MuscleBlog » Base científica que sustenta el artículo sobre los mitos del culturismo.


Base científica que sustenta el artículo sobre los mitos del culturismo.9.4105 large_red-pill-or-blue-pill-5936894

Al hilo del artículo controvertido 5 grandes mentiras de la industria de los suplementos, aquí os traigo las conclusiones de unos cuantos ensayos clínicos y revisiones. El 90% son investigaciones posteriores a 2006. Solo te prometo la verdad Neo. Tu eliges.



Anti-oxidants, controversies and perspectives: How can the failure of clinical studies using anti-oxidants be explained?

First of all, definitions should be reviewed, such as that of free radicals (FR); all of them are not toxic. Some of them, such as nitric oxide, are necessary for the proper physiological functioning of the body, and eliminating them would be a mistake!

Antioxidants do not prevent postexercise peroxidation and may delay muscle recovery.

AOX supplementation does not offer protection against exercise-induced lipid peroxidation and inflammation and may hinder the recovery of muscle damage.

Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases.

Vitamin A, beta-carotene, and vitamin E may increase mortality. Future randomised trials could evaluate the potential effects of vitamin C and selenium for primary and secondary prevention. Such trials should be closely monitored for potential harmful effects. Antioxidant supplements need to be considered medicinal products and should undergo sufficient evaluation before marketing.

Antioxidants: not for prevention.

In spite of substantial evaluation, the preventive effect of antioxidants remains hypothetical. Some antioxidants have been associated with higher mortality rates.

Can antioxidants prevent atherosclerosis?

Most of the placebo-controlled studies for primary or secondary prevention failed to show a protective effect even after administration of high doses. In addition, other studies demonstrated a risk for adverse effects due to antioxidant supplementation (beta-carotene and vitamin E).The obtained results suggest that supplementation of antioxidants cannot be recommended for the normal population.

The Antioxidant Paradox in Diabetes Mellitus.

The divide between the robust experimental evidence of the pathogenetic role of increased oxidative load in diabetes and the overwhelming failure of antioxidants to show any health benefits in clinical trials may well be characterized as the «antioxidant paradox».


Ascorbic acid increases the severity of spontaneous knee osteoarthritis in a guinea pig model.

Ascorbic acid worsened the severity of spontaneous OA. This worsening of OA with ascorbic acid supplementation suggests that ascorbic acid intake should not be supplemented above the currently recommended dietary allowance (90 mg/day for men and 75 mg/day for women).

Multivitamin supplementation of Wistar rats during pregnancy accelerates the development of obesity in offspring fed an obesogenic diet.

High multivitamin intake during pregnancy increases the phenotypic expression of obesity and components of the metabolic syndrome in both female and male rats fed an obesogenic diet

British Medical Journal: Vitamin E supplementation and cardiovascular events in high risk patients

According to the authors, this study did not demonstrate any significant reduction in the incidence of cardiovascular events by the administration of 400 units of vitamin E for four to six years. They describe and comment on the results of four randomized clinical trials of vitamin E:

A chinese trial that randomized patients to a combination of vitamin E, beta carotene and selenium or placebo. This trial showed a 9 percent decrease in all-cause mortality, but no decrease in cardiovascular events. The effect of vitamin E could not be separated out, and the nutritional status of the population is different from that in the population studied here.

The ABC trial (Alpha- Tocopherol, Beta Carotene Cancer Prevention) studied over 29,000 male smokers between the ages of 50 and 70. Fifty mg of vitamin E daily showed no significant beneficial effect on cardiovascular events.

The Cambridge Heart Antioxidant Study assigned patients with coronary disease to vitamin E (400 IU or 800 IU) or placebo. There was a significant decrease in the number of nonfatal MI’s, but not in cardiovascular mortality. The numbers were small, the effects were seen too quickly to be easily attributable to the antioxidant properties of vitamin E and there were imbalances in the study groups.

An Italian study randomized 11,000 post-MI patients to 300 IU vitamin E or placebo; there was no statistically significant effect on cardiovascular events.

American Heart Association: Antioxidant Vitamin Supplements and Cardiovascular Disease

Clinical trials have failed to demonstrate a beneficial effect of antioxidant supplements on CVD morbidity and mortality. With regard to the meta-analysis, the lack of efficacy was demonstrated consistently for different doses

Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance.

Vitamin C supplementation decreases training efficiency because it prevents some cellular adaptations to exercise.

Short-term vitamin A supplementation at therapeutic doses induces a pro-oxidative state in the hepatic environment and facilitates calcium-ion-induced oxidative stress in rat liver mitochondria independently from permeability transition pore formation.

We show here that mitochondria are a target of vitamin-A-associated toxicity also in vivo

Pro-oxidant effect of α-tocopherol in patients with Type 2 Diabetes after an oral glucose tolerance test – a randomised controlled trial

There was a significant increase in oxidative DNA damage in the α-tocopherol treatment group

High dose supplementation with α-tocopherol primes mononuclear cells from patients with type 2 diabetes for a potentially damaging response to acute hyperglycaemia

Ascorbic acid as a prooxidant:

Pro-oxidant effects of AA and BH(4) can enhance the EDHF phenomenon by generating H(2)O(2), which has previously been shown to amplify electrotonic hyperpolarization-mediated relaxation by facilitating Ca(2+) release from endothelial stores.

Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality.

High dosage Vitamin E supplements (>or = 400IU/d) may increase all cause mortality and should be avoided.

Supplementation with vitamin C and N-acetyl-cysteine increases oxidative stress in humans after an acute muscle injury induced by eccentric exercise.

The subjects receiving vitamin C and NAC had higher levels of lipid hydroperoxides and 8-Iso-PGF2α 2 d after the exercise. This acute human inflammatory model strongly suggests that vitamin C and NAC supplementation immediately post-injury, transiently increases tissue damage and oxidative stress.

Does vitamin C act as a pro-oxidant under physiological conditions?

The Linus Pauling Institute and the Department of Biochemistry and Biophysics, Oregon State University, Corvallis, Oregon 97331, USA

The interaction of vitamin C with `free’, catalytically active metal ions could contribute to oxidative damage through the production of hydroxyl and alkoxyl radicals; whether these mechanisms occur in vivo, however, is uncertain.The data on vitamin C and DNA oxidation in vivo are inconsistent and conflicting.

Scientists expose vitamin C’s pro-oxidant alter ego (The Guardian, 3 nov-09)

If the health foods and supplements industry is to be believed, antioxidants are the panacea of modern times. Vitamin C reacts with dissolved oxygen to generate hydrogen peroxide, a potentially harmful ROS. Reactive oxygen species get a lot of bad press, and it’s true that if we have too many of them in our cells, they can do a lot of damage. But we’re increasingly finding out that they can also have important physiological functions in healthy individuals. Oxidative stress can also cause arteries to constrict by destroying nitric oxide. So future therapies might have to strike a balance between promoting and suppressing oxidativestress.

Pharmacologic doses of ascorbate act as a prooxidant 

Ascorbic acid is an essential nutrient commonly regarded as an antioxidant. In this study, we showed that ascorbate at pharmacologic concentrations was a prooxidant, generating hydrogen-peroxide-dependent cytotoxicity toward a variety of cancer cells in vitro without adversely affecting normal cells.

Vitamin E, vitamin C, beta carotene, and cognitive function among women with or at risk of cardiovascular disease: The Women’s Antioxidant and Cardiovascular Study.

Antioxidant supplementation did not slow cognitive change among women with preexisting cardiovascular disease or cardiovascular disease risk factors. A possible late effect of vitamin C or beta carotene among those with low dietary intake on cognition warrants further study.

Acute and chronic vitamin A supplementation at therapeutic doses induces oxidative stress in submitochondrial particles isolated from cerebral cortex and cerebellum of adult rats.

Vitamin A could be toxic at the sub cellular level, inducing mitochondrial dysfunction and altering cerebral cortex and/or cerebellum-dependent behavior.

Therapeutic vitamin A doses increase the levels of markers of oxidative insult in substantia nigra and decrease locomotory and exploratory activity in rats after acute and chronic supplementation.

Vitamin A supplementation is prooxidant to the rat substantia nigra and effective in altering behavior.

Vitamins C and E and beta carotene supplementation and cancer risk: a randomized controlled trial.

Duration and combined use of the three antioxidants also had no effect on cancer incidence and cancer death. CONCLUSIONS: Supplementation with vitamin C, vitamin E, or beta carotene offers no overall benefits in the primary prevention of total cancer incidence or cancer mortality.

Beta-carotene supplementation and incidence of cancer and cardiovascular disease: the Women’s Health Study.

Among apparently healthy women, there was no benefit or harm from beta-carotene supplementation for a limited period on the incidence of cancer and of cardiovascular disease.

Prooxidant effects of beta-carotene in cultured cells.

A possible mechanism which can explain the dual role of beta-carotene as both a beneficial and a harmful agent in cancer as well as in other chronic diseases is its ability in modulating intracellular redox status. beta-Carotene may serve as an antioxidant or as a prooxidant, depending on its intrinsic properties as well as on the redox potential of the biological environment in which it acts. This review summarizes the available evidence for a prooxidant activity of beta-carotene in cultured cells, focusing on biochemical and molecular markers of oxidative stress, which have been reported to be enhanced by the carotenoid.

Beta-carotene breakdown products may impair mitochondrial functions–potential side effects of high-dose beta-carotene supplementation.

We are striving for safe conditions of carotenoid supplementation in order to protect patients in need of this kind of medical treatment from possible side effects, such as unwanted prooxidative reactions.

Results provide strong evidence that beta-carotene breakdown products are responsible for the occurrence of carcinogenic effects found in the Alpha-Tocopherol Beta-carotene-Cancer prevention (ATBC) study and the beta-CArotene and RETinol Efficacy (CARET) Trial.


Prolonged intake of coenzyme Q10 impairs cognitive functions in mice.

These findings do not support the notion that CoQ(10) is a fitness-enhancing or an «antiaging» substance under normal physiological conditions


Pro-oxidant actions of alpha-lipoic acid and dihydrolipoic acid.

Aside from its antioxidant role, in vitro and in vivo studies suggest that LA and its reduced form DHLA also act as a pro-oxidant properties. The ability of LA and/or DHLA to function as either anti- or pro-oxidants, at least in part, is determined by the type of oxidant stress and the physiological circumstances In further studies, careful evaluation will be necessary for the decision in the biological system whether LA administration is beneficial or harmful.


Prooxidant and cytotoxic action of N-acetylcysteine and glutathione in combinations with vitamin B12b

Prooxidant and cytotoxic effects of thiols N-acetylcysteine (NAC) and glutathione (GSH) were studied in combinations with vitamin B12b It was established that the prooxidant action of NAC (or GSH) combined with B12b, i.e., generation and accumulation of hydrogen peroxide in culture medium, led to intractellular oxidative stress and cell redox imbalance.

Antioxidant and pro-oxidant effect of the thiolic compounds N-acetyl-L-cysteine and glutathione against free radical-induced lipid peroxidation.

Nevertheless, the interaction of thiols with reactive radicals can generate thiyl radicals, which, in turn, may impart a pro-oxidant function (…) antioxidant and pro-oxidant effects of both NAC and GSH and enhanced production of hydroxyl radicals by NAC and GSH.

S-Nitrosothiols signal hypoxia-mimetic vascular pathology

We used the pharmaceutical antioxidant N-acetylcysteine (NAC) as a bait reactant to measure NO transfer reactions in blood and to study the vascular effects of these reactions in vivo. NAC was converted to S-nitroso-N-acetylcysteine (SNOAC), decreasing erythrocytic S-nitrosothiol content, both during wholeblood deoxygenation ex vivo and during a 3-week protocol in which mice received high-dose NAC in vivo. Strikingly, the NAC-treated mice developed pulmonary arterial hypertension (PAH)


The quercetin paradox

The quercetin paradox is that in the process of offering protection, quercetin is converted into a potential toxic product.  Apparently, the potential toxicity of metabolites formed during the actual antioxidant activity of free radical scavengers should be considered in antioxidant supplementation.

Green tea (Camellia sinensis) for the prevention of cancer.

There is insufficient and conflicting evidence to give any firm recommendations regarding green tea consumption for cancer prevention.

Ginkgo biloba is not a smart drug: an updated systematic review of randomised clinical trials testing the nootropic effects of G. biloba extracts in healthy people.

We have found no convincing evidence from randomised clinical trials for a robust positive effect of G. biloba ingestion upon any aspect of cognitive function in healthy young people, after either acute or longer term administration.

Prooxidative effects of green tea polyphenol (-)-epigallocatethin-3-gallate on the HIT-T15 pancreatic beta cell line.

Increasing evidence indicates that EGCG produces reactive oxygen species (ROS) and subsequent cell death.  EGCG did not scavenge exogenous H(2)O(2), but rather, it synergistically increased H(2)O(2)-induced oxidative cell damage in pancreatic beta cells. Together, these findings suggest that in the HIT-T15 pancreatic beta cell line, EGCG mediated the generation of H(2)O(2), triggering Fe(II)-dependent formation of a highly toxic radical that in turn induced oxidative cell damage.

Soy diet worsens heart disease in mice.

We report that dietary modification from a soy-based diet to a casein-based diet radically improves disease indicators and cardiac function in a transgenic mouse model of hypertrophic cardiomyopathy.


The combination of vitamin C and grape-seed polyphenols increases blood pressure: a randomized, double-blind, placebo-controlled trial.

Although the mechanism remains to be elucidated, these results suggest caution for hypertensive subjects taking supplements containing combinations of vitamin C and polyphenols.

Fulminant hepatitis during self-medication with hydroalcoholic extract of green tea.

Despite an ancient reputation for potential phytotherapeutic effects and innocuity, traditional herbal medicine has previously been implicated in severe adverse events. In this study, we report a case of fulminant hepatitis during self-medication with Exolise, requiring liver transplantation


1) No es verdad que los suplementos antioxidantes actúen biológicamente como antioxidantes.

2) La acción estrictamente química antioxidante de una sustancia in vitro no tiene nada que ver con su efecto biológico.

3) No es verdad que los radicales libres sean necesariamente malos.

4) No es verdad que un efecto prooxidante sea malo. El organismo utiliza esa capacidad citotóxica funcionalmente para combatir ciertas patologías o como señalización para ciertos procesos biológicos básicos que son indispensables.

5) No es verdad que un efecto antioxidante sea necesariamente bueno. El antioxidante puede generar un metabolito más tóxico que la reacción oxidativa que se pretendió detener.

6) La alteración o inhibición crónica de esta señalización prooxidante y antioxidante a través de los suplementos tiene consecuencias imprevisibles. Estás impidiendo gran parte de comunicación celular que no es nociva y es fundamental para el correcto funcionamiento del organismo.

7) No existe ni un solo estudio que muestre que aquellos que toman vitaminas vivan más o enfermen menos, excepto en poblaciones muy pobres y desnutridas que presentan déficit alimenticio.

8.) El deporte protege contra la oxidación celular, no es verdad que los radicales libres generados sean dañinos en conjunto, ni es verdad que un deportista necesite más antioxidantes que una persona sedentaria, y mucho menos que un suplemento antioxidante añada una mayor protección celular.

9) La supresión de la señalización celular con suplementos puede retrasar el desarrollo muscular.

10) Aunque un suplemento tenga un efecto antioxidante, puede provocar otras consecuencias sistémicas más graves: por ejemplo en ratones solo 3 semanas de suplementación con N acetil cisteina bastó para provocar hipertensión pulmonar, patología muy grave que provoca disfunción en el ventrículo derecho del corazón y puede derivar en insuficiencia cardíaca. Desconocemos estas consecuencias, y no se sabe si los beneficios superan los riesgos. No se sabrá hasta dentro de muchas décadas, mediante estudios de cohortes retrospectivos.

11) En conclusión, no existe una base científica para elegir un antioxidante, y desechar otro.