True or False: Mycotoxins in Coffee Are a Serious Threat to Our Health and the Only Way to Avoid Them is Abstinence

As we are about to see coffee is by far not the worst aflotoxin offender in the human diet. Still, that does not mean that the coffee related exposure to this form of mold that can befall all sorts of grains, nuts and seeds is harmless.

You will probably remember that I casually touched on the possibility of being exposed to aflotoxins and more importantly ochratoxins as a result of the consumption of mold-infected coffee in previous coffee articles. When the issue of the « coffee ➲ aflotoxin / ochratoxin exposure ➲ serious health » triage resurfaced in a brief facebook conversation, recently, I realized that I was not 100% sure if these mycotoxins that are produced by Aspergillus flavus, Aspergillus ochraceus, Aspergillus niger, and Aspergillus carbonarius do or don't pose a serious health risk.

Well, you know how much I hate unanswered questions, so I kept digging until I'd found what I consider to be a half-way satisfying answer to this life-or-death question ;-)

You can learn more about coffee at the SuppVersity

Remember: With Coffee More Won't Help More

Coffee - The Good, Bad & Interesting

Three Cups of Coffee Keep Insulin At Bay

Caffeine's Effect on Testosterone, Estrogen & SHBG

Coffee + Cacao for Breast Cancer Prevention

"Decaf" Won't Help With Weight, ... Ahh, Fat Loss

"The amount of aflotoxin in the average cup of coffee is a serious threat to our health!"

In 90% of the cases the above statement is FALSE! Despite the fact that it is difficult to tell how much mycotoxins you've been flushing down with your morning coffee today, the exact amount of the more common aflotoxins and their similarly kidney-toxic, pro-carcinogenic and coffee-loving cousins, the ochratoxin, in the average cup of (roasted) coffee is probably way too low to be worried about.

Figure 1: Mycotoxin exposure from coffee; calculated based on data from Europe (Vd Stegen. 1997)

Based on the studies I have reviewed for this article, it appears almost certain to say that the relatively low amount of coffee beans per cup (4-8g) reduces your average mycotoxin exposure from 1-4 cups of coffee per day to levels that are almost certainly within one of the various (multi-)national reference ranges (Van Egmond. 2007):

• Europe: 5µg/kg
• Africa: 10µg/kg

• North America: 20µg/kg

• Asia: 15µg/kg
• Latin America: 20µg/kg

Using a selection of commercially available regular and soluble coffee brands, van der Stegen et al. have actually calculated the average daily mycotoxin intake of Europeans with an average coffee consumption of 1-4  to be in the nanogram range - 19ng and 10ng, specifically, for regular and instant coffee drinkers, respectively.

Please remember: We don't know if / what happens or doesn't happen if you stay within or break the arbitrary intake limits. If you take a look at the available evidence from rodent studies, the results Epstein et al. presented in their 1969 paper (see Table 1) later in this article, would suggest that a sensible intake limit would have to be below the 1µg range if we assume a similar toxicity for the average mycotoxin mixture as for the aflotoxin B Epstein et al. used. This assumption is obviously not realistic, but it should remind you of the arbitrariness of the "intake limits".

Just to make sure, we understand each other, here: That's 1000x less than you'd get from only 20g of some of the Brazilian peanuts Freitas and Brigido analyzed in a 1998 study for their mean and maximal mycotoxin content. With 1099µg/kg the worst offenders in this study would easily have you breach the already lax American (North & Latin America) max. tolerable intake limit of 20µg/kg per day - and that despite the fact that this limit is more than 1000x higher than the amount of mycotoxins you'll have in your average cup of coffee.

Green vs. roasted coffee: Do we have to chose between anti-oxidants and mycotoxins?

It goes without saying that the mere fact that the dangers of being exposed to high amounts of mycotoxins from adequately processed and stored coffee appears negligible, does not warrant ignoring the problem completely. The effects of processing and storage are and will thus always be an important issue.

Given the fact that humid and cool (but not cold) is what mold needs to thrive, you will probably already have suspected that the hot and arid environment of a coffee roastery is not exactly the favorite growth environment for the Aspergillus family.

Figure 2: Ochratoxin content (µg/kg) in green, roasted & soluble coffee, left; total antioxidant activity in TROLOX essay of green (=unroasted), lightly, medium and dark roast coffee (Blanc. 1998; del Castillo. 2002)

A lower mycotoxin content is yet not the only beneficial effect of roasting. Contrary to what 99% of the people will tell you, when you ask them, the roasting process increases not decreases the total antioxidant capacity of coffee (TAC).

What does the latest review say about regular coffee consumption and cancer? "The epidemiological evidence consis-tently indicates that coffee protects against liver cancer, and also point toward protective effects for risk of colorectal cancers (with relative risks of 0.50 (95% CI: 0.42–0.59) and 0.83 (95% CI: 0.75–0.92), respectively, in the most recent meta-analyses)" (Bøhn. 2013). The evidence for protective effects against breast and prostate cancer on the other hand is inconclusive - irrespective of the established chemo-preventive effects of coffee phytochemicals Bøhn et al. list in their soon to be published paper in Molecular Nutrition & Food Research early in 2014.

Due to the formation of a whole host of new antioxidant molecules during the roasting process, light or mildly roasted coffee beans have a higher total antioxidant capacity than green ones - irrespective of the reduced chlorogenic acid content, for which the green beans are currently (over-)hyped. If you look at the data in Figure 2 you will see that even the heavily roasted, tar-black coffee beans still have a minimally higher anti-oxidant activity than the "natural" green coffee beans (del Castillo. 2002) - an observation that has been made both in the Petri dish, as well as ex vivo rodent studies (Daglia. 2002).

You've been drinking tons green coffee, lately?

Don't worry! Your past green coffee consumption probably isn't a real problem either. It does after all look as if those beans were yet another example for the infamous "nature kows best" principle. I mean, can it really be "coincidence" that the beans come with "anti-mycotoxin agents" in form of cafestol and kahweol. These coffee-specific diterpenes have been shown to ameliorate the aflotoxin B induced genotoxicity (Cavin. 1998) and the subsequent pro-carcinogenic effects (Cavin. 2001) and can be expected to exert protective effects against ochratoxin toxicity, as well.

In view of the fact that similar evidence exists for chlorogenic acids (CGA), dodecyl chlorogenates (DCGA) and a high(er) coffee consumption, in general (Suárez‐Quiroz. 2013; Ferk. 2013), it is actually not surprising that studies like Shank et al. (1972)  or Bulatoa-Jaym et al. (1982) found links between aflotoxin contaminated corn, grains, potato, peanuts & co., but could not identify an increased risk in liver cancer for coffee aficionados. Consequently, it's (imho) relatively unlikely that your health has already taken a beating - irrespective of the amount of the number of cups of green coffee you've been consuming over the past weeks.

Coffee is not the worst mycotoxin offender in the human diet: In a case-control dietary study of primary liver cancer in humans Bulatoa-Jaym et al. found that 51.2% of their subjects daily aflotoxin exposure came from cassava, 20.3% from corn, 6.8% frompeanuts and 5.8% from sweet potato (Bulatao-Jaim. 1982). On the other hand, many scientists argue that the ochratoxin content of coffee is the real danger, anyway (Bayman. 2006)

I would still like to remind you that even the sum of the previous remarks must not be misunderstood as an incentive to willy nilly forget all previously harbored concerns about "moldy coffee beans"... and I say this in spite of the existing epidemiological evidence that a high coffee consumption decreases the risk of developing and dying from liver cancer (Kurozawa. 2005; El–Serag. 2007). The liver is after all not the only organ that may be affected by the pro-carcinogenic toxins. The kidneys are at least as susceptible to the toxic assault from the mycotoxin filtrate that passes through them.

The liver is not the only organ that's taking a beating

It may thus be hypothetical, but not impossible that a 2x / 2.6x increased risk to develop renal cell carcinoma Mimi et al. report in a 1986 paper on the associations between coffee consumption and kidney cancer may at least be partially related to the higher mycotoxin exposure in those 61 study participants who consumed 1-4 cups of coffee per day (Mimi. 1986).

That mycotoxins can promote the development of kindey cancer had been demonstrated 17 years before the publication of Mimi's paper by Epstein, Bartus & Farber (1969) whose Wistar rats developed renal epithelial neoplasms after being exposed to food-borne aflatoxin B1.

Table 1: Incidence of renal epithelial and malignant hepatic tumors in male Wistar rats ingesting aflatoxin B1 for 147 days; the indces a, b, c provide irrelevant (in this context) extra information (Epstein. 1969)

In that, it's quite remarkable that even the lowest aflotoxin dosage the researchers used in their study (0.25µg/kg chow; HED  ~1.2ng/kg body weight, ; see Table 1) lead to significant rates of cancerous growth in both kidney (28%, if we count both developing and full-blown renal neoplasms) and liver  within the 21 week study period.

There is just one no-go: Storing unroasted beans for years in your humid basement

In view of the large regional difference in aflotoxin infection rates, the different susceptibility of the various coffee cultivars and the influences of weather, storage conditions, blending, processing, and all the other factors that increase or decrease the amount of mold and mycotoxins on coffee (see Figure 3), I would still be hesitant to exclude the possibility that stocking up on highly aflotoxin contaminated unroasted coffee you possibly even stock in a very humid basement of yours to consume the coffee over the course of months if not years could have negative effects on the health of your organs, in general, and the function of your kidney and liver, in particular.

Figure 3: Percent infection of coffee cherries and beans byAspergillusspecies potentially capable of producing ochratoxin A in four Brazilian coffee growing regions from the 1999 and 2000 harvests (Taniwaki. 2003)

I mean, look at the data in Figure 3. It's probably no coincidence that the otherwise virtually uninfected beans of coffee from the 1999 and 2000 harvests in the Cerrado Miniero exhibits a 4% infection rate after being stored intermediately before it is either roasted, shredded or both or simply forwarded "raw" to the mailbox of an "unroasted coffee enthusiast". Similar effects can be expected when the huge coffee manufacturers mix harvests from various regions. If only one is infected, all it takes to have Aspergillus flavus literally "all over the place" is enough time in one of the huge storage silos or the hold of one of the container ships that transport coffee from the "New" back into the "Old World".

Figure 4: The amino acid make up of coffee changes upon roasting (data from Cirilo. 2003).

Life kills, anyway! Let's be honest. In the end, living is a pretty deadly undertaking, anyway. Against that background the uncertainty with respect to the tolerable intake of mycotoxins should not bother you so much to ignore the existing evidence of the beneficial effects of regular coffee consumption (see "Coffee - The Good, the Bad & The Interesting" | read more).

One thing you may keep in mind, though, is that this evidence is based on data from average coffee drinkers, people who drink coffee that's made of roasted beans. Beans that are virtually mycotoxin-free (see Figure 2, left) and have a higher, not lower antioxidant capacity than green coffee beans.

What roasted beans lack, though, are chlorogenic acid and trace amounts of amino acids (see Figure 4), including serotonin. If you are looking for one of these molecules specifically, you are yet probably better of with a hopefully aflotoxin and mycotoxin free green coffee extract and a bottle of pills with the serotonin precursor 5-HTP, anyways.

References:

• Bayman, P., & Baker, J. L. (2006). Ochratoxins: a global perspective. Mycopathologia, 162(3), 215-223. 
• Blanc, M., Pittet, A., Muñoz-Box, R., & Viani, R. (1998). Behavior of ochratoxin A during green coffee roasting and soluble coffee manufacture. Journal of agricultural and food chemistry, 46(2), 673-675.
• Bøhn et al. (2013) Coffee and cancer risk, epidemiological evidence, and molecular mechanisms. Molecular Nutrition & Food Research [early view article]
• Bulatoa-Jaym J, et al. (1982). A Case-Control Dietary Study of Primary Liver Cancer Risk from Aflatoxin Exposure*. International journal of epidemiology, 11(2), 112-119.
• Cavin, C., Holzhäuser, D., Constable, A., Huggett, A. C., & Schilter, B. (1998). The coffee-specific diterpenes cafestol and kahweol protect against aflatoxin B1-induced genotoxicity through a dual mechanism. Carcinogenesis, 19(8), 1369-1375.
• Cavin, C., Mace, K., Offord, E. A., & Schilter, B. (2001). Protective effects of coffee diterpenes against aflatoxin B< sub> 1</sub>-induced genotoxicity: mechanisms in rat and human cells. Food and Chemical toxicology, 39(6), 549-556.
• del Castillo, M. D., Ames, J. M., & Gordon, M. H. (2002). Effect of roasting on the antioxidant activity of coffee brews. Journal of Agricultural and Food Chemistry, 50(13), 3698-3703. 
• Cirilo, M. P., Coelho, A. F. S., Araújo, C. M., Gonçalves, F. R., Nogueira, F. D., & Glória, M. B. A. (2003). Profile and levels of bioactive amines in green and roasted coffee. Food Chemistry, 82(3), 397-402.
• Daglia, M., Papetti, A., Gregotti, C., Bertè, F., & Gazzani, G. (2000). In vitro antioxidant and ex vivo protective activities of green and roasted coffee. Journal of Agricultural and Food Chemistry, 48(5), 1449-1454.
• Epstein, S. M., Bartus, B., & Farber, E. (1969). Renal epithelial neoplasms induced in male Wistar rats by oral aflatoxin B1. Cancer Research, 29(5), 1045-1050.
• El–Serag, H. B., & Rudolph, K. L. (2007). Hepatocellular carcinoma: epidemiology and molecular carcinogenesis. Gastroenterology, 132(7), 2557-2576. 
• Ferk, F., Huber, W. W., Grasl‐Kraupp, B., Speer, K., Buchmann, S., Bohacek, R., ... & Knasmüller, S. (2013). Protective effects of coffee against induction of DNA damage and pre‐neoplastic foci by aflatoxin B1. Molecular nutrition & food research. 
• Freitas, V. P., & Brigido, B. M. (1998). Occurrence of aflatoxins B1, B2, G1, and G2 in peanuts and their products marketed in the region of Campinas, Brazil in 1995 and 1996. Food Additives & Contaminants, 15(7), 807-811.
• Kurozawa, Y., Ogimoto, I., Shibata, A., Nose, T., Yoshimura, T., Suzuki, H., ... & Tamakoshi, A. (2005). Coffee and risk of death from hepatocellular carcinoma in a large cohort study in Japan. British journal of cancer, 93(5), 607-610. 
• Mimi, C. Y., Mack, T. M., Hanisch, R., Cicioni, C., & Henderson, B. E. (1986). Cigarette smoking, obesity, diuretic use, and coffee consumption as risk factors for renal cell carcinoma. Journal of the National Cancer Institute, 77(2), 351-356.
• Shank, R. C., Wogan, G. N., & Gibson, J. B. (1972). Dietary aflatoxins and human liver cancer. I. Toxigenic moulds in foods and foodstuffs of tropical South-East Asia. Food and Cosmetics Toxicology, 10(1), 51-60.
• Taniwaki, M. H., Pitt, J. I., Teixeira, A. A., & Iamanaka, B. T. (2003). The source of ochratoxin A in Brazilian coffee and its formation in relation to processing methods. International Journal of Food Microbiology, 82(2), 173-179. 
• Van Egmond, H. P., Schothorst, R. C., & Jonker, M. A. (2007). Regulations relating to mycotoxins in food. Analytical and bioanalytical chemistry, 389(1), 147-157. 
• Vd Stegen, G., Jörissen, U., Pittet, A., Saccon, M., Steiner, W., Vincenzi, M., ... & Schlatter, C. (1997). Screening of European coffee final products for occurrence of ochratoxin A (OTA). Food Additives & Contaminants, 14(3), 211-216. 
• Yamato, T., Yamasaki, S., Misumi, Y., Kino, M., Obata, T., & Aomine, M. (2002). Modulation of the stress response by coffee: an in vivo microdialysis study of hippocampal serotonin and dopamine levels in rat. Neuroscience letters, 332(2), 87-90.

The Potato Manifesto - Part 2/2: The Sweet Potato, Is It More Than Just the "En Vogue Tuber of the Year"?

Image 1: A mixer like this would be one of the best choices to turn your healthy low-GI sweet (or regular) potato into a high GI "nightmare".

If you've read yesterday's first part of the Potato Manifesto, you should by now be aware that the common notion of the pro-diabetic high-glycemic regular potato is another of the numerous black-or-white nutrition myths that do not become right, no matter how many bloggers and forum posters reiterate them. In today's second part of the series I will try to elucidate, whether the sweet potato, of which I would venture to say that she is the "en vogue tuber of the year", is not still the "safer starch alternative". So bear with me while I am using my scientific peeling knife to check whether there is a bitter truth hidden beneath skin of the sweet potatoes ;-)

Come on sweety, show me what's beneath your skin!

Now, if we take a look at the literature, a review of the glycemic index of 33 commonly available foodstuffs from the 1990s lists sweet potatoes with a glycemic index of 49 as #17 (with #1 peanuts and a GI of 11 and #32 cornflakes and a GI of 83 as the "extremes"; Nishimune. 1991). It is "outperformed by spaghetti (GI 47) and closely followed by Buckwheat, Yam (both GI 51) and you guessed it the good old "regular" potato, to which Takahiro Nishirnune and his colleagues assign a GI of 54, which - as you should know from yesterday's installment of the Potato Manifesto is nothing but an average on a scale that ranges from 10 to 110!

Figure 1: Difference in plasma glucose concentrations (expressed as the increase due to the "high GI" normal potato vs. the "low GI" sweet potato) in response to the ingestion of 50g of carbohydrates in form of bush potato or regular potato in 7 Aborigines and 7 Caucasians (data adapted Thorburn. 1986)

A brief note on the fallacy of common arguments for "traditional diets" (=sweet potato diets): I recently started listening to archived episodes of Jimmy Moore's Living La Vida Low Carb show and encountered time and again the 99% nonsensical argumentation that the XYZ thrived on whatever diet and that by just mimicking their diet(s), we would thrive, as well. To me this is like saying: "Look, the Panda bears thrive on a 100% bamboo diet! So, the ice-bears in our zoo should get along pretty well, if we stopped feeding them meat." Now, this is obviously a provocative comparison, but if I look at myself and then look at an Aborigine, the difference may not be as significant as the one between panda and ice-bear and yet, according to the results of a 1986 study by Anne W. Thorburn et al. (Thorburn. 1986) our glucose responses to the ingestion of 50g of carbohydrates from either the sweet-potato'esque bush potato and a "normal" western potato would be completely different (cf. figure 1). While the poor Aborigine would encounter the typical blood sugar ups and downs that are so characteristic for the ingestion of "high GI" carbs, my body would probably not care whether I eat the 100% paleo bush potato or its readily available, cheap cousin. The futility of common "neo-paleolithic" reasoning aside, this example also shows that genetic individualities are another major determinant of the glycemic index.

Three yeas later, in 1994, Thomas Wolever and his colleagues from the University of Toronto tested the glucose response of diabetic patient to 102 complex carbohydrate foods (Wolever. 1994). "Complex", in this case, indicates that they tested combinations of foods like they could appear on someone's dinner table and lo and behold, the "low GI" sweet potato took a close second to the "high GI" boiled white potato, when the both were boiled and served to 16 diabetic patients along with tomatoes. The 1 GI point difference between sweet and white potato (60 vs. 59) is yet well within the statistical margin.

Identical glycemic index, but differing free sugar compositions

Although, I hope that I should by now have convinced you that the glucose response is no convincing argument in favor of the sweet potato. I am even convinced that, if people abused their sweet potatoes in similar ways as their "regular" potatoes, i.e. mashed, fried, pureed, powdered and instantized it, we would soon see the (contemporarily) sexier sister of the regular potato on the list of "foods to avoid if you want to lose wait or just live a long and healthy life". Nevertheless, taste and name of the sweet potato, leave no doubt that there must be a sugary difference between her and her white brethren.

Figure 2: Free sugar composition (in mg/g) of 16 "regular" and 3 sweet potatoes cultivars (comparison based on data from Zhu. 2011 and Dincer. 2011)

And in fact, as my juxtaposition of data from a 2010 study on the relation between amino acid and sugar content of commercially available regular potatoes and its effect on the formation of acrylamite during heating (Zhu. 2011) and data from the previously mentioned (cf. Part 1) study by Cuneyt Dincer and his (or her) colleagues from the Akdeniz University in Ankara, Turkey (Dincer. 2011) shows (cf. figure 2), there is a non-negligable difference in the amount and composition of "free sugars" (vs. sugars in the form of starch). Although I am not 100% about the exact nature of the exotic Chinese potatoes, it is quite obvious that, despite large varieties in the absolute and relative sugar content of "regular" potatoes, the "classic" potato has a lower absolute free sugar content and contains more fructose and glucose than her sweet sister, 90% of the free sugar content of which is plain table sugar (=sucrose = glucose + fructose).

Figure 3: Mean free sugar composition (in mg/g) of fresh "regular" and sweet potatoes (comparison based on data from Zhu. 2011 and Dincer. 2011)

This "sugary" pattern does yet broaden, when you expose the sweet potato to heat in the form of either boiling or baking (cf. figure 4). In that, the cultivar-dependent slight reductions in glucose and fructose carry little weight compared to the sudden appearance of significant amounts of maltose, which had been beyond the detection before the sweet potatoes were boiled or baked (cf. figure 4).

Figure 4: Free sugar content (mg/g dry weight) of fresh and cooked sweet potatoes (data adapted from Dincer. 2011)

From a chemical perspective, the latter is not really surprising and its formation in response to heat treatment has been reported as early as 1923, when H.C. Gore published a paper in the Journal of Industrial and Engineering Chemistry (Gore. 1923), in which he makes the important observation that the formation of sugars from starch takes place within the first minutes of heating:

The  raw  potatoes  contained  0.34  per cent of  reducing  sugar calculated as maltose, the  cubes  cooked for  5  minutes in boiling water contained 8.32 per cent, and the cubes cooked for 1  hour,  7.82 per  cent.  Thus,  no sugar formation  occurred  at the  boiling point.

In view of this immediate heat-induced increase in the high GI free sugars, maltose (maltose has a ~10% higher GI than glucose), it should not surprise you that a study that was conducted by Jamaican scientists (Bahado-Singh. 2011), only a few months ago, found statistically significant increases in glycemic index and the area under the incremental glucose curve after boiling, frying, baking or roasting 10 sweet potato cultivars, which are commonly consumed in Jamaica (cf. figure 5):

Figure 5: Glycemic indices and glucose AUC of 10 common Jamaican sweet potato cultivars after boiling, frying, baking and roasting (data adapted from Bahado-Singh. 2011)

If we disregard the differences between the 10 cultivars and focus on the overall pattern, it is quite obvious that on the "less to worst thing you can do with your sweet potatoes if you are concerned about GI"-scale boiling is at the most benign end of the continuum, while baking and roasting compete for the position at the other end - a pattern, those of you who have already read Part 1 of the Potato Manifesto should be familiar with: Contrary to common believe new boiled (regular / sweet) potatoes are in fact a low GI food. In our kitchen (and even more so in the industrial processing machinery of the food industry), where the harmless tubers are mashed, pureed, dried, instantized, fried, baked, roasted etc., both, regular, as well as sweet potatoes do yet acquire at least some resemblance to the "pro-diabetic frankenfood", as which they have gotten labeled within the blogosphere, all along.

Figure 5: Comparison of regular and sweet potato glycemic indices after boiling, frying, baking and roasting.

If we now take a final look at the comparison of the average GI (figure 6 is based on data from both installments of the Potato Manifesto) of regular and sweet potatoes after boiling, frying, baking and roasting, it seems as if the main differences were that on average the regular potato has a slightly higher baseline GI (I do not need to remind you that according to Soh. 1999 boiled Desiree potatoes have a GI of 10!, do I?) and tends to be more resistant to heat-induced deteriorations in her starch / free sugar composition.

So, are boiled sweet and baked and roasted regular potatoes the way to go?

In view of the fact that probably 99% of the average and maybe 70% of the health conscious consumers don't even know the name of the potato cultivar they are using, let alone their age, storage temperature, the amount of phosphate in the soil on which it was grown, and all the other countless variables that have an impact on the "basal" GI of a potato, I honestly doubt that switching from one of the waxier, new regular potatoes (low basal GI) to a random (I mean, how many sweet potato cultivars are available at your grocery store?) sweet potato cultivar, would make you healthier, help you lose weight or offer any other GI-related benefits.

Image 2: Tapioca, another purpoted "health food" with a surprisingly high glycemic index GI of 84

Just as an aside, the Wolever study also examined the glucose response to another of the funky foods that are resurfacing on the Internet as "health foods", these days: Tapioca - also known as cassava, manioc, aipim, bitter-cassava, boba, mandioca, macaxeira, manioca, tapioca plant, yuca. With a GI of 84 it easily outperforms, corn chips (GI 76) and even waffles (GI 79).

Note: Wherever this was necessary I converted GIs that were given with white bread as a reference to the glucose as a reference.

Whether you could benefit from the (again, on average and in this case specifically referring to the white variety of the regular potato) higher beta-carotene and vitamin C content of sweet potatoes would depend on the rest of your diet. If the latter is "99% paleo" ;-), the likelihood that you would not get enough of these antioxidants is close to zero and it should thusly not really make a difference whether you go for the "paleo-" or the "neolithic" potato, as long as you don't (over-)process her into another of the innumerable frankenfoods the average member of the neolithic convenience society is so fond of.