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Telomeres: Measures of Vitamin Benefits

In the last couple of years, new research has discovered another benefit for taking multiple vitamins. This is a "Gold Standard" benefit that can be measured to show value.

Telomeres are a special protein cap on the ends of chromosomes that protects them from damage during DNA and cell division. As cells continue to divide and form daughter cells, the telomeres shorten until this protein cap is so short it can not longer offer this protection against DNA damage and the cell dies. Multiple vitamin users had on average just over 5% longer telomeres than those not taking vitamins. BEWARE: Those taking IRON supplements had 9% LESS length of telomeres.

DO NOT TAKE IRON SUPPLEMENTS UNLESS YOU ARE ANEMIC. 

Longer telomere lengths are associated with anti-oxidant vitamins C and E and also Fish oils. The active ingredient in red vine, resveratrol, is a big protective factor here.


Antioxidant Overkill

If you are looking for this topic in search engines, it will be found under "antioxidant overload". Evidently, the body likes harmony and balance in opposing reactions. Testing megadose antioxidant vitamins without knowing how they affect redox reactions in the body is like a blind man turning on the lights when entering a room. How can any results truly reflect the situation. The fact that you may not have read about this topic on you favorite health website is more a reflection on what little science knows about this topic rather than its credibility.

WHY IS SCIENCE ABSENT ON THIS VITAL ISSUE

This topic is still relatively new. Science doesn't yet have a clue where the balance point is between free radical generation and vitamin antioxidant load. Partly, this could be due to the adaptability of the body to control reactions between moderate level differences, or those generated just from food sources. The truth is that there is most likely a point at which taking extra of some antioxidant vitamins overwhelms body adaptability and detrimental effects start. It would be valuable to know this point, one that will of course be different between subsets of the public.

ONE STUDY REVEALS EVIDENCE 

The SELECT study looking into Vitamin E and Selenium on Prostate health found that selenium at the tested level of 200 mcg slightly increased the diabetes risk. How? One possible theory: Selenium forms a cellular antioxidant that attacks and destroys a certain free radical before it can perform a necessary body function. In this case, the radical facilitates in switching on the uptake of insulin with glucose by cells. ref  ref  ref

The Vitamin E form used in this study is only one of 4 tocopherols found in natural foods. Testing just the alpha form most likely upset cellular balance by suppressing the levels of the other needed vitamin E forms, especially gamma which protects the prostate cell membranes against a certain type of radical that the alpha form doesn't effect. There are two types of radicals, either oxygen or nitrogen based. Without knowledge of these facts, the $114 million dollar SELECT study was sure to fail, which it did. OR, is the result really a positive one for showing the balance point for selenium and that using just one fraction of nature's vitamin E family as alpha tocopherol by itself may have limitations? ref

SIDEBAR: Just the alpha tocopherol from of vitamn E is tested in most research for heart disease. A researcher wanting to see if vitamin E as alpha tocopherol was lower in heart disease patients amazingly found levels were not different from those in healthy people. And he also discovered that another of the four tocopherols, gamma, was lower. If the alpha levels are nearly the same, why would one assume that taking extra would help? Won't it be wiser to add the gamma form as well?

SIDEBAR: Another vitamin E antioxidant overkill story comes out of breast cancer studies. It has long been debated whether vitamin E is beneficial for breast cancer. Observational research shows advantages to those eating foods with higher vitamin E, but supplement E does not always show benefits, although the antioxidant theory says it should. Here is a possible reason. Alpha Linolenic acid (Flax Oil) and Gamma Linolenic Acid (Evening Primrose, contain omega 3 fats that have antitumor effects through a lipid peroxidation process.  When these oils are added to test tubes with breast cancer cells, the cancer cells die at an increased rate from a process of membrane interruption. When Vitamin E is added to the test tube, this die off process stops by virtue of its antioxidant protection. Of note here is that other vitamin E family members other than alpha tocopherol appear to have stronger anti-cancer cell effects without the same level of antioxdiant activity. -end 

Another beneficial radical is created by the immune system white blood cells to help kill invading viruses. A study discovered that seniors who took vitamins had colds that lasted longer than the seniors not on vitamins. The antioxidant vitamins too quickly neutralized the "good" radicals before they could get to and kill the viruses. This allows the viruses to multiply and the colds lasted longer.

Not many vitamin company formulators of wellness products are aware of this fact. Education in this area will be slow to become public knowledge due to the current mechanics of information sharing. The government has limited information channels and the vitamin industry won't be in a hurry to put out this type of advice. Mass media will just sensationalize it and the public will be left with a skewed view of exactly how to maximize benefits from vitamin antioxidants without crossing the overkill line. Thus until a better informational system is in place, enter RightWay's vitamin criteria.

The Following studies point out the relationships of antioxidant loads to beneficial functions:

Cell Death and Differentiation (2005) 12, 1259–1262. doi:10.1038/sj.cdd.4401694; published online 10 June 2005

NF-kappaB meets ROS: an 'iron-ic' encounter

S Papa1, C Bubici1, C G Pham1, F Zazzeroni1,2 and G Franzoso1

1The Ben May Institute for Cancer Research, The University of Chicago, 924 East 57th Street, Chicago, IL 60637, USA

Correspondence: G Franzoso, The Ben May Institute for Cancer Research, The University of Chicago, 924 East 57th Street, Chicago, IL 60637, USA. Tel: +773 834 0020; Fax: +773 702 1576; E-mail: gfranzos@midway.uchicago.edu

2Current address: Department of Experimental Medicine, The University of L'Aquila, Via Vetoio-Coppito 2, 67100 L'Aquila, Italy

"Since becoming abundant in the atmosphere approximately 2.3 billion years ago, oxygen has been a defining element for life on our planet. One needs not be a biologist to know the importance of oxygen for sustaining life – termed in fact 'aerobic' life. Our body is built around the need to maximize exploitation of oxygen for the production of energy. The respiratory and cardiovascular systems are exemplary illustrations of this need. Like all good things, however, oxygen can also be extremely harmful. Its original accumulation on Earth caused the extinction of most existing life forms, defenseless against oxidative damage. Even a layperson is aware of this potential toxicity of oxygen. Indeed, nowadays antioxidants are among the most heavily advertised dietary supplements on the market. Yet, it would surprise most to know that the potent reactivity of oxygen and its products – so-called reactive oxygen species (ROS) – is purposefully used by nature to transduce signals that actively trigger cell suicide or programmed cell death (PCD), as well as other biological responses.

One pathway that seems to fully exploit this reactivity of ROS for inflicting cell death is that initiated by TNFalpha engagement of TNF-R1, a pathway that plays a central role in immunity, inflammation, cell growth, cell death and differentiation.1, 2, 3 This pathway is also crucial for pathogenesis of human diseases such as cancer and chronic inflammatory conditions, including rheumatoid arthritis (RA) and inflammatory bowel disease (IBD).1, 3, 4 Not surprisingly, it has been the subject of intense investigation for over one century.1 TNFalpha-induced killing is antagonized by activation of NF-kappaB-family transcription factors3, 4 – which act as master coordinators of immune and inflammatory responses.4 The prosurvival activity of NF-kappaB is also crucial for lymphocyte development, tumorigenesis and cancer chemoresistance.4, 5 In recent years, remarkable progress has been made in our understanding of the mechanisms governing TNFalpha-induced death and NF-kappaB-mediated survival.3, 4 As it turns out, ROS have now taken center stage in the intricate multitude of players that control cell fate downstream of TNF-R1, as they appear to be at an obligatory crossroads of the opposing pathways for life and death elicited by stimulation of this receptor. Indeed, now there is hope that this new understanding of TNF-R-induced pathways may lead to the development of new approaches for treatment of widespread human diseases."  

Antioxidants Blunt Exercise Benefit     May 11, 2009

...Vitamins C & E block creation of free radicals that promote insulin sensitivity according to researchers...


MONDAY, May 11 (HealthDay News) -- "Exercise helps increase insulin sensitivity and ward off diabetes, but taking supplemental antioxidants such as vitamins C and E actually blunts that benefit, researchers report.

Exercise helps increase the body's sensitivity to insulin by making reactive oxygen species, or "free radicals," which antioxidants work against. These free radicals are thought to damage cells and speed the aging process, but they are also used by the body to prevent cell damage after exercising, the researchers say.

"When you exercise you do improve your insulin sensitivity, and if you are at risk for diabetes improving insulin sensitivity is good," said researcher Dr. C. Ronald Kahn, the Mary K. Iacocca Professor at the Joslin Diabetes Center and Harvard Medical School.

Part of the reason that exercise improves insulin sensitivity is that it causes oxidative stress on the muscles. The muscles respond to this stress by creating free radicals, Kahn said.

"If you take antioxidants like vitamins C 1000 mg and E 400 I.U., you block the oxidative stress response, but you also block the beneficial effects of exercise on insulin sensitivity," he said.

The report is published in this week's online edition of the Proceedings of the National Academy of Sciences.

For the study, Kahn's team looked at the benefit of exercise in increasing insulin resistance in 39 young men, roughly half of whom were taking supplemental vitamins C and E.

Kahn's group found that men taking vitamin supplements had no change in their insulin resistance, but men not taking vitamins had an increase in free radicals, which increases insulin resistance. A month after stopping the vitamin supplements insulin sensitivity was restored, the researchers noted.

"If you are exercising, in part, to reduce diabetes risk, you shouldn't take vitamin C and E, because you are going to block some of the beneficial effect of the exercise to prevent the diabetes," Kahn said.

Dr. David L. Katz, director of the Prevention Research Center at Yale University School of Medicine, thinks this study raises doubts about the benefits of taking antioxidant supplements, but not about the value of these vitamins in the foods people eat.

"We have long held out hope that antioxidant supplements, among them vitamin C, vitamin E, beta carotene, and more recently lycopene and others, would help prevent diseases from the common cold to cancer, heart disease to diabetes," Katz said. "But to date, virtually all of the best research evidence is contrary to this hope."

This study has a counter-intuitive conclusion, namely that antioxidant supplements may actually interfere with the beneficial effects of exercise on insulin sensitivity, Katz said.

"This is a small and short-term study, and thus cannot tell us definitively that antioxidant supplements are harmful in diabetes or the insulin-resistant state that often precedes it. But that is precisely what the study suggests may be true," Katz said.

For now, there is substantial uncertainty about any health benefits and the potential harms of antioxidants as supplements, Katz said. "But we have no such confusion about the powerful health-promoting effects of wholesome, mostly plant-based diets and regular physical activity."

If this study was the only one to observe these facts, that would not carry much weight. But since the SELECT study was halted due to slight increases in diabetes rates in the selenium group, and animal studies have verified the antioxidant mechanism involved, enough is available to use the precautionary principle until further research settles this issue.

This is a very small study and one has to be careful how these results are interpreted. Here is one scientist's review. Note that he is associated with a vitamin company.

Vitamin-exercise study questioned

By Stephen Daniells, 12-May-2009

Reports that vitamins C and E may blunt the positive effects of exercise are misleading, according to an antioxidant expert.

German researchers have reported that antioxidant vitamins C and E may blunt the positive effects of exercise, with respect to insulin sensitivity. Findings were published in the Proceedings of the National Academy of Sciences.

Reacting to the study , Alexander Schauss, PhD, from AIBMR Life Sciences, a nutraceutical products consultancy, told NutraIngredients.com that the title of the study (Antioxidants prevent health-promoting effects of physical exercise in humans) was misleading.

 “The primary objective of this study was to study the effect of a 4-week intensive 5-days a week exercise program on insulin sensitivity. Yet the title of the paper leads one to believe otherwise,” he said.

 “This is a small gender-biased study of 40 male subjects, 25 to 35 years of age. When I read through the study for the first time I had to wonder how could the authors have come up with such a title for their paper?” he asked.

In addition to questioning the study design, particularly with respect to assigned both trained and untrained people to an intensive exercise programme of underwent 85 minutes of exercise five days per week for four weeks, Dr Schauss also questioned the conclusions drawn from the data.

 “Skeletal muscle biopsies were obtained from the right vastus lateralis muscle of study subjects. But some of the data is missing for a number of subjects, and reported as such by the authors,” said Dr Schauss.

 The authors noted that biopsies for the ‘early’ time-point were only obtained from five people in the vitamin group, and four in the placebo group. “Yet the authors conclude a “strong induction of PGCl-alpha, PGCl-beta, and PPAR-gamma expression in skeletal muscle following 4 weeks of exercise training in previously untrained, antioxidant naïve individuals” and “markedly reduced exercise-related induction” in those taking antioxidants, based on these limited number of biopsies,” said Dr Schauss.

 

“Would it not have made more sense to appropriately increase the intensity and duration of exercise slowly and then see if the subject’s bodies didn’t accommodate handling of ROS without a significant change in induction of these markers?” he said.

 The study reflects a ‘transient’ increase in ROS during ‘limited periods of physical exercise only’, noted Dr Schauss, “whereas the bulk of the literature, including that in non-primate models have not observed these concerns obtained in models of ‘continuous exposure to increased levels of ROS’”, he said.

Dr Schauss also noted that the authors presented no evidence of adverse effects by any of the individuals from vitamin C and E supplementation.

 

British Nutrition Foundation comment

Adding to the debate, Dr Elizabeth Weichselbaum, nutrition scientist from the British Nutrition Foundation, said: “This study shows that just because something is good for you, it does not mean that more of it is better! Vitamins C and E are antioxidants naturally occurring in many foods, mainly fruits and vegetables (vitamin C), and vegetable oils (vitamin E).

NOW the delimma surfaces: First, if you take too many antioxidants, they might stop benefical free radicals from switching on glucose/ insulin uptake. Then, blood sugar levesls increase which damage tissues. High amounts of antioxdiants are protective against this damage. The following research shows that low levels of antioxidants are often associated in diabetes.:

From: Duke University Medical Center

Antioxidants May Reduce Harmful Complications Of Diabetes

SAN FRANCISCO -- Duke University Medical Center researchers have found that the depletion of body chemicals called antioxidants may increase the risk of complications from the most common form of diabetes.

The scientists recommend that diabetics take antioxidant supplements, such as vitamin C or E, to help stave off or even forestall the hallmark complications of diabetes, including blindness, kidney failure, amputation and even death.

Antioxidants neutralize oxygen "free radicals," highly reactive chemicals that are the potentially destructive byproducts of the body's process of turning food into energy. Normally, the body produces enough antioxidants of its own to keep the reactive oxygen from causing damage.

"We were able to show that patients with poor control of their diabetes who were beginning to show signs of complications had depleted their store of antioxidants," said Duke researcher Dr. Emmanuel Opara in an interview. "Further, we found a significant correlation between high blood-sugar levels and depletion of antioxidants.

"It appears that this depletion is a major risk factor for developing complications, and that antioxidant supplements could lower this risk," he concluded.

Opara prepared the results of his studies for presentation Sunday (April 19) at Experimental Biology `98, the annual scientific meeting of the Federation of American Societies for Experimental Biology (FASEB).

The researchers studied 50 similar people with Type II diabetes -- also known as non-insulin-dependent or adult-onset diabetes. In this form of the disease, insulin produced in the body is unable to trigger the lowering of high blood sugar. Type II diabetes afflicts about 90 percent of the estimated 10.7 million Americans diagnosed with the disease and the 5.4 million believed to have undiagnosed cases, according to the Centers for Disease Control and Prevention.

Insulin is the hormone that normally regulates the level of sugar (glucose) in the blood and is produced by cells in the pancreas. Insulin is secreted when the level of blood glucose rises -- as after a meal.

All diabetic patients in the study were taking only drugs referred to as sulfonylureas, which increase the sensitivity of receptors to insulin throughout the body. Half the patients exhibited microalbuminuria, the excretion of tiny amounts of protein in the urine that is considered a precursor of kidney disease, while the other half did not.

The researchers took blood samples from all 50 patients, as well as a control group of 20 similar people without diabetes, and determined levels of antioxidants in their blood.

"We found that the non-diabetics' ability to defend against damage from the oxygen free radicals was almost twice that of those patients exhibiting microalbuminuria," Opara explained. "And while the difference between the two diabetic groups was not as pronounced, the difference was still statistically significant. Also, antioxidant depletion correlated with high blood sugar after meals only in the group with microalbuminuria."

The researchers determined antioxidant levels by a new chemical assay developed at King's College in England that enabled them to measure all known antioxidants in the blood and to obtain a more global picture of the body's total antioxidant capacity, Opara said. Other assays are only specific for individual antioxidants.

Using the newly developed assay, the scientists rated the ability of the non-diabetics to defend against free radical damage at 2.7, compared with 1.4 for those with microalbuminuria and 1.7 for the diabetics without microalbuminuria.

Though the exact mechanism of action of the oxygen free radicals is not yet clear, these findings confirm in humans earlier animal studies of the chemicals' role in damage in diabetes, Opara said. Previous Duke studies by Opara have shown that vitamin E can delay the development of diabetes in obese rats with Type II diabetes, and that the depletion of the antioxidant glutathione caused diabetes in another rat model.

"The results we've been seeing in our animal studies are now being borne out in humans,' Opara said. "I recommend that since the body has many antioxidants, diabetics should take a number of these agents, including vitamins C and E, and N-acetylcysteine."

The diabetic patients involved in the current study come from Eygpt, and their samples were brought to Duke by E. Abdel-Rahman, one of Opara's collaborators.

Joining Opara in the study, which was partly funded by the Duke department of surgery, were, from Duke, Dr. Somaya Soloma, Dr. James Lowe, and Dr. Salah Abdel-Aleem.

 

More information

For more information on antioxidants, visit the U.S. National Library of Medicine.

 

Until science is aware of and incorporates these parameters for supplemental antioxidants into research, results will continue to be faulty and not fully applicable to current nutritional and health realities.