The Potato Manifesto - Part 1/2: A (Re-)Evaluation of the Contemporary Discrimination of "the" Ordinary Potato

Image 1: The grunty regular (left) and the cute sweet potato (left), which one would you commit your health to? (img. menshealth.co.uk)

This is a blogpost, which eventually turned out to be the first part of a series, is a post with a history, a rather complex one, to be precise. It is rooted (not tubered ;-) in my amazement over the contemporary craving for sweet potatoes within the ever-growing neo-paleolithic community on the Internet and was sparked by the recent publication of a study on sweet potatoes, I stumbled upon on my daily tours of the most recent scientific literature. To make long story short, instead of immediately summarizing the data, drawing some graphs and commenting on the real-world implications of this study, I decided to use the holiday to descend into the archives and take a closer look at what science has to say on the bitter truth about the grunty regular and the starchy promises of cute sweet potato (cf. image 1 ;-)...

When wheat was devils excrement, would regular potatoes then be his horns?

According to the official obesity statistics of the European Union, British women are the fattest in Europe (Eurostat. 2011): 23.9% were classified as being obese (BMI > 30) in the year 2008 to 2009. This certainly raises the not altogether serious question, whether the British obesity problem (the obesity rate among the men was 22.1% and thusly topped only be the Maltese with 24.7%) is due to the fried fish or the fried (regular) potatoes in the unofficial British national dish, fish & chips.

Image 2: Obese British woman's rear view (img. BBC.co.uk)

A note to my dear American friends: Don't crow too soon, the obesity rate in the US tops the one in the UK by more than just a margin. According to a 2010 paper by Flegal et al. that was published in the Journal of the American Medical Association, the estimated obesity rate in the US amounts to 35.5% among the women and 32.2% among the men (Flegal. 2010). And a constantly increasing percantage (currently 4.7%) of the American population is already "extremely obese" and has a BMI > 40! Just to put that into perspective. A man or woman with a BMI beyond 40 and a height of 5 foot and 7 inches (170cm) would weigh at least (!) 254.85lbs (115.6kg) - this is already "Kig-Size Homer"-territory (cf. Intermittent Thoughts).

If we follow the current dietary paradigms and ignore the frying procedure, the answer to this question does not appear to be very difficult. I mean, when wheat was devil's excrement, then regular potatoes would be his horns or even nastier body parts, I do not want to mention here... and though a reasonable explanation for the widespread vilification of potatoes still escapes me, the contemporary nutritional paradigm within the health and nutrition blogosphere suggests that regular white potatoes have an awfully high glycemic index, will spike your blood sugar levels and have your neolithic body pump out tons of insulin - even if the rest of your diet is 99% paleo, as many of the listeners of Robb Wolf's podcast like to describe the way they are eating after having read his (widely read, yet controversial - esp. wrt to starches / carbs, fish oil and a few other topics) book ;-)

Figure 1: Names and characteristics of eight common potato cultivars in the British diet (left) and experimentally evaluated area under the glucose curve and glycemic indices (right; data based on Henry. 2005)

If we take a look at the data in figure 1, which shows both the incremental area under the glucose curve (AUC) and the GI of eight commercially available and commonly consumed British potato cultivars, it should however be quite obvious that the concept of the bad high-GI regular potato is about as misguided as the racist or religious prejudices some of our fellow human beings are still harboring against other members of the human race. With glycemic indices that range from 56 for the "waxy" Marfona to 94 for the "firm" Maris Peer, the "bad" regular potatoes cover the exact same GI range as their "healthy" sweet cousins (come back tomorrow for Part II of this series with more information on sweet potatoes).

Cultivar, processing, serving temperature and more have profound influences on the GI

The type  (=cultivar) of the (classic) potato, is yet neither the only, nor the most important determinant of the glycemic index of a potato meal. The processing method and, to my own surprise, even the food temperature have considerable influence on the glucose response to otherwise identical test meals, as well:

Figure 2: Incremental areas under the curve (AUC) and glycemic index values for 50 g available carbohydrate portions of white bread and seven potato meals tested in a cohort of 12 healthy subjects (data adapted from Fernandes. 2005)

On the left = "better than white bread"-side of figure 2, we have cold, boiled red potatoes (GI 56.2) and, surprise, frensh fries (GI 63.6) and roasted Californian white potatoes  (GI 72.3, but lower AUC than white bread). On the right = "worse than white bread"-side, instant mashed potatoes (GI 87.7) and the hot variety of the "low GI" red potatoes (GI 89.4) are competing for the red lantern.

With regard to the unexpected differences between cold and hot red potatoes, it is important to note that the results of a 2011 study by Kinnear et al. confirm that the latter is not an artifact of the Fernandes study. In their trial, the scientists from the University of Toronto found an average GI reduction of -37% (mean GI for the tested cultivars ~47), when the freshly boiled potatoes were refrigerated at 4°C for 24–28h before they were served to the 10 healthy study participants (Kinnear. 2011). As far as the reasons for this temperature-dependence of the glycemic index is concerned, Kinnear et al. speculate that it is an effect "due to starch retrogradation", which is a process that takes place in gelatinized starch, when the amylose and amylopectin chains realign themselves and thusly causes the liquid to gel. This is quite interesting, as it stands in line with the low GI of the Marfona potato (cf. figure 1), the texture of which is described as "waxy". The long-established relation of the phosphate content and the degree of starch gelatinization (and thusly digestibility and GI), on the other hand, could explain difference between crops and differences between identical crops grown on soil with different phosphate contents.

Figure 3: Areas under the glucose curves (AUC) in 32 healthy volunteers to 50g carbohydrates from mashed potatoes with or without 10g fructose administered 0, 30 or 60min before the meal. Measure by Accu Check finger-prick glucometer and YSI glucose oxidase analyzer (data adapted from Heacock. 2002)

Did you know that fructose, of all, is able to reduce the postprandial increase in serum glucose in nondiabetic adults (mean age: 26)? In their 2002 study, Patricia M. Heacock and her colleagues were able to show that pre-ingestion of 10g of fructose 60min and 30min before the ingestion of a 50g carbohydrate meal (from potatoes) reduced the area under the glucose curve (glucose AUC; cf. figure 3) by 25% and 27%, respectively (Heacock. 2002). The immediate co-administration of 10g of fructose with the potato meal (figure 3, 0 min), on the other, did not induce any statistically significant changes in the glucose AUC of the 13 male and 19 female study participants whose blood glucose levels were measured by finger-prick capillary blood (Accu Check) and glucose oxidase analyzers (YSI).

Furthermore, a 1999 study by Soh and Brand-Miller from the University of Sidney (Soh. 1999) shows that the real-world glucose responses of different individuals to differently processed and stored potato cultivars cover an even broader spectrum (especially on the low GI side) than the results of the previously cited studies suggested. The GI values, the Australian scientists calculated based on the glucose response to a 50g carbohydrate portion of eight different potato meals (three varieties, four cooking methods, two states of maturity) differed by as much as +/- 55pts, with canned new potatoes (GI 65) at the upper and boiled Desiree potatoes (GI 10) at the very lower end of the spectrum. And as if things were not complicated enough, already, Soh and Brand-Miller also introduce yet another variable into the equation - the size of the tuber, which showed a statistically significant correlation with the glucose response of the study 10 healthy participants (correlation between GI and tuber size: r=0.83, p < 0.05).

Black-and-white thinking and ineradicable prejudices

If we base our argumentation solely on the glycemic index, which is in fact the main argument that is brought forward against "regular" potatoes in the public debate, it is quite clear that the poor (regular) potato is another victim of the human propensity to black-and-white thinking and the public's stubborn adherence to convential nutritional wisdom. With reference to the "unjustified generalization" that "all potatoes have a high glycemic index", Anette E. Buyken and Anja Kroke, two researchers from the Research Institute of Child Nutrition in Dortmund, Germany, write in their letter to the editor of the British Journal of Nutrition (Buyken. 2005):

Figure 4: GI values (glucose reference) for potatoes by different cooking methods; the horizontal bars indicate the minimal and maximal glycemic index; the dotted vertical lines mark the conventionally accepted  "low GI" <55 (left) and "high GI" >70 (right) cut-off points (the figure was taken directly from Buyken. 2005)

[...] as with all GI data, the GI values of potatoes may depend on cooking method, processing, variety and the composition of the meal. This fact deserves attention since mashed potatoes, French fries, baked potatoes and potatoes cooked in a microwave are characterised by GI values mostly exceeding the upper limit for a high GI value of 70; whereas conventionally boiled potatoes appear to have a GI value on average below 70. The values of conventionally boiled potatoes do vary considerably though, so it may also be that some potato varieties have an inherently low GI what-ever the cooking method (Najjar. 2004; Fernandes. 2005). In this context, it should be considered that most currently available GI values are based on mature potato varieties (Ontario, Prince Edward Island, Desiree, Pontiac, Sebago). The starch of more mature potatoes is, however, easier to digest, presumably due to increased amylopectin branching and hence lower resistance to gelatinisation, which in turn results in a higher GI (Soh. 1999).

Buyken and Kroke support their argument by the means of an illustration of the broad range of the glycemic responses (and respective GI) of study participants to 46 different potato meals (cf. figure 4) and emphasize that there are significant differences in both the preferred potato cultivars, as well as the respective cooking / processing methods between European and US customers. While the former "prefer potato varieties characterised by a lower GI", the prevailing potato varieties in the US are mature and exhibit significantly higher glycemic indices. This trend toward higher glycemic indices in US potato meals is reinforced by the average American's preference to fry, bake, mash, roast or microwave his potatoes, so that it would  be "thoughtless" for any European, or American who selects less mature, low GI cultivars and refrains from frying, baking, mashing, roasting or microwaving his potatoes to follow the grossly over-generalized recommendation to eat less potatoes.

Ok, not all regular potatoes are made equal, but sweet potatoes are still king, right?

Against the background that my grand father who lived a 100% healthy, diabetes-free life into his late 90s, competed in track and fields and swam laps until about 6 months before he died, had regular potatoes with every dinner, I may be somewhat biased as far as the "bad potatoes" are concerned. This does yet not compromise the value of the rational arguments and scientific evidence against the unjust and, above all, over-generalized vilification of regular potatoes I have brought forward in this first installment of the Potato Manifesto. If you are interested in how the "holy" sweet potato which is currently hailed as the savior of the neo-paleolithic race compares, come back tomorrow for Part II of the Potato Manifesto ;-)

Is Hypoglycemia Obesogenic? Is the GI Totally Worthless? Is Mild, But Chronic Stress Behind the Diabesity Pandemic? Is Leptin Obesogenic? And How Do You Calculate the Energy Requirements of Diabetics?

One of the mistakes researchers and dieters make time and again, using the scale as their only guide

Since I had a couple of interesting, but not earth-shatteringly exciting studies on obesity, body weight gain, the GI, leptin and a couple of other things lying around, I thought I'd compile a brief potpourri for you to get you on par with the helplessness with which researchers are still facing the diabesity pandemic. So don't expect any of the one-size-fits-it-all solutions the scientists still appear to be looking for from any of the following items. What you may find, however, is some inspiration when you read between the lines or follow up on the suggested reads, I mention. And if that's not the case, you can still browse previous articles on fat loss or simply go to the gym and try the fat loss example routine from the SuppVersity "Step By Step Guide for Your Own Workout Routine" or simply go to be early to preserve your circadian rhythm.

• Going "Hypo" time and again will make you fat (McNay. 2012) -- Usually you think of hyogylcemia as a sign of a lack of energy, yet despite the fact that this may well be the case this very lack in energy has recently been shown to exert obesogenic effects in a rodent model.
  
  

  

  Often a picture says more than 1000 words: Normal (left) and repeatedly hypoglycemic rodents after 8 months of weekly insulin injections (McNay. 2012)

  The weekly injections Ewan C McNay and his colleagues administered to their rodents and the subsequent episodes of hypoglycemia lead to profound weight gain in the absence of diabetes, hyperphagia, changes in hypothalamic NPY or POMC mRNA expression and  the other usual suspects that could explain this phenomenon. The one thing that's left is therefore what the researchers call a "multi-faceted deficit in metabolic regulation" (McNay. 2012) - interestingly enough the 69.5% higher body weight at 12 months went hand in hand with the usual laziness (-25% activity) of people whose brains are starving in abundance (e.g. type II diabetics).
  
  What remains to be seen, though, is whether similar effects would occur in response to "regular" non-insulin induced hypoglycemia. In view of the easy with which crash dieters and people with roller-coaster blood glucose levels gain weight, it is yet not unlikely that it is actually the avoidance of (reactive) hypoglycemia and not so so much the prevention of hyperglycemia that makes low GI diets successful for weight maintenance (for weight loss the picture is more complicated, since this will require a energy deficit and that's a game changer).

• Dietary glycemic index and load are not associated with type II diabetes risk in 12,403 Europeans (Sluijs. 2012) -- Apropos GI, scientists from the University Medical Center in Utrecht did not find statistical significant correlations dietary glycemic index and/or glycemic load and the risk to develop type II diabetes in in a subcohort of the European Prospective Investigation into Cancer and Nutrition Study (n = 12,403 participants).
  
  Even when they compared participants in the highest and lowest quantiles, the increase in risk was only 5% and 7% for GI and GL respectively. Since this is by no means the first study that suggests that the still propagated concept of the beneficial health effects "low GI diets" is faulty, I would suggest you rather watch the actual food items, than their respective glycemic indexes if you intend to ward off obesity and diabetes. Potatoes for example may have a high GI (including sweet potatoes, by the way), but their high potassium and overall mineral content, as well as the mere fact that you can hardly eat the same amount of total carbohydrates you can easily annihilate, when you are eating pasta still makes them one of the best sources of starchy carbs you have (learn more in the Potato Manifesto, Part I & II).

• 

  Figure 1: There were no statistically significant difference in terms of weight gain or loss, but the 2-week re-feed had a greater impact on blood glucose and insulin levels in the high GI group (Lagerpusch. 2012)

  There is use for the GI on a bulk or after a diet, but only if you are concerned about insulin sensitivity (Lagerpusch. 2012) -- While the general value of the GI as a means to distinguish good from bad carbohydrate sources is certainly questionable, the recently published results from a study that was conducted at the Institute of Human Nutrition and Food Science, of the -Albrechts University in Kiel, Germany, does suggest that monitoring the GI of your diet and adding additional fiber to reduce the insulin response to your meals can come quite handy, in phases, where you are particularly prone to store body fat. On a bulk, for example, or even more so when you have been dieting and are trying to return to a normal caloric intake.
  
  According to the results Lagerpusch et al. present in the November issue of the British Journal of Nutrition even healthy young men who were subjected to a 3-week diet phase (-50% in caloric intake) and subsequent overfeeding (+50% in caloric intake) the subjects in the high GI study arm had a 135% higher increase in fasting insulin levels during the refeed than those in the low GI group. In view of the fact that the glucose clearance (measured in an oral glucose tolerance test) was identical, it is not only no wonder that the weight gain did not differ either (see figure 1), but also unlikely that we would see significant differences as far as the fat gains are concerned (the latter were unfortunately not measured in the study at hand). At the same time, longer hyper-caloric high GI diets are certainly a risk factor for both insulin resistance and obesity, so that you are probably still at lower risk with 65g instead of 27g of fibre per day and a mean GI of 40 vs. 74.
  
  If you are interested in the influence of different diets on weight gain and health during overfeeding, I suggest you check out the following two SuppVersity posts: "194 Bananas in Three Weeks" and "A Tale of Macro- and Micronutrient Modifications".

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  Figure 2: Chronic mild stress leads to an overactivation of the HTPA and subsequen metabolic dysregulations (Takahashi. 2012)

  Further evidence that chronic mild stress is to blame for the obesity pandemic (Takahashi. 2012) -- As researchers from the Tohoku University Graduate School of Medicine in Japan report in the latest issue of the  American Journal of Physiology - Endocrinology & Metabolism, the localized re-setting of the clock genes in the liver, yet not the hypothalamic suprachiasmatic nuculeus (SCN), of BALB/c mice in response to chronic mild stress exposure elevated and phase-shifted serum corticosterone levels (see figure 2).
  
  Takahashi et al. argue that the observed changes are indicative of an overactivation of the HPA axis, which induced disturbances in the rhythmic expressions of core clock genes, e.g. Clock, Npas2, Bmal1, Per1 and Cry1 in the liver and subsequently circadian patterns of glucose and lipid metabolism-related genes such as the proliferator activated receptor (PPAR) family which favor the storage and hamper the oxidation of fatty acids.
  
  If you want to learn more about clock genes and how you can modify them, (re-)read the SuppVersity Circadian Rhythm Series!

• Scientists develop improved formula to calculate the resting energy expenditure of diabetics (Ikeda. 2012) -- While I would hope that you don't belong to the group who would have to use the new and improved formula scientists from the Department of Diabetes and Clinical Nutrition at the Kyoto University in Japan have now proposed, you may have clients or relatives who could benefit from its high predictive validity (78% +/- 103kcal vs. 50% for Harris-Benedict; 38% for Oxford, 42% for Liuand 63% for Ganpule):
  
  
  What you should keep in mind though, is that this equation was tested on Japanese individuals. Since we know from other studies that there are certain metabolic differences between people with different ethnic backgrounds I would remain a "healthy skeptic" as far as the outcomes of this equation are concerned - the same obviously goes for any other equation, e.g. the ones for athletes I provided in part III of the Female Athlete Triad series.

• 

  If you are interested in ways to modulate your leptin levels that may facilitate weight gain, I suggest you take a look at my second "Carbs Past 6PM Won't Make You Fat" post.

  Leptin induced weight gain? 13% more body fat in 2 weeks, when it hits the wrong part of the brain (Harris. 2012) -- With the mixed results from intervention trials, the enthusiasm around leptin has abated over the past months, the general consensus is yet still that leptin and leptin resistance loom large in the metabolic dysregulation that's at the heart of the diabesity pandemic. Against that background, the results Ruth B.S: Harris presents in her latest paper in the American Journal of Physiology - Endocrinology & Metabolism are unquestionably surprising.
  
  When Harris injected twice the amount of leptin (0.6 µg leptin/day) that had previously been shown to decreased 24 food intake, body fat and lean tissue, when it was injected into the third ventricle of the hindbrain, into the fourth ventricle of her lab rats, the rodents gained an almost incredible amount of 13% body fat within only 2 weeks! And that in the absence of statistically significant change in daily food intake, suggests an "increase in efficiency of energy utilization" (Harris. 2012). Fortunately, further experiments showed that the pro-obesogenic effects of leptin in the 4th ventricle was antagonized when both the 3rd and the 4th ventricle were exposed to leptin. In this scenario the leptin exposure of the 4th ventricle did even protect the lean mass of the rodents from the negative effects the exclusive exposure of the 3rd ventricle had. Overall, the study is yet somewhat chaotic and a clearcut message aside from "look people things are even more complex than we already thought", is probably not going to contribute to a solution of the obesity dilemma in the near future. 

There are, as usual more news on Facebook, some of them, such as the relation between hypothyroidism during pregnancy and the diabetes risk of the offspring later in life, are even related to the topic at hand. And if that's nothing you are interested, you may want to read about ...

• the non-existent effects of coffee consumption before bed on the sleep quality of habitual coffee drinkers (read more),
• the problem with inaccurate vitamin D tests and the absence of a reliable and scientifically sound definition of "vitamin D deficiency" (read more), or
• the strength promoting in-vitro effects of sodium bicarbonate, or in other words, a rather alkaline milieu on muscular force production (read more)

... and if neither of those can satisfy your thirst for more information from the realms of exercise and nutrition sciences, you can still wait for the next serving of facebook news or tomorrow's SuppVersity article :-)


References:

• Harris RB. Leptin-induced increase in body fat content of rats. Am J Physiol Endocrinol Metab. 2012 Dec 4.
• Ikeda K, et al. A new equation to estimate basal energy expenditure of patients with diabetes. Clinical Nutrition. 2012 [article in press] 
• Lagerpusch M, Enderle J, Later W, Eggeling B, Pape D, Müller MJ, Bosy-Westphal A. Impact of glycaemic index and dietary fibre on insulin sensitivity during the refeeding phase of a weight cycle in young healthy men. Br J Nutr. 2012 Nov 28:1-11.
• McNay EC, Teske JA, Kotz CM, Dunn-Meynell A, Levin BE, McCrimmon RJ, Sherwin RS. Long-term, intermittent, insulin-induced hypoglycemia produces obesity without hyperphagia or insulin resistance: a model for weight gain with insulin therapy. Am J Physiol Endocrinol Metab. 2012 Nov 20.
• Sluijs I, Beulens JW, van der Schouw YT, van der A DL, Buckland G, Kuijsten A, Schulze MB, Amiano P, Ardanaz E, Balkau B, Boeing H, Gavrila D, Grote VA, Key TJ, Li K, Nilsson P, Overvad K, Palli D, Panico S, Quirós JR, Rolandsson O, Roswall N, Sacerdote C, Sánchez MJ, Sieri S, Slimani N, Spijkerman AM, Tjønneland A, Tumino R, Sharp SJ, Langenberg C, Feskens EJ, Forouhi NG, Riboli E, Wareham NJ; on behalf of the InterAct consortium. Dietary Glycemic Index, Glycemic Load, and Digestible Carbohydrate Intake Are Not Associated with Risk of Type 2 Diabetes in Eight European Countries. J Nutr. 2012 Nov 28.
• Takahashi K, Yamada T, Tsukita S, Kaneko K, Shirai Y, Munakata Y, Ishigaki Y, Imai J, Uno K, Hasegawa Y, Sawada S, Oka Y, Katagiri H. Chronic mild stress alters circadian expressions of molecular clock genes in the liver. Am J Physiol Endocrinol Metab. 2012 Dec 4.