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.

"An Apple A Day" & More: Alex Leaf's Reviews Folk Wisdom and Scientific Evidence on a Forbiddenly Healthy Fruit Item

Forbidden fruit or not: You got to love your daily apples ;-)

Guestpost by Alex Leaf

An apple a day keeps the doctor away. I’m sure you’ve heard this before. And while there are many ways in which we could keep the doctor at bay with an apple (target practice anyone?), our wellbeing demands we eat the luscious fruit. Truthfully, the old adage could not be truer for a variety of reasons. So to keep things organized I am going to worm through the benefits of apples categorically. Also remember we are dealing with the apple fruit, not the apple fritter or apple flavored candy or the iPhone.

I suppose the best starting point is the apple’s nutritional worth. As you can see in the nutritional label to the right, a single medium apple is less than 100 Calories and provides over 10% of the RDA for fiber. Apples also contain every vitamin needed by the body with the exception of Vitamin B12, which is only found in animal products, and Vitamin D, which you can produce by eating your apple under the sun. The same applies to minerals, with apples providing a little of everything except selenium.

A hearty bite for a healthy heart

If you have ever looked at an apple you may have noticed it resembles the humble heart, and for good reason. A comprehensive review of nine human studies conducted by researchers at the British Nutrition Foundation in London examined the effects of apples on cardiovascular disease risk factors and found that apple polyphenols, a type of antioxidant, have a positive influence on blood lipids and blood pressure in human beings (Weichselbaum, Wyness and Stanner 2010). Furthermore, don’t think that apple juice has you covered, since these compounds are most concentrated in the peel of the apple (Wolfe, Wu and Liu 2003). In fact, whole apples have an average of 57 times more polyphenols than commercial apple juice (Hyson 2011; cf. Figure 1).

Figure 1: Phenols in whole apples vs. juices (Markowski. 2005)

Not for juicers (addendum by Adel)! I won't tire and repeat it once again. If you want to eat fruit, do so - EAT it, don't juice it, or buy juices from the supermarket. Why? Just take a  look at the phenol loss in juices in Figure 1 and you have your answer.

I know that some of you are juice-o-holoics, so in case you still insist on juicing, keep the pomace and throw away the juice, not the other way around ;-)

Okay, so heart health is from the antioxidants in apples and I can get those in any fruit or vegetable. Well, not quite. In one study of nonsmoking healthy middle-age adults who ate apples less than twice a month, simply eating one apple per day lowered blood levels of oxidized LDL – a substance linked to hardening of the arteries – by 40% (Ohio State University 2012). And it’s not just because of the polyphenols either, since a group in this study that took a polyphenol supplement instead of eating the apple had similar but not as pronounced effects. Even dried apples show promise, with a separate study concluding that daily dried apple consumption “can significantly lower atherogenic cholesterol levels” (Chai, et al. 2012). The only caveat is that you need to eat the equivalent of two apples per day if dried rather than fresh.

Apples can help with weight management and protect against cancer

In a very recent study, researchers from the University of Navarra in Spain sought to determine the mechanisms through which the beneficial effects of apple polyphenols act on diet-induced obesity (Boqué, et al. 2013). Overall, they found that apple polyphenols exerted potent anti-obesity and anti-diabetic effects through prevention of fat cell growth, decreased intestinal glucose uptake, and increased fat breakdown. These effects were observed at both the surface and genetic level. The researchers even conclude their study with the acknowledgement that apple polyphenols can act “as a promising functional food ingredient for the management of obesity and its metabolic complications”.

Figure 2: Vitamin & Mineral content of one large apple relative to RDA. Data based on USDA food database for 09003, Apples, raw, with skin (USDA. 2013) - left;  Nutritional label of one raw apple with skin - right (skipthepie.org. 2013)

A review summarizing the current knowledge on potential cancer preventive effects of apples conducted by a lone researcher at the German Cancer Research Center in Germany found that apples influence multiple mechanisms relevant for cancer prevention on the genetic level, and regular consumption of one (or more) apple per day has been shown to prevent skin, breast, and colon cancer (Gerhauser 2008). And it all comes back to the whole fruit, with some of the most potent anti-cancer compounds residing in the peel (Cornell University 2007).

Apples can do even more!

The antioxidants in apples have been shown to extend the average lifespan of fruit flies by 10% (American Chemical Society 2011). Granted the relevance to humans is debatable, but it’s interesting nonetheless. Apple polyphenols may even provide protection against some autoimmune diseases such as ulcerative colitis and Crohn’s disease (Federation of American Societies for Experimental Biology 2011). Another unique compound found in apple peels, ursolic acid, prevents muscle loss during illness and aging, and “animals given ursolic acid also became leaner and had lower blood levels of glucose, cholesterol and triglycerides” (Cell Press 2011).

And it doesn’t end there. In a review and analysis of apples and related compounds, Dianne Hyson (Hyson 2011) from the Department of Family and Consumer Sciences, California State University concluded that, There are current data suggesting that [apple polyphenols] might be linked to reduced risk of several forms of cancer, cardiovascular disease, and asthma. [Apple polyphenols] may also have beneficial effects on outcomes related to Alzheimer’s disease, cognitive decline of normal aging, diabetes, weight management, bone health, and gastrointestinal protection from drug injury.

Red Delicious is king, when it comes to its antioxidant power.

Talk about natural medicine! While everyone has their own apple preferences, some of us may want to know how to capitalize on this apple investment. If that’s the case, then I present the Red Delicious apple. Studying the antioxidant amounts of every apple variety would be difficult, but less broad comparisons have been done. One of these studies looked at eight popular apple varieties grown on the same farm under similar conditions and found that the Red Delicious had the most antioxidant activity (American Chemical Society 2005).

This makes sense when you think back to “eating the rainbow” in fruits and vegetables, since the above study also found the antioxidants to be five times higher in the skin than the flesh of the apples, and Red Delicious apples are renowned for their seductive red coating. It’s also better to go organic with this one as organic apples have on average higher antioxidant capacity than their conventional counterparts (Stracke, et al. 2009). So if you ever needed more reasoning for heading down to farmer Joe…

Oh, and before I forget. Apples are harvested in the fall, which makes local organic difficult to find during other times of the year. Usually, a bunch of apples will be picked and stored through the winter until the next harvest. Fret not, since “long-term storage, both at refrigerator temperature and under controlled atmosphere conditions, was found not to influence flavonoid concentration or antioxidant activity” (van der Sluis, et al. 2001) of the apple.

Emotional Eating

Have your head in the clouds from choosing to eat that apple with lunch? I’m not surprised, given that recent research has shown that eating fruit and vegetables may promote emotional wellbeing (White, Horwath and Conner 2013). More specifically, “on days when people ate more fruits and vegetables, they reported feeling calmer, happier and more energetic than they normally did" (IANS 2013). Even just eating apples in everyday life has been shown to reduce hunger and elevate mood (Macht and Dettmer 2006). Eating more apples isn’t challenging either. Actually, it’s as simple as buying a new fruit bowl. People are more likely to eat apples when they are visible and easily accessible (Privitera and Creary 2012). So keep your fruits close, and your apples closer. Especially during stressful times, as you may find yourself a little less anxious (Hyson 2011).

Promise me! Never throw away the pomace, if you insist on juicing your apples, then keep the pomace in whatever the result may be. This is where all the good stuff is and this is what made the difference between a 5% reduction in type II diabetes risk for apple eaters and a 8% increase in type II diabetes risk for apple (and other) juice drinkers in a recent analysis of three prospective longitudinal cohort studies by Muraki et al. (2013).

Bottom line (by Adel): If you are not convinced of the benefits of apples (not Apple!), yet, you may want to have a parting look at a study that made a direct comparison between statins and apples with respect to their cardio- and stroke-protective effects in otherwise healthy adults over 50 years.

The results of the model the scientists fed with data from previous studies are quite astonishing: With a assumed compliance of 70% compliance in the "an apple a day" arm of the study, the scientists except a reduction in vascular mortality of 12%. Now, allegedly that's based on the estimate that this would be the necessary consequence of the "apple-induced" reduction in low density lipoprotein... but alas, it's better than the hilarious and obviously 100% irrelevant witch-hunt on apples and other "high fructose fruit items" *rofl* - I mean, I find it "lustig" (German word for "funny") that people believe that someone would develop diabetes & NAFLD from eating whole apples.

References:

• American Chemical Society. Eating apples extends lifespan of test animals by 10 percent. March 8, 2011. http://www.sciencedaily.com/releases/2011/03/110302121702.htm (accessed May 13, 2013). 
• —. Red Delicious, Northern Spy Apples Have Most Antioxidants, Chemists Find. May 23, 2005. http://www.sciencedaily.com/releases/2005/05/050523234141.htm (accessed May 16, 2013). 
• Boqué, Noemi, et al. "Prevention of diet-induced obesity by apple polyphenols in Wistar rats through regulation of adipocyte gene expression and DNA methylation patterns." Molecular Nutrition & Food Research, 2013: [ePub ahead of print].
• Cell Press. Apple Ingredient Keeps Muscles Strong: Component of Apple Peels Found to Help Prevent Muscle Weakening in Mice. June 7, 2011. http://www.sciencedaily.com/releases/2011/06/110607131718.htm (accessed May 13, 2013).
• Chai, S C, S Hooshmand, R L Saadat, M E Payton, K Brummel-Smith, and B H Arjmandi. "Daily apple versus dried plum: impact on cardiovascular disease risk factors in postmenopausal women." J Acad Nutr Diet 112, no. 8 (2012): 1158-1168.
• Cornell University. An Apple Peel A Day Might Keep Cancer At Bay. June 3, 2007. http://www.sciencedaily.com/releases/2007/06/070601181005.htm (accessed May 13, 2013).
  Federation of American Societies for Experimental Biology. Scientists discover anti-inflammatory polyphenols in apple peels. December 15, 2011. http://www.sciencedaily.com/releases/2011/11/111130100455.htm (accessed May 13, 2013).
• Gerhauser, Clarissa. "Cancer Chemopreventive Potential of Apples, Apple Juice, and Apple Components." Planta Medica 74, no. 13 (2008): 1608-1624.
• Hyson, Dianne A. "A Comprehensive Review of Apples and Apple Components and Their Relationship to Human Health." Advances in Nutrition 2, no. 5 (2011): 408-420.
  IANS. Eating fruits, vegetables linked to emotional well being. January 30, 2013. http://cooks.ndtv.com/article/show/eating-fruits-vegetables-linked-to-emotional-well-being-321793 (accessed May 16, 2013).
• Macht, M, and D Dettmer. "Everyday mood and emotions after eating a chocolate bar or an apple." Appetite 46, no. 3 (2006): 332-336. 
• Markowski, J., W. Plocharski, and M. Mieszczakowska. "Effect of cultivar and processing on phenolics and antioxidant activity of apple products." I International Symposium on Human Health Effects of Fruits and Vegetables 744. 2005.
• Muraki, Isao, et al. "Fruit consumption and risk of type 2 diabetes: results from three prospective longitudinal cohort studies." BMJ: British Medical Journal 347 (2013).
• Nutritional Info: Raw Apple with skin. 2013. http://skipthepie.org/fruits-and-fruit-juices/apples-raw-with-skin/?weight=182 (accessed May 2, 2013). 
• Ohio State University. An apple a day lowers level of blood chemical linked to hardening of the arteries, research suggests. October 2, 2012. http://www.sciencedaily.com/releases/2012/10/121002143220.htm (accessed May 13, 2013).
• Privitera, G J, and H E Creary. "Proximity and Visibility of Fruits and Vegetables Influence Intake in a Kitchen Setting Among College Students." Environment and Behavior, 2012.
  Stracke, B A, C E Rüfer, F P Weibel, A Bub, and B Watzl. "Three-year comparison of the polyphenol contents and antioxidant capacities in organically and conventionally produced apples ( Malus domestica Bork. Cultivar 'Golden Delicious')." J Agric Food Chem 57, no. 11 (2009): 4598-4605.
• U.S. Department of Agriculture. "USDA National Nutrient Database for Standard Reference, Release 26." 2013.
• van der Sluis, A A, M Dekker, A de Jager, and W M Jongen. "Activity and concentration of polyphenolic antioxidants in apple: effect of cultivar, harvest year, and storage conditions." J Agric Food Chem 49, no. 8 (2001): 3606-3613. 
• Weichselbaum, E, L Wyness, and S Stanner. "Apple polyphenols and cardiovascular disease – a review of the evidence." Nutrition Bulletin 35, no. 2 (2010): 92-101.
• White, Bonnie A, Caroline C Horwath, and Tamlin S Conner. "Many apples a day keep the blues away – Daily experiences of negative and positive affect and food consumption in young adults." British Journal of Health Psychology, January 2013.
• Wolfe, Kelly, Xianzhong Wu, and Rui Hai Liu. "Antioxidant Activity of Apple Peels." J. Agric. Food Chem 51, no. 3 (2003): 609-614.

Fructose-Nation: No Change in Fructose Availability in the US Since the Early 1970s. So Why Are We Fat, Then?

From fat to Fructose - just another scapegoat for a fundamental problem?

Over the past 5 years or so, the idea that that fructose is to blame for the ever-increasing rates of diabesity has become so popular that hypotheses such as "the fructose consumption has exploded over the past decade" are usually accepted as scientifically verified facts.

A recent paper from the Department of Nutrition and Health Sciences at the University of Nebraska did now remind me that not all things that appear logical and consistent with our believes are necessarily true.

Do we even consume that much fructose?

As Trevor J Carden and Timothy P Carr point out, "the consumption pattern of fructose and other key nutrients" in the past 4 decades, "remains a topic of debate" (Carden. 2013). To determine whether fructose consumption in the US has increased sufficiently to be a casual factor in the rise in obesity prevalence Carden and Carr analyzed the USDA Loss-Adjusted Food Availability Database.

The researchers found that the food availability of glucose and fat, but not fructose, increased in the US between 1970 and 2009.

To calculate the percent change in energy from food groups and individual nutrients, Carden and Carr started initially compiled the available data on the per capita loss-adjusted food availability for 132 individual items were. In a second step they analyzed the corresponding nutrient profiles and used their findings to determine the availability of energy as well as macronutrients and monosaccharides during the years 1970-2009. By comparing the values for a given year to the baselinen in 1970, they did eventually determine the percent change in energy from food groups and individual nutrients.

Figure 1: Change in food energy availability per capita, 1970-2009 (Carden. 2013)

If you take a glance at the data in Figure 1 it's easy to see that their findings indicate that during this 40 year period the total energy availability increased by +10.7%. In that, the main "offenders" were grains and oils, the net change in total fructose availability, on the other hand was 0% - in other words, the added sweeteners (1%) were not even fructose based. Furthermore, Carden and Carr observed that the ...

"[e]nergy available from total glucose (from all digestible food sources) increased 13.0% [and ended up being] more than 3-times greater than fructose." (Carden. 2013)

With 14.6%, the amount of fat increased to a very similar extend as that of glucose. That's a 3x higher increase than for protein (+4.7) and am 1.6x higher increase in energy availability than for carbohydrates ,in general (+9.8).

So, it's the fat and sugar that's to blame? Not the fructose?

Despite the fact that I am not particular fond of the "fructose theory of everything evil", I believe that we got to be cautious about the significance of Trevor J Garden's and Timothy P Carr's conclusion, that their data would "suggest" that fructose is "unlikely to have been a unique causal factor in the increased obesity prevalence". If you take a look at the supplemental data they provided you will find, that their list of 132 foods used to calculate USDA food availability, i.e.

• Head Lettuce
• Kale
• Lima Beans
• Whole flavored milk
• Buttermilk
• Lowfat flavored milk
• Plain 1-percent milk
• Plain 2-percent milk
• Skim milk
• Eggnog and Half and Half (dairy and fat share of)
• Sour cream
• Yogurt
• Cheeses
• Lowfat cottage cheese
• Reg. cottage cheese
• Frozen yogurt and other misc
• Ice cream
• Lowfat ice cream
• Condensed bulk and canned skim milk
• Condensed bulk whole milk
• Condensed canned whole milk
• Dry buttermilk
• Dry whole milk
• Nonfat dry milk
• Barley products
• Corn flour and meal
• Corn hominy and grits
• Corn starch
• Durum flour
• Oat products
• Rice
• Rye flour
• White and whole wheat flour
• Beef
• Lamb
• Pork
• Veal
• Chicken
• Turkey
• Fish and Shellfish
• Eggs

• Great N. Beans
• Butter
• Edible beef tallow
• Lard
• Margarine
• Other edible fats and oils
• Salad and cooking oils
• Shortening
• Beer
• Wine
• Distilled Spirits
• Garlic
• Frozen Veggies
• Mushrooms
• Mustard Greens
• Navy Beans
• Okra
• Onions
• Canned Veggies
• Other Dry Beans
• Peas and Lentils
• Pinto Beans
• Potatoes
• Pumpkin
• Radishes
• Red Kidney Beans
• Lettuce
• Snap Beans
• Spinach
• Squash
• Sweet Corn
• Sweet Potatoes
• Tomatoes
• Turnip Greens
• Peanuts
• Tree Nuts
• Coconuts
• Refined sugar
• Dextrose
• Glucose
• HFCS
• Edible syrups
• Honey
• Plain whole milk
• Green Peas

• Collard Greens
• Avacado
• Bananas
• Blackberries
• Blueberries
• Canteloup
• Cherries
• Cranberries
• Dates
• Figs
• Grapefruit
• Grapes
• Honeydew
• Kiwifruit
• Lemons
• Limes
• Mangos
• Olives
• Oranges
• Frozen Berries
• Papayas
• Peaches
• Pears
• Pineapple
• Plums and Prunes
• Raisins
• Raspberries
• Stawberries
• Tangerines
• Watermelon
• Artichokes
• Asparagus
• Bell Peppers
• Black Beans
• Broccoli
• Brussel Sprouts
• Cabbage
• Carrots
• Cauliflower
• Celery
• Cucumbers
• Eggplant
• Apples
• Apricots
• Chili Peppers
• Escarole & Endive

... is representative of the variety of foods US citizens eat, but it does not tell you which of these foods, they will eventually select. Let's take apples, coconuts, and white and whole wheat flour as an example triplet. I guess if you had to rank them according to their contribution to the total energy intake of the average US citizen, none of you would hesitate to give me an answer like this: "White and whole wheat flour > apples > coconuts". Without the corresponding "weights" that would tell the scientists that white and whole wheat flour has a 10x higher impact on the average macronutrient composition of the average American diet, we be talking about the nutrient and fructose availability, not the actual intakes.

Better treat the data with the appropriate caution

Unfortunately, the scientists provide only rudimentary information about the impact of food choices, i.e. how much of the items listed above, the average US citizen actually consumes, namely:

• The food categories that increased the most during this time were grains and fats/oils, having increased 24.2% and 25.3%, respectively. 
• Caloric sweeteners (including both sucrose and HFCS) increased a modest 1.3%. 

With respect to the sweeteners Carden and Carr emphasize that the "sugar" availability, or as they put it the "monosaccharides available for metabolic absorption" is more than 3x higher than that of fructose.

In other words: Despite the fact that fructose appears to have become ubiquitous, overeating on plain sugar is still 3x easier. That this does not imply that you cannot do so, is the main and in my humble opinion crucial problem Carden and Carr fail to address. The result of their study do after all not exclude that a significant parts of the US population increased their fructose intake, in spit of the fact that its availability remained essentially the same.

The availability of a given nutrient on the shelves of US supermarket may provide a realistic image of the diets of a society of identical clones, who wheel their carts back and forth through the whole supermarket and buy foods from all each and every shelf. The "real" American, however, is no clone. On the contrary! He has his preferences and for a large part of the society these preferences can be found in the "highly processed, high sugar, high fat"-shelves of the super market. He does not care about the coconuts, apples, kale, mushrooms, olives and all the other foods in the "whole foods" section of the supermarket. They are available, but not what he is looking for.

Figure 2: The increase in total energy intake is one of the most fundamental contributers to the obesity epidemic (adapted from Carden. 2013)

Bottom Line: Despte the disconnect between availability and consumption you will be hard pressed to debate the scientists' conclusion that "increased total energy intake, due to increased availability of foods providing glucose (primarily as starch in grains) and fat" are the major contributors to the increased obesity in the US.

What is annoying, though, is the fact that a vast majority of the researchers fails to realize that their studies already account for the obesogenic effects of nutrient density. The average "high fat diets are bad for ..." is after all based on experiments, where animals or humans are fed diets that are high in both fat and carbohydrates.

Despite the fact that these studies provide a realistic portrayal of the average Western diet, the messages people infer, when they read about these results in the mainstream media is flawed.

It's not about eating less, fat, fructose, sugar or whatever scapegoat the author of the corresponding article believes was to blame for our misery. It's about nothing else than turning our whole way of eating upside down. It's about the right foods, not the right macros and it's about moderation and mindfulness.

References:

• Carden, T. J., & Carr, T. P. (2013). Food availability of glucose and fat, but not fructose, increased in the US between 1970 and 2009: analysis of the USDA food availability data system. Nutrition journal, 12(1), 130.

Fructose Impairs Fatty Acid Oxidation: Replacing 26g of Starch and Lactose in low GI Meal by Fructose Decreases Postprandial and Exercise Fatty Acid Oxidation by -21%

Image 1: With just bacon and eggs for breakfast you would not run the "risk" of reducing fatty acid oxidation.

A carby meal, i.e. a meal with a high amount of carbohydrates, right before workout triggers a shift in substrate utilization, i.e. the type of energy resource, your body will use to fuel the subsequent workout, from fats to carbohydrates, right!? But does it make difference whether you eat a Snickers bar or drink a can of Coca Cola, if both contained the same amount of carbs? Or, in other words, does the source and/or the glycemic index of your pre-workout meal have an impact on the respiratory quotient (RQ), which is the quotient of the amount of exhaled CO2 and inhaled oxygen, with higher RQs (towards 1.0) indicating that you are predominantly running on carbs, and low RQs (towards 0.7) indicating that you derive a greater part (not all!) of your energy from fatty acids.

Orange juice with breakfast? Better not...

The question, whether GI and carbohydrate type of a meal would have a significant impact on the postprandial glucose, lactate and free fatty acids levels, as well as the insulin response and the subsequent carbohydrate and fatty acid oxidation in the course of a low intensity 1h walk, has been bothering Feng-Hua Sun and his (or her?) colleagues from the Department of Sports Science and Physical Education at the Chinese University of Hong Kong, too. In a counter-balanced crossover design (>=7 days between trials; identical, recorded diet in the 3 days before each trial), all 10 healthy male subjects reported fasted (10-12h) at the laboratory, where they consumed one out of three meals with identical macronutrient composition, yet varying carbohydrate sources and glycemic indexes (cf. figure 1).

Figure 1: Macronutrient (in g) and ingredient composition of
the three test meals (according to Sun. 2011)

As you can see, the meals have identical caloric values and macronutrient compositions. Unfortunately, the differences between the ingredients go beyond their plain sugar vs. starch vs. fructose content. After all, spaghettis are not rice and milk is not ham ... this is a design flaw, of which I think that it impairs the significance of the results, but hey! At least the Chines have grasped the idea that calorie is not a calorie...

After all participants had finished eating their "delicious" breakfast, they remained seated for another 120min, in the course of which they had to drink 2ml of water per kg of body weight every 30 minutes "to ensure adequate hydration and balance the water content of the meals".

After these sedentary 2 hours, the subjects performed a standardized 5 min warm-up at 40%  of their individual VO2 and then completed 60 min of brisk walking at 50% of their VO2max.

Figure 2: Differential postprandial (2 hours) glucose (left) and insulin (right) response to the three test meals
(data adapted from Sun. 2011)

As you can see in figure 2, there were significant difference in the postprandial (120 min before exercise) glucose and insulin response to the different meals. Yet, while the difference between the low and high GI meals was something you should have expected, judged by the GI, the fructose enriched LGF meal should not have produced greater glucose (+63% area under the curve, cf. figure 2, left, small graph) and insulin (+62% area under the curve, cf. figure 2 right, small graph) responses than the low GI, no fructose meal, which, in fact, had a slightly lower glycemic index.

Figure 3: Postprandial (2 hours) lactate concentration in the 10 subjects after ingestion of the three test meals
(data adapted from Sun. 2011)

What is yet even more striking is the profound increase in lactate concentration during the prostprandial (not the exercise phase) in the subjects who consumed the fructose-containing meal (cf. figure 3). With +211% (lactate AUC) the postprandial lactate concentration in the LGF group is more than 3x higher than in the LG group! A clearcut sign for an increase in hepatic glycolysis and probably part of the reason that we are seeing increased carbohydrate and decreased fatty acid oxidation rates in the course of the subsequent walking exercise (cf. figure 4).

Figure 4: Postprandial, during exercise and total substrate utilization (in g) subsequent to the ingestion of the three different test meals (data adapted from Sun. 2011)

Postprandially, the increase in carbohydrate oxidation is even more pronounced in the LGF group than in the HG (sugar) group. That being said, the total reductions in fatty acid oxidation are -21% for the low GI fructose (LGI) and -23% for the high GI sugar (HG) group and thusly, within their respective statistical margins, identical!

With respect to the underlying reasons of this disadvantageous shifts in substrate utilization, Sun et al. speculate, that the mechanism

[...] behind this may be the reduced hyperglycemia and hyperinsulinaemia during the postprandial period following LGI meal consumption. [...] In addition, it is well known that insulin can suppress the lipolysis. This suppression appears to be long lasting, even when insulin concentration has returned to basal levels.

The last part, here, is of particular interest, because, obviously, after a few minutes of walking and with the increased need for carbohydrates the insulin levels of all subjects (regardless of the composition of their prior meals) dropped to levels ~2-3mU/L. Now the insulin response in the LGF group was still smaller than the one of the high GI (HG) group, so that the scientists assume that the ability of the fructose to bypass first rate-limiting enzymes of glycolosis in the liver, which renders it readily available for oxidation, must explain why the ratio of carbohydrate to fat oxidation was still similarly skewed in both, the low GI, plus fructose, and the high GI groups.

Image 2: I wonder if nutritionists will ever understand that there is difference between fructose powder (left) and an apple (right)

Although these results stand in line with the detrimental effects of fructose sweetened foods, I would still like to see two methodologically flawless studies with a) meal 1 not using different foods (I mentioned that in the 4th paragraph of this post already) and b) fructose from whole fruit and not in the form of the powdered poison Sun et al. just dissolved in water and added to their meals... and you know, in case these studies will be done - sometime in the distant future, when mainstream nutritionists will finally understand that not only is a calorie not a calorie, but that powdered fructose is also not an apple, you will read about that on the SuppVersity, first!

-16% Abdominal Fat on a Cornstarch Diet? No Problem If You Add 4 Teaspoons of Black Pepper to Your Meals!

Image 1: According to Wood et al. (1988) black pepper contains between 3-8% piperine. A teaspoon of black pepper would thus deliver have 60-160mg piperine, which would mean that you would have to swallow roughly 4 of those to get the fat loss effect (if it does translate to humans)

I don't know if you have realized it, but if you are taking any "high quality" dietary supplements, chances are that one of the minor ingredients on its label is "piperine", the alkaloid that is responsible for the pungent taste of black pepper. The reason, why manufacturers keep adding this spicy ingredient to their formulas is not its anti-oxidant potency, not its stimulating effect on the digestive enzymes of pancreas or even its ability to significantly reduce the gastrointestinal food transit time, no it is because piperine messes with the way your liver metabolizes drugs (piperine inhibits both the drug transporter P-glycoprotein and the major drug-metabolizing enzyme CYP3A4; Bardhwaj. 2002). Yet, while everybody seems to be freaking out about possible medical interactions of St. John's Wort, nobody appears to care about piperine... the credo seems to be "As long as it enhances the delivery of my curcumin it must be a good thing!" That it could as well enhance the bioavailability of a lot of other things, you'd rather have your liver clear from your system as fast as possible, is largely ignored, though.

Note: It always amazes me how scientists design their experimental diets. Usually we have those "high fat diets" that then turn out to be high fat + high carb (like 40% carb, 50% fat, 10% protein). So I was curious what a "high carbohydrate, high fat" diet (HCHF) would look like. Well, let me put it like that. I am not sure, whether the control diet that consisted of a meat-free rat and mouse feed (Specialty Feeds, Australia) that was mixed with cornstarch (yes, the devil! ;-) and water was so much "healthier" than the fattening HCHF diet where part of the cornstarch and the water was replaced with condensed milk, fructose and beef tallow... I mean, condensed milk and beef tallow do sound pretty good, and let's be honest even "normal" corn starch is probably not much better than pure fructose... what do you say? "Scientific Idiocy?" Well, I didn't say that ;-)

So far for the bad news. Now for the good one: A recent study from the University of Southern Queensland found that the addition of ~30mg piperine per kg body weight to the chow of 8-9 week old male Wistar rats, who were fed a high carbohydrate + high fat diet for 16 weeks (cf. red box above), ...

[...] reduced blood pressure, improved cardiac and liver structure and function, reduced oxidative stress, and attenuated inflammatory and metabolic changes induced by HCHF diet as compared to CS diet.

Moreover, the addition of 30mg/kg piperine (=4.86mg/kg for humans) kept the rats on the "typical Western diet" (high carbs + high fat) healthy, it also kept them reasonably lean and, more importantly, it also reduced the weight of the abdominal fat pads by -16% in the "control" (=high carb) group (cf. figure 1).

Figure 1: Changes in dietary intake and body composition of male Wistar rats receiving 30mg/kg piperine in their cornstarch (control) or high carbohydrate + high fat (HCHF); values relative to unsupplemented control (data calculated based on Diwan. 2011)

If you have a closer look at the dietary and body compositional data, I've compiled for you in figure 1, you will also realize that all that happened, although the rats who received the piperine in their chow consumed +7% (cornstarch) and +16% (HCHF) more calories than their peers. This is not only further evidence for the ludicrousness of the calories in vs. calories out hypothesis it also goes to show that the rats did not simply stop eating, because they felt that their chow was too spicy ;-)

Figure 2: Changes in inflammatory markers and anti-oxidant status of male Wistar rats receiving 30mg/kg piperine in their cornstarch (control) or high carbohydrate + high fat (HCHF); values relative to unsupplemented control (data calculated based on Diwan. 2011)

For those of you who are also interested in their health (for the general public, I often get the impression that looking good is more important for many than feeling good), it may also be worth to have a look at the changes in inflammatory markers and anti-oxidant status in figure 2. After all, the data indicates that the piperine supplemented animals exhibited statistically significant (* p<0.05) reductions in the high carb + high fat induced elevations in C-reactive protein (one of the few markers of which scientists still believe that it is a realiable predictor of heart disease), uric acid and reactive oxygen specimen. Moreover, the total antioxidant status of the HCHF + piperine fed rats improved and was not statistically different from the rats in the cornstarch group at the end of the 16 weeks treatment period.

A potential fat-burner with a bitter after taste

Although Kim et al. observed similar effects in another recent study on mice, who were fed the classic high-fat diet for 3 weeks (the study compared piperine to pipernonaline, and dehydropipernonaline, Kim. 2011), these positive results do yet still have a peppery, ahh... I mean bitter after-taste. Yes, piperine exerted beneficial effects on body composition in both groups and had ameliorated the negative effects of the high carbohydrate + high fat diet on inflammatory markers (most importantly C-reactive protein) and anti-oxidant status and thusly prevented fibrosis, inflammation, and the accumulation of mast cells in the heart and liver of the animal, BUT in view of the colorful poly-pharmacological OTC self-doctoring approaches of many of the self-proclaimed "health conscious" consumers, I am kind of worried that the addition of 400mg of piperine per day (that would be the HED for an 80kg human being) could have unpredictable consequences. That being said, I am not even convinced that we would see similarly profound effects in human studies. After all, it would not be the first "proven" fat burner that turns out to be a non-starter in human trials... if you insist on trying it, do me a favor and not mix it with a lot of other supplements or even medical drugs!

1.3g of Grape-Seed Extract Could Protect You From Oxidative Damage, Viral Infections, Obesity and Insulin Resistance, Reduce Your Heart Rate and Blood Pressure and Increase Your Nitric Oxide Production by >25%

Image 1: Bought in bulk, grape-seed extract is actually reasonably cheap... and it does not even taste as awful as some other herb / seed extracts ;-)

After initially being hailed as the yet another anti-oxidant panaceum, grape-seed extract (GSE) has been displaced by newer, fancier "superfoods" from the headlines of the major health and wellness newscasters. Therefore, even you, as a highly self-educated student of the SuppVersity could have missed out on a handful of recently released studies which reported antiviral effects of GSE (Su. 2011) and confirmed its ameliorative effect on diet-induced obesity (Ohyama. 2011) and (high) fructose-induced insulin resistance (Meeprom. 2011). Moreover, a meta-analysis of nine controlled with more than 300 human subjects and daily doses ranging from 250mg to 2,000mg of GSE, which was published in the Journal of the American Dietetic Association (Feringa. 2011), found that ...

[b]ased on the currently available literature, grape seed extract appears to significantly lower systolic blood pressure and heart rate, with no effect on lipid or CRP levels.

These results suggest that we (at least some of) the beneficial health effects that have been observed in rodent studies actually translate to human beings - something  we cannot (yet?) say for some of the next generation "panacea" ;-) This is also important in view of the significance of the results GSE-administration had on exercise-induced oxidative stress in a more recent study by scientists from the universities of Konya and Dicle in Turkey (Belviranli. 2011), which was published in the latest issue of the British Journal of Nutrition.

The experiments were carried out with 64 adult male Sprague Dawley rats who were randomly assigned to one of the following six groups:

• sedentary control (C, n=10), 
• chronic exercise control (CEC, n=11), 
• acute exercise control (AEC, n=11), 
• GSE-supplemented control (GC, n=10), 
• GSE-supplemented chronic exercise (GCE, n=11), and 
• GSE-supplemented acute exercise (GAE, n=11)

The rats in the treatment groups received a standardized GSE extract containing 54% dimeric, 13% trimeric, 7% tetrameric and <5% monomeric proanthocyanidines and undisclosed amounts of cathechines and oligomeric proanthocyanidines, at a daily dose of 100mg/kg body weight in their drinking water for 6 weeks.

Image 2: Click here to learn how to calculate human equivalent doses (HED)

Rat to human equivalent dosage calculation: If you have already read my dissertation on how to calculate the so-called human-equivalent-dose (HED), you will probably already have whipped out your calculator and are just about to type "100mg times the K-value for rats, which is 6; divided by the K-value for humans, which is 37" ... and what does your calculator tell you? Correct! The HED of 100mg/kg GSE in rats is 16.33mg/kg - in other words, if you weigh 80kg you will have to take roughly 1,300mg of grape-seed extract per day to mimic the dosage that was used in the study.

The dosage, according to the scientists, was chosen because it had elicited beneficial anti-oxidant effects in previous studies on alloxan induced diabetes (El-Alfy. 2005) and age-related oxidative damage (Balu. 2006). And, as Belviranli et al. had suspected, it exhibited similar protective effects against the oxidative stress triggered by both chronic, 5x a week treadmill exercise at 25m/min for 45 minutes, as well as, acute running on the treadmill at 30m/min until exhaustion.

Figure 1: Effects of acute or chronic exercise and grape seed extract (GSE) supplementation on plasma malondialdehyde (MDA) levels (data calculated based on Belviranli. 2011).

As you can see in figure 1, administration of 100mg/kg grape-seed extract per day augmented the beneficial effect of 6 weeks of chronic exercise on muscle MDA levels (-37% vs. -18% in the control group) and ameliorated the acute +22% increase in MDA levels due to increased lipid peroxidation during exhaustive treadmill running.

Figure 2: Effects of acute or chronic exercise and grape seed extract (GSE) supplementation on plasma nitric oxide (NO) levels (data calculated based on Belviranli. 2011).

GSE supplementation also increased the expression of nitric oxide (NO in  plasma; on average +25%) in all animals (cf. figure 2). Moreover, GSE ameliorated the increase in xanthine oxidase and adenosine deaminase activities due to acute exercise and triggered an overall increase in antioxidant enzyme activities.

So, even if your favorite anti-aging and health (onilne-)magazine or vendor appears to have forgotten about grape-seed extract. For a physical culturist like you and me, it may yet well be worth to (re-)include the extract from the seeds of the fruits of Vitis vinifera, which are a particularly rich source of vitamin E, linoleic acid and, most importantly, oligomeric proanthocyanidins, into our supplement regimen. And if the current study does not convince you, it may help, if I remind you of the 2006 study by Kijima et al. who were able to show that GSE due to its anti-aromatase activity can suppress tumor growth in a breast cancer model (Kijima. 2006) ... ah, and before I forget: don't be stupid and buy over-priced caps. Use google and find yourself a source of bulk grape-seed extract - don't worry the taste is not all too bad ;-)

Fructose as a Dieting Tool: 100g Fructose Per Day Exert Sign. Protein Sparing Effects & Ameliorate the Decline in Thyroid Hormones During Starvation Diet in the Obese

Fructose as an injectable Dieting Aid? Sounds crazy, but it works!

Would you ever have remotely considered that a high-fructose corn-syrup based sugar-sweetened beverage could help seven health obese women who are 35%-90% over their ideal weight lose weight? No, ...?

Well, honestly, me neither and if we take a closer look at the experimental design of a 1986 study by Robert A. Gelfand and Robert S. Sherwin from the prestigious Yale University, we will have to relativize the aforementioned claim. Coke alone may not do the trick. Pure fructose, if it's infused right into the bloodstream, on the other hand will "abolishes the entire hormone-substrate response to fasting, and spares body protein without raising insulin above postabsorptive levels." (Gelfand. 1986)

Learn more about fructose at the SuppVersity

Bad Fructose not so Bad, After All! Learn its Benefits.

Fructose From Fruit is NOT the Problem

Americans Don't Eat More Fructose These Days!

An Apple A Day, Keeps... & More (Guestpost)

Fructose is Not Worse Than Sugar

The Obesogenic Fructose Fat Connection

Before we are pondering the results, let's first have a closer look at the actual design of a study was conducted to "examine the influence of low-dose fructose infusion on nitrogen economy and the metabolic response to fasting in man" (Gelfand. 1986 | I know that you should do that in "man", not rodents, but that's costly and has the aforementioned limitations).

To this ends, the aforementioned overweight to obese women who were not diabetic and normal blood glucose and insulin levels, had normal thyroid and liver function and had been consuming a weight maintenance diet with at least 200g of carbohydrates per day before they were recruited for the study, were fasted for a period of 10 days (they did get a multivitamin, a folic acid and a potassium chloride tablet to eat, though ;-) and randomly divided into 2 groups using a crossover design:

• Group 1 (n = 4) received intravenous fructose during the last 3 days of the IO-day fasting period, while 
• Group 2 (n = 3) received fructose for the initial 7 days of the fast 

In all subjects, fructose was administered by continuous intravenous infusion of a 10% solution in water (American McGaw), delivering 100 g of fructose (375 kcal) per day.

Figure 1: Changes in plasma glucose and insulin (left) and active thyroid hormone T3 (right) during the fast with and without fructose (Gelfand. 1986)

As you can see in Figure 1 the first thing the fructose did was to keep the blood sugar and insulin stable and the levels of the active thyroid hormone T3 (iodothyronine) from plummeting. In addition, the levels of the glycogen liberating hunger hormone glucagon remained stable over the course of the whole study period in the fructose arm(s) of the study, while it increased by more than 80% in the women who didn't receive the fructose infusion.

Hormonal changes and real world effects!

Now hormonal changes are one thing. Real world effects which cannot always be predicted solely by endocrine parameters are yet often a whole different animal. What you would maybe have expected, though, is the decrease in ketone production during the supplement phases, which are indicative of "less starvation" (Blood beta-hydroxybutyrate is only a sign positive ketosis, when you actually eat tons of fat, not when you fast - in that case they are a starvation response; see Table 1)?

Table 1: Inhibitory Effect of Fructose on Starvation-Induced Ketosis. FFA Elevation,
Acidosis. and Hyperuricemia (Gelfand. 1986)

What you probably also expected are are the decreases in bicarbonate and increases in uric acid, of which the latter have previously been reported to contribute to the metabolic derangements that occur with high fructose intakes on top of an already obesogenic diet (Sahebjami. 1971; Nakagawa. 2006).

Figure 2: Urinary ammonium loss with sodium bicarbonate (G2) or potassium + calcium carbonate (G3) vs. no buffer (G1) on a 93g all protein starvation diet (Gougeon-Reyburn. 1991)

Did you know that the addition of sodium bicarbonate or a combination of potassium bicarbonate and calcium carbonate can "buffer" the increased acidity that occurs on very low energy diets and minimize the urinary nitrogen loss in form of ammonia (see Figure 2)? No, well... I guess it's about time you learn more about sodium bicarbonate, then ;-) It can, for example, also buffer the reduction in growth hormone production that occurs, when the acid level in your body is rising (see Figure 3 in previous article). Plus: It's obviously a neat ergogenic.

What is way more important than the previously described changes in serum parameters is the effect the infusion of fructose had on the energy expenditure, of which all of you know that it plummets, when you starve yourself. An effect that has long been touted as the main "risk factor for body-weight gain" (Ravussin. 1988) and thus unsuccessful dieting by scientists.

One of the factors that contributes to the "reduced rate of energy expenditure" is the the previously mentioned decline in thyroid hormone levels, of which you've just learned that it can be ameliorated by fructose injections (see Figure 1). Another one that is partly related to the decline in T3 is the loss of muscle mass - a process of which Byerley et al. (1996) argue showed that it does not have the protein sparing effects many people believe it would have.

Figure 3: Fructose decreases the total urinary nitrogen loss by ~40% (Gelfand. 1986).

In view of the results of Byerley & Heber's human study that investigated the metabolic effects of triiodothyronine replacement during fasting in obese subjects and found no effects when the protein intake was >70g/day (or 50g were complemented by 76g carbohydrates), it is thus much less surprising that the provision of fructose increased the triiodothyronine levels and decreased theh net urinary protein loss. A brief look at the serum amino acid levels of the subjects (not shown in Figure 3) suggests that fructose may have had a BCAA sparing effect, as well.

Bad Fructose? Increased Glycogen Synthesis, Reduced Glycemia, Higher Glucose Oxidation - When Do These Beneficial Effects Occur? And Why Don't They Prevail? | Read more!

Bottom line: Overall, it is unquestionably remarkable how effectively less than 375kcal of energy from fructose can reverse major components of the starvation response in human beings, i.e. abolishes the entire hormone-substrate response (specifically the decline in T3), spare body protein, and reduce urinary mineral (specifically sodium) loss.

Unfortunately, one very important question remains: What will happen if the fructose has to pass by the liver first, i.e. if it is ingested orally, not injected? 

The absence of corresponding research and the question, whether the same effects will be observed if small amounts of fructose are added to a saner form of "crash dieting", e.g. a protein modified fast, make the results of the study at hand interesting, but difficult to interpret.

References:

• Byerley, L. O., and D. Heber. "Metabolic effects of triiodothyronine replacement during fasting in obese subjects." The Journal of Clinical Endocrinology & Metabolism 81.3 (1996): 968-976. 
• Gelfand, Robert A., and Robert S. Sherwin. "Nitrogen conservation in starvation revisited: Protein sparing with intravenous fructose." Metabolism 35.1 (1986): 37-44.
• Gougeon-Reyburn, Réjeanne, François Larivière, And Errol B. Marliss. "Effects Of Bicarbonate Supplementation On Urinary Mineral Excretion During Very Low Energy Diets." The American Journal Of The Medical Sciences 302.2 (1991): 67-74.
• Nakagawa, Takahiko, et al. "A causal role for uric acid in fructose-induced metabolic syndrome." American Journal of Physiology-Renal Physiology 290.3 (2006): F625-F631.
• Ravussin, Eric, et al. "Reduced rate of energy expenditure as a risk factor for body-weight gain." New England Journal of Medicine 318.8 (1988): 467-472.
• Sahebjami, Hamid, and Raymond Scalettar. "Effects of fructose infusion on lactate and uric acid metabolism." The Lancet 297.7695 (1971): 366-369.