frequency of exercise, personal fitness evaluations, and dietary habits and lifestyle. It was found that those who exercised five or more days a week experienced 41% fewer days’ worth of cold symptoms. Also, colds were milder for those in better shape than for those who were sedentary. Dr. Nieman explained that exercise mobilizes the immune system at a higher rate than normal and causes immune cells to attack viruses. (Nieman. 2011)

As opposed to intense, strenuous workouts, moderate exercise reduces the number and severity of colds. Prolonged strenuous exercise opens a window for viral attack by exhausting the first responders of the immune system. Investigators at the Department of Exercise Science of the University of South Carolina learned of increased susceptibility to respiratory viral attack following exercise stress in lab animals that ran a treadmill to the point of fatigue. The animals subjected to such rigors were more likely to succumb to administered viruses than those that rested or were less taxed.  (Murphy. 2008)

When a geriatric populace was examined under the hypothesis that moderate exercise could promote resistance to upper respiratory tract infections, Polish researchers found that, not only was susceptibility to infection reduced, but also that symptoms of depression were ameliorated. In this cohort, there was a distinct negative association between physical activity and sickness.  (Kostka. 2007)

T-cells are a major source of messenger cytokines responsible for the biological effects of the immune system. They have antigen-specific receptors on their cell surfaces to allow them to identify invaders. Th1 cytokines produce the pro-inflammatory response that kills intracellular parasites and perpetuates autoimmune responses. Interferon gamma is the star player. If this gets out of hand, there can be excessive tissue damage, so there is a balancing mechanism in Th2 cytokines, which include interleukins 4, 5, and 13. These promote the IgE responses that are common to skin and mucus membranes. Interleukin 10, also a Th2, is seriously anti-inflammatory.  In the best case scenario, Th1 and Th2 will be balanced at the exact ratio needed to face an immune challenge. It was discovered at the University of Illinois that moderate exercise (pay attention to the word “moderate”) would shift immune response from the pro-inflammatory Th1 to the anti-inflammatory Th2 cytokines, thereby reducing lung pathology and influenza protein expression, thus improving survival after virus infection. (Lowder. 2006)

Current study is examining nutritional supplements as countermeasures to exercise-induced immune changes and infection risk.  Quercetin, beta-glucan, and curcumin are cited as being able to reduce the magnitude of such immune system insult and resultant risk of URI.  (Nieman.  2008)

Now we have another reason to get up from the couch and leave the remote behind.

References

Chubak J, McTiernan A, Sorensen B, Wener MH, Yasui Y, Velasquez M, Wood B, Rajan KB, Wetmore CM, Potter JD, Ulrich CM.
Moderate-intensity exercise reduces the incidence of colds among postmenopausal women.
Am J Med. 2006 Nov;119(11):937-42.

Douglas RM, Hemilä H, Chalker E, Treacy B.
Vitamin C for preventing and treating the common cold.
Cochrane Database Syst Rev. 2007 Jul 18;(3):CD000980.

Eccles R.
Understanding the symptoms of the common cold and influenza.
Lancet Infect Dis. 2005 Nov;5(11):718-25.

Friman G, Wesslén L.
Special feature for the Olympics: effects of exercise on the immune system: infections and exercise in high-performance athletes.
Immunol Cell Biol. 2000 Oct;78(5):510-22.

Kostka T, Praczko K.
Interrelationship between physical activity, symptomatology of upper respiratory tract infections, and depression in elderly people.
Gerontology. 2007;53(4):187-93. Epub 2007 Feb 21.

Lowder T, Padgett DA, Woods JA.
Moderate exercise early after influenza virus infection reduces the Th1 inflammatory response in lungs of mice.
Exerc Immunol Rev. 2006;12:97-111.

Martin SA, Pence BD, Woods JA.
Exercise and respiratory tract viral infections.
Exerc Sport Sci Rev. 2009 Oct;37(4):157-64.

Murphy EA, Davis JM, Carmichael MD, Gangemi JD, Ghaffar A, Mayer EP.
Exercise stress increases susceptibility to influenza infection.
Brain Behav Immun. 2008 Nov;22(8):1152-5. Epub 2008 Jun 21.

Nieman DC.
Immunonutrition support for athletes.
Nutr Rev. 2008 Jun;66(6):310-20.

D C Nieman, S J Stear, L M Castell, L M Burke
Nutritional supplement series
A–Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance: part 15
Br J Sports Med 2010;44:1202-1205

David C Nieman, Dru A Henson, Melanie D Austin, Wei Sha
Upper respiratory tract infection is reduced in physically fit and active adults
Br J Sports Med. 2011 Sep;45(12):987-92. Epub 2010 Nov 1.

Woods JA, Keylock KT, Lowder T, Vieira VJ, Zelkovich W, Dumich S, Colantuano K, Lyons K, Leifheit K, Cook M, Chapman-Novakofski K, McAuley E.
Cardiovascular exercise training extends influenza vaccine seroprotection in sedentary older adults: the immune function intervention trial.
J Am Geriatr Soc. 2009 Dec;57(12):2183-91.

Wright PA, Innes KE, Alton J, Bovbjerg VE, Owens JE.
A pilot study of qigong practice and upper respiratory illness in elite swimmers.
Am J Chin Med. 2011;39(3):461-75.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

AGE’s and Curcumin

high-blood-sugarThe title of this may be misleading because, although it’s about AGE, it isn’t actually about age.  The two—the acronym and the word—are related, however.  AGE is the acronym for Advanced Glycation End-products, substances that have something to do with aging, but that are part of a bigger picture. An AGE forms after a chain of chemical reactions that yield glycation, which is the result of a sugar molecule bonding to a protein or lipid molecule without the controlling action of an enzyme. AGE’s may form outside the body by cooking sugars with proteins or inside the body via normal metabolism and aging. In certain circumstances, such as the oxidative stress that occasionally accompanies the hyperglycemia of diabetes, AGE formation can exceed normal levels.

What Do AGE’s Mean For Me?
In diabetes-related AGE formation, high glucose levels ultimately cause reactive oxygen species (ROS) that have the potential to attack DNA and to become prime factors in aging and in age-related chronic diseases. From this come the vascular complications of diabetes, where a cascade of events leads to inhibition of vascular dilation (contributing to elevated blood pressure), to the oxidation of low-density lipoprotein (LDL), and to the secretion of pro-inflammatory chemicals that increase oxidative stress.  In the long run, atherosclerosis, arthritis, myocardial infarction (heart attack), retinopathy, or any of several other conditions may develop.

AGE’s may be more reactive than the sugars from which they are made, two of which are fructose and glucose. Glycation is a haphazard process, and is not the same thing as glycosylation, which is controlled by enzymes. Glycation occurs in the Maillard reaction, the phenomenon that makes food taste exceptional when it gets browned.  Remember that this entails an amino acid and a sugar in an event that is enhanced in an alkaline environment. Toasted bread, fried onions, roasted coffee, maple syrup, biscuits, dark-colored sodas, donuts, barbecued meats and tater tots are examples.  Although the results are similar to the naked eye, caramelization is quite a different process. Yes, both involve heat, but caramelization excuses amino acids from the party and relies solely on some kinds of sugars. Once in a while Maillard and caramelization occur at the same time. High temperature, low moisture and alkaline conditions promote the Maillard reaction. Browning doesn’t happen until water is vaporized at a temperature exceeding the boiling point.

What Happens Inside The Body?
Maillard-type reactions occur inside the body, albeit at much lower temperatures. There are slow, complex reactions that cause the formation of AGE’s, some of which are believed to be responsible for the amyloid proteins that lead to Alzheimer’s disease.  Degenerative eye disease and diabetes have received the most attention, however, followed by recent interest in an association of glucose to neurodegeneration. Recent study has associated type 2 diabetes with cerebral atrophy, cognitive impairment and dementia at glucose levels deemed to be within normal range (Herbuin, 2012).

Some animals, notably rats and mice, either already have, or can be bred to have, physiological traits that parallel those of human body systems and mechanisms. Animal models can develop diabetes, for example, either spontaneously via breeding or by chemical or surgical means. Of course, for each advantage there may be a limitation, but it is recognized that without such laboratory partners there would be little progress in medical research (Chatzigeorgiou, 2009). Oxidative stress has been studied as a factor in degenerative diseases for years. Its inhibition has been the goal, and appears to have been realized in experiments with diabetic rats performed in India in the late 1990’s, where AGE’s and the cross-linking of collagen were addressed by the use of curcumin, the active ingredient of the turmeric spice. Doses as high as 200 mg/kg of body weight, for a period of two months, attenuated not only degradative processes, but also the accumulation of lipid peroxidation by-products (Sajithlal, 1998).

Malondialdehyde is an organic compound used as a marker for the specific oxidative stress resulting from the corruption of polyunsaturated fats (PUFA’s). As a reactive aldehyde, malondialdehyde is analogous to AGE’s. One of the wear-and-tear pigments remaining after this assault on PUFA’s is called lipofuscin, whose presence is viewed as a symptom of membrane damage or of damage to the mitochondria. Accumulation of lipofuscin is implicated in Alzheimer’s disease, Parkinson’s disease, ALS, COPD, and macular degeneration, among other disorders. Calorie restriction and increased glutathione are but two approaches to control this symbol of aging and its sequelae.   The anti-oxidant and anti-aging characteristics of curcumin were found to wield considerable influence in the prevention of malondialdehyde and lipofuscin formation, even at comparatively low doses of 30 mg/kg (Sarvalkar, 2011).

Those suffering the diabetes complications that corrupt vision, renal function, nerves, blood vessels, and the skin have found hope in the interruption of protein glycation by curcumin, where it was seen to be one of several natural substances to interfere with the reaction of glycated materials and their respective receptors. The therapeutic potential in delaying or preventing diabetic complications using curcumin is viewed as a safe and simple complement to conventional therapies (Elosta, 2012) (Ahmed, 2005).

Besides the diminution of AGE potency, curcumin inhibits the unfavorable activities tied to enzymes such as the pro-inflammatory COX2, the peroxide-forming lipoxygenase and the unfriendly nuclear factor kappa beta. Remarkably, curcumin also was discovered to have probiotic characteristics and to enhance treatment routes for such refractory conditions as Crohn’s, certain cancers, cirrhosis of the liver, and COPD (Chronic Obstructive Pulmonay Disease) (Bengmark, 2009).

It has become clear that some natural substances can replace drugs, without side effects. Anti-AGE strategies, addressing more than one body system and using curcumin in the arsenal, are here right now.

References

Ahmed N.
Advanced glycation end products–role in pathology of diabetic complications.
Diabetes Res Clin Pract. 2005 Jan;67(1):3-21.


Bengmark S, Mesa MD, Gil A.
Plant-derived health: the effects of turmeric and curcuminoids.
Nutr Hosp. 2009 May-Jun;24(3):273-81.


Ishita Chattopadhyay, Kaushik Biswas, Uday Bandyopadhyay, and Ranajit K. Banerjee
Turmeric and curcumin : Biological actions and medicinal applications
Current Science. 2004, 10 July; 87 (1): 44-53


Chatzigeorgiou A, Halapas A, Kalafatakis K, Kamper E.
The use of animal models in the study of diabetes mellitus.
In Vivo. 2009 Mar-Apr;23(2):245-58.


Cherbuin, Nicolas, Sachdev, Perminder, MD, PhD, Anstey, Kaarin.
Higher normal fasting plasma glucose is associated with hippocampal atrophy: the path study.
Neurology Journal. September 2012 Volume 79 Issue 10: Pages: 1019-1026


Elosta A, Ghous T, Ahmed N.
Natural products as anti-glycation agents: possible therapeutic potential for diabetic complications.
Curr Diabetes Rev. 2012 Mar;8(2):92-108.


Goldberg T, Cai W, Peppa M, Dardaine V, Baliga BS, Uribarri J, Vlassara H.
Advanced glycoxidation end products in commonly consumed foods.
J Am Diet Assoc. 2004 Aug;104(8):1287-91.


Alison Goldin, BA; Joshua A. Beckman, MD; Ann Marie Schmidt, MD; Mark A. Creager, MD
Basic Science for Clinicians: Advanced Glycation End Products—Sparking the Development of Diabetic Vascular Injury
Circulation. 2006; 114: 597-605


Jakus V, Rietbrock N.
Advanced glycation end-products and the progress of diabetic vascular complications.
Physiol Res. 2004;53(2):131-42.


Krajcovicová-Kudlácková M, Sebeková K, Schinzel R, Klvanová J.
Advanced glycation end products and nutrition.
Physiol Res. 2002;51(3):313-6.


Manmei Li, Zhong Liu, Zhulin Zhang and Lin Ma
Inhibitory effects of curcumin derivatives on nonenzymatic glucosylation in vitro
Frontiers of Chemistry in China . Volume 1, Number 2 (2006), 227-231


Lin J, Tang Y, Kang Q, Chen A.
Curcumin eliminates the inhibitory effect of advanced glycation end-products (AGEs) on gene expression of AGE receptor-1 in hepatic stellate cells in vitro.
Lab Invest. 2012 Jun;92(6):827-41.


Lin J, Tang Y, Kang Q, Feng Y, Chen A.
Curcumin inhibits gene expression of receptor for advanced glycation end-products (RAGE) in hepatic stellate cells in vitro by elevating PPARγ activity and attenuating oxidative stress.
Br J Pharmacol. 2012 Aug;166(8):2212-27. doi: 10.1111/j.1476-5381.2012.01910.x.


Ji-ping Liu, Liang Feng, Mao-mao Zhu, Ru-Shang Wang, Ming-hua Zhang, Shao-ying Hu, Xiao-bin Jia, Jin-Jie Wu
The In Vitro Protective Effects of Curcumin and Demethoxycurcumin in Curcuma longa Extract on Advanced Glycation End Products-Induced Mesangial Cell Apoptosis and Oxidative Stress
Planta Med. 2012; 12: 1311-1398 DOI: 10.1055/s-0032-1315257


Okamoto T, Yamagishi S, Inagaki Y, Amano S, Koga K, Abe R, Takeuchi M, Ohno S, Yoshimura A, Makita Z.
Angiogenesis induced by advanced glycation end products and its prevention by cerivastatin.
FASEB J. 2002 Dec;16(14):1928-30. Epub 2002 Oct 4.


Rees DA, Alcolado JC.
Animal models of diabetes mellitus.
Diabet Med. 2005 Apr;22(4):359-70.


Sajithlal GB, Chithra P, Chandrakasan G.
Effect of curcumin on the advanced glycation and cross-linking of collagen in diabetic rats.
Biochem Pharmacol. 1998 Dec 15;56(12):1607-14.


P. P. Sarvalkar, M. V. Walvekar and L. P. Bhopale
Antioxidative effect of curcumin (Curcuma longa) on lipid peroxidation and lipofuscinogenesis in submandibular gland of D-galactose- induced aging male mice
Journal of Medicinal Plants Research. 30 September, 2011 Vol. 5(20): 5191-5193

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Treat Your Asthma Gingerly

ginger-rootIf numbers can be trusted (99% of all statistics being made up on the spot), there are almost 25 million cases of asthma in the United States. Out of almost 314 million people in the country, that equates to almost 8% of the population. More than 3,000 Americans die from asthma each year. The annual cost for prescription drugs exceeds 6 billion dollars, and, as reported in 2012, asthma cases have increased 48% in the last ten years. (http://www.statisticbrain.com/asthma-statistics/, from the American Lung Association). Wow, that’s quite an indictment.

Asthma is a condition in which airways become narrowed, swell and produce extra mucus, making it difficult to breathe. It triggers coughing, wheezing and shortness of breath. For the lucky few, it’s only a minor nuisance; for others, it can be a major problem that interferes with daily life and might lead to a life-threatening asthma attack. Although asthma has no cure, it can be controlled. Once in a while symptoms flare up in certain situations, such as the exercise-induced asthma that worsens when the air is cool and dry, or the occupational asthma that assaults people in a workplace where exposure to fumes, chemicals or gases are the norm.

The odds of developing the condition increase among smokers, those whose mothers smoked during pregnancy, those assailed by second-hand smoke, people having other allergic conditions, or those having a blood relative with asthma. Symptoms that interfere with sleep, work or recreational activities need serious attention and a visit to a physician.

The inhaled corticosteroids commonly prescribed to treat asthma claim to have fewer adverse effects than the oral steroids used for other inflammatory conditions, such as arthritis and allergies. But that is purely subjective. These medications are used for the long haul, as are the oral leukotriene modifiers that include Singulair and its kin. Leukotrienes are endogenous chemicals that mediate responses in allergic reactions and inflammation, and their modification with drugs is linked, albeit weakly, to psychological reactions characterized by aggression, agitation, hallucinations, depression and suicidal thoughts. No completed suicides have been reported, however (Philip, 209). That’s reassuring. Yep. Other medications are used in combination with inhaled corticosteroids, but have the nasty habit of occasional exacerbation of symptoms. A drug seldom used nowadays is theophylline, a pill that relaxes the muscles around the airways to keep them open. Originally extracted from tea leaves and later found in cocoa, theophylline is one hundred percent bioavailable, but its side effects are equally disturbing, and are worsened in the presence of fatty meals.

But the future is bright. On the horizon are compounds extracted from ginger, the zingy spice that livens up our baked goods. Traditionally used to treat stomach upset, including that from motion sickness (Langner, 1998), ginger has found its way into the grab bag of integrative medicine, where its anti-inflammatory nature finds favor with sufferers of arthritis, hypercholesterolemia (Madkor, 2011), elevated glucose (Akhani, 2004), and even hypertension (Ghayur, 2005) and worms (Mostafa, 2011) (Lin, 2010).

Researchers at Columbia University have discovered that the bronchoconstriction of asthma can be attenuated with ginger compounds that work synergistically with  medications called beta-agonists, the best-known probably being Albuterol. The relaxation of airway smooth muscle is the goal. When the drug and the natural components were combined, relaxation response was remarkable (Townsend, 2013). Of the ginger isolates, one called 6-shogaol was most effective in its relaxing effects. This constituent of ginger is similar in structure to the better-known gingerol, the most active ingredient of the herb which is related to compounds appearing in chilies and black pepper, capsaicin and piperine respectively. Shogaol is produced when ginger is dried or cooked. As far as pungency, it falls between capsaicin and piperine on the heat scale.

In the lungs there is an enzyme called PDE4D which interferes with the relaxation of the airways. The elements of ginger stop this enzyme from flaunting its attributes. To further aggravate asthma, there also exists a protein structure that plays a role in the constriction of airways and the contraction of muscles, named F-actin filament.
6-shogaol dissolves these filaments rapidly. While there is support for the idea that asthma can be outgrown as musculature matures (Chitano, 2005), there is comfort in knowing that management of the disease is readily obtainable and that all-natural adjuvants are in the offing. Calcium signaling is part of the muscle contraction process. With some blood pressure medicines, calcium is inhibited and vessels relax to allow the smooth passage of blood. It was found that ginger has an activity like that of verapamil, a calcium-channel blocker, in that it can ease the contraction of the smooth muscle that controls airways (Ghayur, 2008).

In the decade preceding the 21st century, plants have been documented to be useful in the treatment of various respiratory disorders, including asthma. In fact, the use of natural products has increased dramatically all over the world. Not only have they affected bronchodilation, but also mast cell stabilization, anaphylaxis, and overall leukotriene modulation (Mali, 2011). (Mast cells, by the way, are those that release histamine in response to injury, allergy or inflammation.) To the delight of alternative-minded practitioners, many of these medicinal plants provide relief of symptoms equal to allopathic medicines (Bielory, 1999).

We might be reminded to enjoy our spices, especially those with anti-inflammatory characteristics, such as ginger and its close cousin, turmeric, but to be prudent if taking blood thinners. That the therapeutic value of ginger is enhanced by its mineral constituents (Latona, 2012) adds another dimension to the study of its universal appreciation.

References

Akhani SP, Vishwakarma SL, Goyal RK.
Anti-diabetic activity of Zingiber officinale in streptozotocin-induced type I diabetic rats.
J Pharm Pharmacol. 2004 Jan;56(1):101-5.

Bielory L, Lupoli K.
Herbal interventions in asthma and allergy.
J Asthma. 1999;36(1):1-65.

Chitano P, Wang L, Murphy TM.
Mechanisms of airway smooth muscle relaxation during maturation.
Can J Physiol Pharmacol. 2005 Oct;83(10):833-40.

Ghayur MN, Gilani AH.
Ginger lowers blood pressure through blockade of voltage-dependent calcium channels.
J Cardiovasc Pharmacol. 2005 Jan;45(1):74-80.

Ghayur MN, Gilani AH, Janssen LJ.
Ginger attenuates acetylcholine-induced contraction and Ca2+ signalling in murine airway smooth muscle cells.
Can J Physiol Pharmacol. 2008 May;86(5):264-71.

Hirst SJ.
Airway smooth muscle as a target in asthma.
Clin Exp Allergy. 2000 Jun;30 Suppl 1:54-9.

Langner E, Greifenberg S, Gruenwald J.
Ginger: history and use.
Adv Ther. 1998 Jan-Feb;15(1):25-44.

Latona DF, Oyekele GO, Olayiwola OA
Chemical analysis of Ginger Root
IOSR Journal of Applied Chemistry (IOSRJAC). Volume 1, Issue 1; May/June 2012: 47-49

Levy AS, Simon O, Shelly J, Gardener M.
6-Shogaol reduced chronic inflammatory response in the knees of rats treated with complete Freund’s adjuvant.
BMC Pharmacol. 2006 Oct 1;6:12.

Lin RJ, Chen CY, Lee JD, Lu CM, Chung LY, Yen CM.
Larvicidal constituents of Zingiber officinale (ginger) against Anisakis simplex.
Planta Med. 2010 Nov;76(16):1852-8.

H Ling, H Yang, S-H Tan, W-K Chui, E-H Chew
6-Shogaol, an active constituent of ginger, inhibits breast cancer cell invasion by reducing matrix metalloproteinase-9 expression via blockade of nuclear factor-κB activation
British Journal of Pharmacology. Volume 161, Issue 8, pages 1763–1777, December 2010

Madkor HR, Mansour SW, Ramadan G.
Modulatory effects of garlic, ginger, turmeric and their mixture on hyperglycaemia, dyslipidaemia and oxidative stress in streptozotocin-nicotinamide diabetic rats.
Br J Nutr. 2011 Apr;105(8):1210-7.

Mali RG, Dhake AS.
A review on herbal antiasthmatics.
Orient Pharm Exp Med. 2011 Aug;11(2):77-90.

Mostafa OM, Eid RA, Adly MA.
Antischistosomal activity of ginger (Zingiber officinale) against Schistosoma mansoni harbored in C57 mice.
Parasitol Res. 2011 Aug;109(2):395-403.

Philip G, Hustad C, Noonan G, Malice MP, Ezekowitz A, Reiss TF, Knorr B.
Reports of suicidality in clinical trials of montelukast.
J Allergy Clin Immunol. 2009 Oct;124(4):691-6.e6.

Ramji, Divya; ho, chi; Huang, Qingron; Rafi, Mohamed; Huang, Mou
Isolation of gingerols and shogaols from ginger and evaluation of their chemopreventive activity on prostate cancer cells and anti-inflammatory effect on 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced mouse ear inflammation
RUcore – Rutgers University Community Repository. 2007
http://mss3.libraries.rutgers.edu/dlr/showfed.php?pid=rutgers-lib:21328

Sehwan Shima, Sokho Kima, Dea-Seung Choia, Young-Bae Kwonb, Jungkee Kwona
Anti-inflammatory effects of [6]-shogaol: Potential roles of HDAC inhibition and HSP70 induction
Food and Chemical Toxicology. Volume 49, Issue 11, November 2011, Pages 2734–2740

Townsend EA, Yim PD, Gallos G, Emala CW.
Can we find better bronchodilators to relieve asthma symptoms?
J Allergy (Cairo). 2012 ;2012:321949. doi: 10.1155/2012/321949. Epub 2012 Oct 2.

Townsend EA, Siviski ME, Zhang Y, Xu C, Hoonjan B, Emala CW.
Effects of ginger and its constituents on airway smooth muscle relaxation and calcium regulation.
Am J Respir Cell Mol Biol. 2013 Feb;48(2):157-63.

Wang L, Pozzato V, Turato G, Madamanchi A, Murphy TM, Chitano P.
Reduced spontaneous relaxation in immature guinea pig airway smooth muscle is associated with increased prostanoid release.
Am J Physiol Lung Cell Mol Physiol. 2008 May;294(5):L964-73.

Wu H, Hsieh MC, Lo CY, Liu CB, Sang S, Ho CT, Pan MH.
6-Shogaol is more effective than 6-gingerol and curcumin in inhibiting 12-O-tetradecanoylphorbol 13-acetate-induced tumor promotion in mice.
Mol Nutr Food Res. 2010 Sep;54(9):1296-306.

Zick SM, Djuric Z, Ruffin MT, Litzinger AJ, Normolle DP, Alrawi S, Feng MR, Brenner DE.
Pharmacokinetics of 6-gingerol, 8-gingerol, 10-gingerol, and 6-shogaol and conjugate metabolites in healthy human subjects.
Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):1930-6.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Get Something Free… Radicals The Saga of Vitamins A, C and E

vitamins-foodThe same oxygen you need to stay alive and to burn food for energy makes you oxidize just as fast as a rusty fender on the old jalopy in the back yard…or maybe in the driveway if your surname is Clampett at 90210. If your apples turn brown and your fish or butter becomes rancid, blame it on oxygen. Lungs, eyes, skin, fruits, vegetables, herbs, you name it. If it has cells, it’ll oxidize and those cells will change. But it’s a normal part of living. Fret not. The Creator gave us a way to intercept the free radicals and undo their dastardly deeds. These molecules are “free” because they have parts missing, and they scour the neighborhood looking for replacements, sort of like the original equipment manufacturer you look for when rebuilding your ’57 Chevy. Being on a mission, these molecules will rampage to hook up with another molecule and steal electrons. Frankly, it would be simpler if free radicals just killed a cell and left it at that. But nope, it has to start the dominoes falling. If a cell were bumped off, the body would make a new one. Instead, the cell’s DNA gets damaged enough to set the stage for disaster.

Broken DNA can make a cell mutate and set up a chain reaction for other cells to do the same thing. Not good. Free radicals damage a bunch of cells. Overexposure to the sun, cigarette smoke (either first-hand or second-hand), vehicle exhaust (diesel is the worst), comestibles that are called food but really are not, booze, heavy metals and a few other hazards can work over time to create chronic sickness, including cancer, heart disease, Alzheimer’s disease and Parkinson’s. How do we fix things? Maybe it’s easier to put the brakes on oxidation in the first place. Waddya think?

Antioxidants are molecules that work to prevent damage due to both normal body processes and exposure to some chemicals and environmental perils. One of the benefits of antioxidants is their ability to slow oxidation in the smallest parts of the body—proteins and DNA. There are antioxidants made by the body and those that come from food or supplements. The water-soluble ones react with oxidants in the blood and in the free spaces inside cells. The fat-soluble protect cell membranes from a process known as lipid peroxidation. Some body tissues might have more of one antioxidant than another. For example, one may be plentiful in the kidney, but almost absent from the heart, while the opposite might apply to a different antioxidant. Some may appear at the same concentration in every part of the body.

The body has its own antioxidant defense system, one that relies partly on minerals for proper functioning. Superoxide dismutase (SOD) needs copper, zinc and manganese; glutathione peroxidase needs selenium; and catalase depends on iron. Except for selenium, minerals are not defined as antioxidants, but as cofactors in their manufacture. Although this endogenous system demands respect, we’re going to focus on the most commonly used exogenous antioxidants—vitamins A, C, and E. In most activities, biochemical as well as psycho-social, the buck stops somewhere. With antioxidants, the buck stops at glutathione, so we’ll give that molecule the respect it merits, particularly for the work it does in the lungs (Rahman, 2006) (Nadeem, 2008).

Vitamin A is a general term for a group of related fat-soluble substances, including retinal and retinol, cited as preformed vitamin A. Retinal is converted to retinoic acid, the form that influences gene transcription. Beta-carotene and other carotenoids are referred to as provitamin A compounds. Beta-carotene, the carotenoid that comes from yellow and orange foods, is converted by the liver to retinol. Some forms of this vitamin are occasionally used in pharmacological doses to treat a few conditions, including retinitis pigmentosa (Berson, 1993), acute promyelocytic leukemia (Thurnam, 1999) (Ross, 1999), and various skin conditions (Ross, 1999). However, it’s important to realize that high doses of retinoids, especially if synthetic, can override the body’s own control mechanisms and present toxicities.

Preformed vitamin A is available as retinyl palmitate or acetate, overdose of which is easy to happen because people don’t read labels and often get the vitamin from more than one source, such as from a multi-vitamin or fortified food and later from a separate supplement.  The chief concern is that vitamin A is rapidly taken up, but slowly cleared from the body. Alcohol depletes vitamin A stores from the liver, but taking vitamin A while drinking is an accident waiting to happen. Keeping intake from a supplement at 2500 IU (750 mcg) should do the trick, while avoiding adverse effects on bone in the geriatric crowd. Getting vitamin A from foods is not normally a problem of overdose unless the food is fortified with it (Promislow, 2002). Beta-carotene, by the way, has about half the potency of preformed A, where 2 mcg of supplemental beta-carotene can be converted to 1 mcg of retinol. With foods, though, it takes 12 mcg to make 1 mcg of retinol. Can you see why it’s hard to overdose on cantaloupe?  Pumpkin, carrots, sweet potatoes, mangoes and collards are decent sources.

Water-soluble vitamin C is ascorbic acid, not citric acid, the latter made commercially by the fermentation of molasses. Even though citric acid can be found in oranges, there aren’t enough oranges on the planet to meet a fraction of the demand from the food industry.  Besides being an antioxidant, vitamin C is required for the synthesis of collagen, the structural element that holds us together. Additionally, it helps to make the neurotransmitter norepinephrine. Most animals can make the vitamin C they need; humans and guinea pigs cannot (Linster, 2007). Like all reducing agents, vitamin C itself becomes oxidized. Such an entity donates one or more electrons to a substance that already has become oxidized and is a free radical. In this instance, an antioxidant can become a damaging molecule, running around, looking for an electron to replace the one it just donated. But there is a rescue molecule, where the buck stops, as mentioned earlier. Too much ascorbic acid may cause kidney stones, since oxalates are metabolites of vitamin C, but doses up to 2000 mg a day shouldn’t be a concern for healthy people (Taylor, 2004) (Auer, 1998). The original RDA was barely enough to prevent scurvy, the reason for the RDA in the first place. Citrus, bell peppers, broccoli, potatoes, tomatoes, and strawberries are good sources.

Vitamin E is a fat-soluble family of eight antioxidants—four tocopherols and four tocotrienols. Any adverse publicity you read about vitamin E is based only on alpha-tocopherol, synthetically produced at that and administered to people with pre-existing conditions. The alpha- form of tocopherol is the one most often encountered because it’s actively maintained in the body and has the greatest nutritional significance, although the beat-, delta-, and gamma- forms have merit. It is an antioxidant that prevents the oxidation of fats (rancidity). This is especially important to the cell membrane. After vitamin E gives up an electron, it becomes a free radical itself, but vitamin C and A sacrifice themselves for its salvation. Besides being antioxidant, vitamin E appears to modulate some genes, to inhibit cell proliferation, and to control platelet aggregation and monocyte adhesion. It might even interact with enzymes, structural proteins and lipids (Zingg, 2004) (Ricciarelli, 2002), and regulate cell signaling (Rimbach, 2002). The body recognizes synthetic forms of vitamin E as sham, so it pays to find the d- form, not the dl-form. Oils, avocados and nuts are good sources. If there be a caveat, it is that too much can interfere with blood clotting. Therefore, if taking an anti-coagulant medication, check with the doctor before supplementing. If a tooth extraction or more serious surgery is in the offing, stop supplementation days ahead of time.

Once an antioxidant gives up an electron it can act like the thugs it’s trying to sequester. It needs its own savior. Here comes glutathione to the rescue. This is the body’s master antioxidant, made from amino acids.  As long as sulfur-containing amino acid stores are adequate and are regularly refilled through diet or supplementation (N-acetyl cysteine is such a source), glutathione is able to spare an electron here and there to replace the ones lost by vitamins A, C and E. The dysregulation of glutathione is known to be a prime factor in pathology, from diabetes to pulmonary fibrosis (Lu, 2009), so it pays to consume enough sulfur foods to get the methionine, taurine and cysteine that glutathione needs to keep itself in perfect form. The crucifers, onions and garlic, and animal products, including egg yolks, are substantial sources.

Having the best home run hitter in the league doesn’t guarantee a championship season. You need defense, too; you need a team. The same applies to antioxidants. The overall collection rather than the heavily advertised super antioxidant is what it takes because different antioxidants counteract damage by different types of free radicals within different cellular compartments. Natural and balanced is the rule.

References

Abdullah Acar, M. Ugur Cevik, Osman Evliyaoglu, Ertugrul Uzar, Yusuf Tamam, Adalet Arıkanoglu, et al
Evaluation of serum oxidant/antioxidant balance in multiple sclerosis
Acta Neurologica Belgica. September 2012, Volume 112, Issue 3, pp 275-280

Auer BL, Auer D, Rodgers AL.
The effect of ascorbic acid ingestion on the biochemical and physicochemical risk factors associated with calcium oxalate kidney stone formation.
Clin Chem Lab Med. 1998 Mar;36(3):143-7.

Mehmet Balci, Erdinc Devrim and Ilker Durak
Effects of Mobile Phones on Oxidant/Antioxidant Balance in Cornea and Lens of Rats
Current Eye Research.2007, Vol. 32, No. 1 , Pages 21-25

Berr C, Richard MJ, Gourlet V, Garrel C, Favier A.
Enzymatic antioxidant balance and cognitive decline in aging–the EVA study.
Eur J Epidemiol. 2004;19(2):133-8.

Berson EL, Rosner B, Sandberg MA, Hayes KC, Nicholson BW, Weigel-DiFranco C, Willett W.
A randomized trial of vitamin A and vitamin E supplementation for retinitis pigmentosa.
Arch Ophthalmol. 1993 Jun;111(6):761-72.

Hassan Boskabadi, Mahdieh Moeini, Fatemeh Tara, Shima Tavallaie, Hamidreza Saber, Raheleh Nejati, Golkoo Hosseini, Hesam Mostafavi-Toroghi, Gordon A. A. Ferns, Majid Ghayour-Mobarhan
Determination of Prooxidant–Antioxidant Balance during Uncomplicated Pregnancy Using a Rapid Assay
Journal of Medical Biochemistry.June 2013. Volume 32, Issue 3, Pages 227–232

Cristóvão, C.; Cristóvão, L.; Nogueira, F.; Bicho, M.
Evaluation of the oxidant and antioxidant balance in the pathogenesis of chronic obstructive pulmonary disease
Revista Portuguesa de Pneumologia. 2013;19:70-5.

Dringen R
Metabolism and functions of glutathione in brain.
Prog Neurobiol. 2000 Dec;62(6):649-71.

Firuzi O, Miri R, Tavakkoli M, Saso L.
Antioxidant therapy: current status and future prospects.
Linster CL, Van Schaftingen E.

Curr Med Chem. 2011;18(25):3871-88.
Vitamin C. Biosynthesis, recycling and degradation in mammals.
FEBS J. 2007 Jan;274(1):1-22.

Lu SC.
Regulation of glutathione synthesis.
Mol Aspects Med. 2009 Feb-Apr;30(1-2):42-59.

Lu SC.
Glutathione synthesis.
Biochim Biophys Acta. 2013 May;1830(5):3143-53.

Celestyna Mila-Kierzenkowska, Alina Woźniaka, Tomasz Boraczyński, Michał Szpinda,  Bartosz Woźniak, Alicja Jurecka, Anna Szpinda
Thermal stress and oxidant–antioxidant balance in experienced and novice winter swimmers
J of Thermal Biology. Volume 37, Issue 8, December 2012, Pages 595–601

Nadeem A, Masood A, Siddiqui N.
Oxidant–antioxidant imbalance in asthma: scientific evidence, epidemiological data and possible therapeutic options.
Ther Adv Respir Dis. 2008 Aug;2(4):215-35.

Promislow JH, Goodman-Gruen D, Slymen DJ, Barrett-Connor E.
Retinol intake and bone mineral density in the elderly: the Rancho Bernardo Study.
J Bone Miner Res. 2002 Aug;17(8):1349-58.

Rahman I, Biswas SK, Kode A.
Oxidant and antioxidant balance in the airways and airway diseases.
Eur J Pharmacol. 2006 Mar 8;533(1-3):222-39.

Ricciarelli R, Zingg JM, Azzi A.
The 80th anniversary of vitamin E: beyond its antioxidant properties.
Biol Chem. 2002 Mar-Apr;383(3-4):457-65.

Rimbach G, Minihane AM, Majewicz J, Fischer A, Pallauf J, Virgli F, Weinberg PD.
Regulation of cell signalling by vitamin E.
Proc Nutr Soc. 2002 Nov;61(4):415-25.

Ross AC. Vitamin A and retinoids. In: Shils M, Olson JA, Shike M, Ross AC. ed. Modern Nutrition in Health and Disease. 9th ed. Baltimore: Lippincott Williams & Wilkins; 1999:305-327.

Amirhossein Sahebk, Akram Mohammadi, Ali Atabati, Shamim Rahiman, Shima Tavallaie Mehrdad Iranshahi, Saeed Akhlaghi, Gordon AA Ferns, Majid Ghayour-Mobarhan
Curcuminoids Modulate Pro-Oxidant–Antioxidant Balance but not the Immune Response to Heat Shock Protein 27 and Oxidized LDL in Obese Individuals
Phytother. Res. Article first published online: 15 MAR 2013. doi: 10.1002/ptr.4952

Taylor EN, Stampfer MJ, Curhan GC.
Dietary factors and the risk of incident kidney stones in men: new insights after 14 years of follow-up.
J Am Soc Nephrol. 2004 Dec;15(12):3225-32.

Thurnham DI, Northrop-Clewes CA.
Optimal nutrition: vitamin A and the carotenoids.
Proc Nutr Soc. 1999 May;58(2):449-57.

Zingg JM, Azzi A.
Non-antioxidant activities of vitamin E.
Curr Med Chem. 2004 May;11(9):1113-33.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.