Tara

I was involved in a discussion with an elite runner on the topic of whether it's necessary to eat fruits and vegetable or if one can instead obtain all needed nutrition from eating a diet void of fruits and vegetables and supplementing with vitamins.

The importance of fruits and vegetables is certainly preached everywhere, but I cannot actually think of a reason why vitamin supplements cannot replace fruits and vegetables in the diet. The only issue I can think of that may present a problem is the lack of fiber contained in such a diet.

I can see why it would not be in some people's best interest to exclude fruits and vegetables from their diet because they may gain weight by substituting more calorie dense foods in place of less caloroc veggies and fruit, but consider an athlete who must eat 4000 calories a day and actually has difficulty meeting such high caloric needs.

The following was written by such an athlete:

"The nutritional value of vegetables is way over rated. Show me a vegetable that has more than 1 or 2 different vitamins in it (all that are easily obtained from pills). I still don't understand the concept of an empty calorie since calories are the only reason why we eat - protein to build muscle and carbs for fuel. Vitamins are much easier to get in pill form than by eating 10 different vegetables a day (since each only has 1 or 2 vitamins) in sufficient quantities to supply them - I would whither away.

I suspect that for some people, who are averse to getting their vitamins from pills, it is more an ideological than sound nutritional objection - they simply don't like the idea that people can get by with "bad" behavior without suffering consequences. I get regular blood tests and I am deficient in no vitamins (most were through the roof). "

So why exactly do we need to eat fruits and vegetables when we can obtain the same nutrients from popping a multi-vitamin? Maybe I should first ask, can we obtain all of the same nutrients from supplements?

nogods4me

Calories are the only reason we eat?

We eat because we are hungry. we need the vitamins and the fiber and the sugars and the carbs. Sure one could substitute for these. Heck eventually we may all be able to subsist on some tasteless, shapeless mush, or by taking a couple of pills. But count me out, Id rather have the steamed broccolli or the peach, the spinach salad, a banana or plum.

Godot

I'll answer your two questions backwards.
Of those we know about, yes. Is it a good idea? No.
In a single word: antioxidants.
Many of the known antioxidants are available as part of a multi-vitamin. However, there exists phytochemical cofactors in foods that enhance the action of antioxidants. I'll pimp myself out by posting part of a paper I wrote which discussed the differences between using food and pill sources of antioxidants (apologies if the formatting is a bit rough on the eyes):
Pills vs. Food Sources
A consistent methodology has not been used across studies attempting to measure similar variables; some use antioxidant supplements, others modify the diet to include rich antioxidant food sources. Due to the aforementioned phytochemical cofactors present in food that act to enhance the effect of antioxidants, the outcome of a study can vary dramatically; an effect not taken into account in the methodologies of many studies.
Pill Supplements
Dawson et al (2002) and Schröder et al (1999) both attempted to measure changes in oxidative stress as a result of antioxidant supplementation (in pill form). Each of these studies endeavours to measure the cumulative effects of a multiple antioxidant supplement; most studies in this area have tended to look at antioxidants individually, without taking into consideration potential interactions between these substances. No mention in either study was made whether the supplements used were synthetic or not: the different forms exhibit different absorbance patterns, and therefore are likely to vary in effect (Clarkson and Thompson, 1999). The participants in these studies were advised against consuming any additional supplements for the duration of the study, but no controls or protocols were established to account for the antioxidants obtained from dietary sources.
Schröder et al (1999) made an effort to incorporate diet into the design via a 24-hour recall questionnaire, but this tool was only used an additional measurement device. They neglected to include a protocol for a “washout” period at the onset of the study to allow for the changes in behaviour/intake to be validly considered real. The single blind design also allows for investigator bias. Their results indicate that the mean average intakes for each of the measured antioxidants were higher in the placebo group than in the supplemented group, yet they somehow manage to conclude a positive significance for antioxidant supplementation in athletes. Clearly, some bias is present.
Unlike Schröder et al (1999), Dawson et al (2002) did include a “washout” period at the onset of the study to normalise the starting conditions of the subjects, in addition to another “washout” at the crossover. Interestingly, this study attempted to measure both the effectiveness of antioxidant supplementation to reduce oxidative stress and if this relationship was dose-dependant. In this study, both direct (muscle biopsy) and indirect (blood analysis) measures of oxidative damage biomarkers were taken. As no significant differences in circulating antioxidant levels were evidenced between the high and low supplemented groups, the data were pooled together to increase the statistical significance of the observation. Despite this attempt to increase the power of the observation, no statistically significant differences in oxidative damage were measured between the supplemented and non-supplemented groups.
Itoh, Ohkuwa, Yamazaki, Shimoda, Wakayama, Tamura, Yamamoto, Sato, and Miyamura (2000) looked at the ability of vitamin E to reduce oxidative damage. They used indirect measures of serum enzymes to determine the extent of tissue oxidation damage, and a double-blind format helped to eliminate investigator bias. However, as with Dawson et al (2000), no controls or protocols were established to account for the antioxidants obtained from dietary sources.
Serum vitamin E levels were increased by supplementation, and the oxidative enzymes measured were significantly reduced after training in the supplemented group compared to the placebo group. The strength of the observations made is reduced since the measures are of an indirect nature; the results are likely due to the theorised reasons, but cannot be confirmed with any degree of certainty.
Food Sources
Van den Berg, van Vliet, Broekmans, Cnubben, Vaes, Roza, Haenen, Bast, and van den Berg (2001) attempted to measure the effects of a high fruit and vegetable diet on antioxidant status and on biomarkers of oxidative damage in smokers. Akin to the extremely active, smokers are exposed to a greater deal of oxidative stress and free radical damage resulting from their lifestyle habit. The investigators employed a single crossover design, including a “washout” period to ensure distinct results for each phase. Their methodology called for the substitution of a regular meal with a known test product manufactured from high-antioxidant sources. Unfortunately, the test product contained antioxidants in lesser quantities than expected and no significant differences in antioxidant status were visible between treatment groups. As a result, no measurable changes were evidenced in the biomarkers of oxidative stress. The researchers did not conclude that antioxidant supplementation was ineffective; the problem was that their study was too limited and small to determine if the differences between groups could be statistically “real.”
Other studies (Aviram, Dornfeld, Rosenblat, Volkova, Kaplan, Coleman, Hayek, Presser, and Fuhrman, 2000; Porrini and Riso, 2000) have shown positive associations between antioxidant intakes from food sources and reductions in oxidative stress.
Aviram et al (2000) examined the effects of pomegranate juice consumption on a number of variables in both men and mice, in both in vitro and in vivo. Although experimental conditions and measures differed for each study group, the consumption of pomegranate juice resulted in favourable changes in levels of oxidative stress for both mice and men. No alterations to usual diet were made for this study; subjects merely had to add the pomegranate juice mixture to their regular intake. It would appear as though the investigators assumed that the role of usual dietary intake in determining antioxidant status was negligible, and therefore not worthy of building into the study design. Additionally, the human component of this study was of extremely limited duration (two weeks) and used a fairly small cohort (13 subjects). Given the narrow window afforded by this investigation, further studies in this area using a larger cohort and of greater duration would be useful.
Porrini and Riso (2000) investigated whether dietary supplementation with tomato puree would increase serum carotenoid concentrations and reduced susceptibility to oxidative stress in an adult female population. This study accounted for dietary antioxidant sources outside of the study parameters; subjects were directed to limit carotenoid intake as well as avoiding consuming lycopene rich foods, with dietary compliance being monitored by a dietician. Clearly, such a protocol will reduce the likelihood of the experimental results being skewed or rendered inaccurate.
The results demonstrate a strong, significant positive relationship between tomato puree consumption and reduced measures of oxidative stress (p< 0.0001). Given the small cohort (n=11), to achieve a significance of this level requires a drastically large effect size. This study also suggests that a dramatic change in resistance to oxidative stress can be realised in a very short period of time, via a very small intervention. Replication of this study using both the identical design and with other antioxidant rich foods needs to be done to determine if these results are unique to lycopene rich foods.
Length of Study
Very few studies have attempted to measure the potential effect of antioxidants for an extended period of time; the duration of a large proportion of studies in this area is under six weeks. Perhaps the lack of conclusive evidence supporting antioxidant supplementation arises from the brief experimental window that is used in many of these studies.
Preziosi, Galan, Herbeth, Valeix, Roussel, Malvy, Paul-Dauphin, Arnaud, Richard, Briancon, Favier, and Hercberg (1998) measured the effects of antioxidant supplementation over a six month period. Like Dawson et al (2002) and Schröder et al (1999), Preziosi et al (1998) utilise a composite of multiple antioxidants as their supplement. Unlike the former, Preziosi et al (1998) also incorporated a double-blind crossover design into their study.
The stated objective of this study was “to test the impact of supplementation with nutritional doses of antioxidant nutrients on biochemical indicators of vitamin and trace element levels.” Compared to the placebo group, the supplementation group had significantly higher serum concentrations for each of the supplemented nutrients (p<0.001). Some indirect measures of oxidation were made (“free radical parameters”), but were inconclusive; whether this is because there was no measurable effect or because this variable was not the focus of the study is unknown. Further long-term research investigating changes in oxidation levels resulting from antioxidant intervention is required.
Conclusions
The literature is generally consistent in demonstrating a positive association between antioxidant supplementation and antioxidant status. It is however, equivocal in demonstrating an effect in altering free radical oxidation as a result of supplementation.
The variability in results for studies investigating the ability of antioxidant supplements to modify oxidative damage can essentially be distilled to three reasons: inconsistencies in supplement dosage (in both active components and in pill frequency), differential measurement sites/methods, and in the length of the study period. The first priority to be addressed is the development of a measurement tool to be recognised as the “gold standard” (for sensitivity and specificity) which would, at the very least, ensure that all future studies in this area will be measuring the same variable as well as ensuring that they do so reliably and consistently. Assuming this task to be possible, once completed the application of this tool will be instrumental in determining the effective ranges for both dosage and the relevant time period involved.
Until such time as these discrepancies are cleared up, no definitive answer regarding the effectiveness of how antioxidant supplementation alters the degree of oxidative stress in the body. It appears likely that any protective benefits to be had from antioxidants will be best achieved through the consumption of foods rich in antioxidants, and not from a supplement.

Godot

I'm sure some may be interested in my sources. Here they are, peruse at your own peril. (some of them are from other parts of the paper, but I couldn't be bothered to remove them. If anyone is strange enough to want to read the paper (unpublished), PM me and I'll arrange to email it to you)

Agarwal, S, and Rao AV. 2000. Tomato lycopene and its role in human health and chronic diseases. Canadian Medical Association Journal; 163(6):739-44.

Aviram M, Dornfeld L, Rosenblat M, Volkova N, Kaplan M, Coleman R, Hayek T, Presser D, and Fuhrman B. 2000. Pomegranate juice consumption reduces oxidative stress, atherogenic modifications to LDL, and platelet aggregation: studies in humans and in atherosclerotic apolipoprotein E–deficient mice. American Journal of Clinical Nutrition; 71: 1062–76.

Baublis AJ, Lu C, Clydesdale FM, and Decker EA. 2000. Potential of Wheat-Based Breakfast Cereals as a Source of Dietary Antioxidants. Journal of the American College of Nutrition: 19 (3); 308S–311S.

Blumberg J, Ji LL, Jenkins R, Goldfarb A, and Clarkson P. 1994. Exercise, Nutrition, and Free Radicals: What’s the Connection? In GSSI Sports Science Exchange Roundtable; 5(1).

Burke, L. Desbrow, B, and Minehan, M. Dietary supplements and nutritional ergogenic aids in sport. In: Burke, L. & Deakin, V. eds. Clinical Sports Nutrition. Sydney: McGraw-Hill, 2002, pp. 455-553.

Carr CA, and Frei B. 1999. Toward a new recommended dietary allowance for vitamin C based on antioxidant and health effects in humans. American Journal of Clinical Nutrition; 69: 1086–107.

Clarkson PM, and Thompson HS. 2000. Antioxidants: what role do they play in physical activity and health? American Journal of Clinical Nutrition; 72(suppl.): 637S-46S.

Dawson B, Henry GJ, Goodman C, Gillam I, Beilby JR, Ching S, Fabian V, Dasig D, Morling P, and Kakulus BA. 2002. Effect of Vitamin C and E Supplementation on Biochemical and Ultrastructural Indices of Muscle Damage after a 21 km Run. International Journal of Sports Medicine; 23: 10-15.

Dröge, W. 2002.Free Radicals in the Physiological Control of Cell Function. Physiological Reviews; 82: 47-95.

Evans, WJ. 2000. Vitamin E, vitamin C, and exercise. American Journal of Clinical Nutrition; 72 (suppl.): 647S-52S.

Fogelholm, M. Vitamin, mineral and antioxidant needs of athletes. In: Burke, L. & Deakin, V. eds. Clinical Sports Nutrition. Sydney: McGraw-Hill, 2002, pp. 312-340.

Halliwell, B. 2000a. The Antioxidant Paradox. Lancet; 355.

Halliwell, B. 2000b. Why and how we should measure oxidative DNA damage in nutritional studies? How far have we come? American Journal of Clinical Nutrition; 72: 1082-7.

Heunks, L. and Dekhuijzen, R. 2000. Respiratory muscle function and free radicals: from cell to COPD. Thorax 2000; 55:704–716.

Itoh H, Ohkuwa T, Yamazaki Y, Shimoda T, Wakayama A, Tamura S, Yamamoto T, Sato Y, and Miyamura M. 2000. Vitamin E Supplementation Attenuates Leakage of Enzymes Following 6 Successive Days of Running Training. International Journal of Sports Medicine; 21: 369–374.

Polidori, MC, Mecocci, P, Cherubini, A, and Senin, U. 2001. Physical Activity and Oxidative Stress during Aging. International Journal of Sports Medicine; 21: 154-7.

Porrini, M. and Riso, P. 2000. Lymphocyte lycopene concentration and DNA protection from oxidative damage is increased in women after a short period of tomato consumption. Journal of Nutrition; 130: 189-192.

Powers SK. 2002. Exercise, Antioxidants, and Cardioprotection. In GSSI Sports Science Exchange; 15(2).

Prasad KN, Kumar A, Kochupillai V, and Cole WC. 1999. High Doses of Multiple Antioxidant Vitamins: Essential Ingredients in Improving the Efficacy of Standard Cancer Therapy. Journal of the American College of Nutrition; 18 (1): 13–25.

Preziosi P, Galan P, Herbeth B, Valeix P, Roussel AM, Malvy D, Paul-Dauphin A, Arnaud J, Richard MJ, Briancon S, Favier A, and Hercberg S. 1998. Effects of Supplementation with a Combination of Antioxidant Vitamins and Trace Elements, at Nutritional Doses, on Biochemical Indicators and Markers of the Antioxidant System in Adult Subjects. Journal of the American College of Nutrition; 17 (3): 244–249.

Salganik, RI. 2001. The Benefits and Hazards of Antioxidants: Controlling Apoptosis and Other Protective Mechanisms in Cancer Patients and the Human Population. Journal of the American College of Nutrition; 20 (5): 464S–472S.

Schröder H, Navarro E, Tramullas A, Mora J, Galiano D. 2000. Nutrition Antioxidant Status and Oxidative Stress in Professional Basketball Players: Effects of a Three Compound Antioxidative Supplement. International Journal of Sports Medicine; 21: 146-50.

van den Berg R, van Vliet T, Broekmans W, Cnubben N, Vaes W, Roza L, Haenen G, Bast A, and van den Berg H. 2001.A Vegetable/Fruit Concentrate with High Antioxidant Capacity Has No Effect on Biomarkers of Antioxidant Status in Male Smokers. Journal of Nutrition; 131: 1714–1722.

Whitney, EN, and Rolfes, SR. 1999. Understanding Nutrition, 8th ed. West Publishing Co. NY.

Yochum LA, Folsom AR, and Kushi LH. 2000. Intake of Antioxidant Vitamins and risk of Death from Stroke in Postmenopausal Women. American Journal of Clinical Nutrition; 72: 476–83.

theyeti

Well, I don't have a dozen sources to back me up, but here's the short answer as I understand it: There have been umpteen different studies showing a positive benefit for eating lots of fruit and vegetables. It was originally believed that this benefit derived from the viatmins present in veggies, but the fact that the benefits cannot be reproduced through vitamin supplements casts doubt on this. No one knows for sure why veggies are good for you. It could be due to cofactors as Godot said. Or it could be due to fiber. Or maybe due to the lack of saturated fat or calories present in other types of food. And it might be a combination of two or more of these. But the fact remains that you cannot reproduce the health benefits of eating vegetables simply by taking vitamin supplements. In fact, it's not clear that there's any benefit to taking vitamin supplements if you're eating a decent diet.

theyeti

scombrid

sound advice

scigirl

scombrid - ROFL!!!

I'm currently working in an exercise physiology lab - they are going to LOVE this!!

Oh haha ha ha!

Ok back to the original question - what godot said!

Lots of studies have indicated that F&V are more beneficial than vitamins - probably because we just don't know all the things in the F&V that are beneficial yet.

However there are cases where dietary supplements are important - in certain disease states, or if you are on certain medications (lasix and potassium for example). Or if you are on a restricted diet for religious or personal reasons - a supplement is better than not getting the vitamin or mineral.

And yes F&V are the only natural way to get fiber. Steak just don't got any!

scigirl

Wyz_sub10

The other thing I'd note is that fruits are an excellent source of water (which you do not get in vitamins...unless you wash them down with lots of water).

BrotherMan

There's a reason why multivitamins et al are called supplements. Vitamins and minerals from pills aren't metabolized the same was as from natural sources.

JGL53

The only problem is that when many Americans hear the word 'vegetable' they think potato, hopefully fried, piled high and covered with R. Reagan's favorite vegetable, catsup - plus a double burger with fake cheese, on a giant pure white bun(wheat's a vegetable), with bits of lettuce, onion, pickles and tomato (Wow, a veritable cornucopia of veggies!). And don't forget the mayo (with added sugar - from beets, ANOTHER vegetable!). The only thing they generally have for lunch that isn't loaded with veggies is the diet drink (but if they switched to regular - Wow, more beet sugar! More vegetables!).

And they think that having a fried pie (apple or peach) is a fruit serving, or, even better, having a three-scoop banana split will give them their daily requirement of three or more fruit servings (Wow, a banana, PLUS pieces of pineapple AND strawberry in syrup! Mmmmmmm. Deliciously HEALTHY!).

With all the 'fruit and vegetables' that Americans eat, you'd think they'd be healthier, on average, huh?