High Fructose Consumption, Inflammation Up (Bad), LDL-to-HDL Ratio Down (Good) - Is That Good or Bad for the Heart?

Remember: If anything fructose from beverages (including juices), yet not fructose from whole fruit is a problem. In fact eating whole fruits will decrease your blood lipids and high sensitivity C reactive protein (hs-CRP) inflammation markers.

Fructose is bad for you, right? Right. According to the latest study from the University of Newcastle, the consumption of only one drink containing containing 50 g of either fructose or glucose or sucrose dissolved in water will have detrimental effects on the #1 indicator of whole body inflammation, which is high sensitivity C-reactive protein (hs-CRP).

Much to the researchers surprise, though, the same amount of fructose had significant beneficial effects on the plasma lipid levels of the healthy male and female adults (n = 14) between the ages of 18-60 years who were recruited by advertisement and underwent study procedures at the Nutraceuticals Research Group Clinic rooms at the University of Newcastle in Australia.

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

Since the exclusion criteria were: diagnosed hyperlipidaemia, diabetes, gastrointestinal disorders, currently on fructose/sugar restricted diet, vegan diet or weight loss program, undergone any surgical procedure for obesity, pregnant or lactating mother, taking lipid-lowering or anti-inflammatory drugs and BMI >30kg/m², the results may well be different in "sicker" individuals, but for the guys and gals who drank the three 50g "sugar" solutions on three different occasions after an overnight fast, the "negative effects" of fructose were far from being conclusive.

Figure 1: Changes in hs-CRP, HDL and LDL in response to the ingestion of the test drinks (Jameel. 2014).

Even if you belong to the ever-increasing numbers of brainwashed fructose haters who believe that fructose and not a general overconsumption of energy was to blame for the obesity epidemic, you will have to admit that the data in Figure 1 leaves the significance of concomitant increases in hs-CRP and significant improvements in the HDL/LDL ratio, as the scientists phrase it, "to be delineated when considering health effects of feeding fructose-rich diets" (Jameel. 2014).

Apples reduce, apple juice increases hs-CRP in healthy volunteers (Ravn-Haren. 2013).

Don't mistake fruits for pure fructose: Studies indicate that a high fruit consumption is associated with reduced hs-CRP scores and a lower mRNA expression in peripheral blood mononuclear cells of some relevant proinflammatory gene markers (Oliveira. 2009; Hermsdorff. 2010). This is yet not the case for fruit juices, as you may remember from a previous SuppVersity post discussing the results of Gitte Ravn-Haren's 2013 study which showed that the intake of whole apples had beneficial, the consumption of apple juice, however, detrimental effects on plasma lipids and - as you can see in the figure to the left - hs-CRP levels of the healthy volunteers (Gitte Ravn-Haren 2013).

Well, yes, but (a) it's only an acute response and (b) while increased levels of hs-CRP have been found to be associated with heart disease (Rifai. 2001; Danesh. 2004), the same can be said for a high LDL/HDL ratio (Fernandez. 2008).

Figure 2: CRP-dependent risk levels for cardiovascular disease according to the American Hear Association.

If we also take into consideration that the baseline hs-CRP level of the subjects was 1.5mg/L and thus low to mid-range for the average Westerner (depending on his or her ethnicity | Albert. 2004), an increase of 10% to a maximal value of 1.65mg/L would not bring them to critical heights of which the Farmingham study says that they start at 3mg/L for Westerners (Wilson. 2005). That's not ana optimal level, but considering the fact that we are talking about "average Joes and Janes" who probably don't work out, eat whatever they like and give a damn about their sleep hygiene (all three factors have previously been linked to elevated hs-CRP levels) that's not astonishing and has absolutely nothing to do with the ingestion of 50g of fructose.

Furthermore, a comparison of the predictive value of different risk markers for cardiovascular disease by Folsom, et al. (2006) indicates that the hs-CRP values did not add to the prognostic value of the standard risk factors which are age, race, sex, systolic blood pressure, smoking status, diabetes and - you guessed it - total and high density lipoprotein cholesterol, which increased by almost 7% while the amount of LDL dropped by maximally 6%. Thus the LDL/HDL ratio decreased from 1.84 to 1.62. That's a 12% decrease that would be health relevant if the subjects' LDL/HDL ratio was not far away from the danger-zone (>5 | see Manninen. 1992), already. Similarly, the total cholesterol to HDL ratio dropped by -1.97 but wasn't in the danger zone before, either.

Incremental area under the curve for glucose and insulin 0-120min after consuming the test beverages (Jameel. 2014).

So what? Overall the results provide no evidence that the occasional consumption of a larg(er) bolus of fructose was unhealthier than the same amount of glucose or sucrose. If you take a parting look at the glucose and insulin response you will also see why fructose has long been haled as the "healthier" alternative to sugar for type II diabetics: there is no increase in glucose or insulin in response to the ingestion of 50g of fructose. And even the dreaded increase in triglycerides that occurs when the liver converts the fructose to fat did not occur (in fact, the levels dropped by ~4%, while they increased when the subjects consumed glucose (+11%) or sucrose (+4%).

So, if you've been drinking your first real coke of 2015 last night, don't worry. It probably didn't hurt your heart. If you plan to continue drinking 1l of the brown sugar-liquid everyday, this year, though, I would not guarantee that the extra pounds you may be gaining and the diabetes you may be developing won't have negative consequences for your heart and maybe liver health  | Comment on Facebook.

References:

• Danesh, John, et al. "C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease." New England Journal of Medicine 350.14 (2004): 1387-1397. 
• Fernandez, Maria Luz, and Densie Webb. "The LDL to HDL cholesterol ratio as a valuable tool to evaluate coronary heart disease risk." Journal of the American College of Nutrition 27.1 (2008): 1-5.
• Folsom, Aaron R., et al. "An assessment of incremental coronary risk prediction using C-reactive protein and other novel risk markers: the atherosclerosis risk in communities study." Archives of internal medicine 166.13 (2006): 1368-1373. 
• Hermsdorff, Helen Hermana M., et al. "Research Fruit and vegetable consumption and proinflammatory gene expression from peripheral blood mononuclear cells in young adults: a translational study." (2010).
• Jameel, Faizan, et al. "Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation." Lipids in Health and Disease 13.1 (2014): 195.
• Manninen, Vesa, et al. "Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment." Circulation 85.1 (1992): 37-45.
• Oliveira, A., F. Rodriguez-Artalejo, and C. Lopes. "The association of fruits, vegetables, antioxidant vitamins and fibre intake with high-sensitivity C-reactive protein: sex and body mass index interactions." European journal of clinical nutrition 63.11 (2009): 1345-1352. 
• Ravn-Haren, Gitte, et al. "Intake of whole apples or clear apple juice has contrasting effects on plasma lipids in healthy volunteers." European journal of nutrition 52.8 (2013): 1875-1889.
• Rifai, Nader, and Paul M. Ridker. "High-sensitivity C-reactive protein: a novel and promising marker of coronary heart disease." Clinical chemistry 47.3 (2001): 403-411.
• Wilson, Peter WF, et al. "C-reactive protein and risk of cardiovascular disease in men and women from the Framingham Heart Study." Archives of internal medicine 165.21 (2005): 2473-2478.

Artificial Sweetened Foods Promote, Not Hinder Fat(!) Loss. 1.2kg Body Fat in 70 Days By Eating Artificially Sweetened Products. Lower Hunger, Higher Fat Oxidation vs. Sucrose

Artificial sweeteners - Could they really be less toxic and obesogenic than half of the blogosphere has it? The study at hand suggests so, but its significance is limited..

The recently posted SuppVersity Classic "Sweet, But Not Innocent!? The Fattening Effects of the Non - Nutritive Sweeteners Erythritol & Aspartame Are On Par With Equally Sweet Sugar Water" (read more) has gotten quite some attention on Facebook, against that background I suppose that today's SuppVersity article will, once more inflame passions. The use of artificial sweeteners as dieting aids is after all highly controversial within the health and fitness community.

If you've read my previous reviews of the corresponding papers, you will yet be aware that there is not a single human study to confirm that any of the "classic" artificial sweeteners (sucralose, aspartame & co) would have negative effects on the loss of body and fat mass during dietary restriction - an still you hear and read corresponding claims on almost every virtual corner of the blogosphere.

You can learn more about sweeteners at the SuppVersity

Unsatiating Truth About Sweeteners?

Will Artificial Sweeteners Spike Insulin?

Sweeteners & the Gut Microbiome Each is Diff.

Sweeter Than Your Tongue Allows!

Stevia, Much More Than Sweet?

Sucralose Raises Cholesterol in Diabetics!?

In this respect, the latest paper by Lone B Sørensen, Tatjana H Vasilaras, Arne Astrup, and Anne Raben is no exception. What is extraordinary, though, is that it describes a relatively tightly controlled single-blind 10-week parallel design study that provides convincing evidence that the association between artificial sweetener consumption and obesity that has been observed in epidemiological studies would be a good example to explain the term "reverse causation" [fat people buy diet products vs. diet products make lean people fat].

In the said study, 24 healthy, overweight subjects had to consume a specific minimum amount of either sucrose-sweetened or artificially sweetened foods and drinks daily.

"The subjects were assigned to 3 different levels of supplements according to their initial body weight: level 1, 2, or 3 corresponding to 60–75, 75–90, and.90 kg, respectively. The minimum intake of the experimental diet was regulated by the sucrose intake and corresponded to a sucrose intake of 125 g/d (level 1), 150 g/d (level 2), and 175 g/d (level 3). This corresponded to a total EI from sucrose supplements of 2.74, 3.29, and 3.83 MJ/d, respectively."

The sweetener group received an equivalent amount (by weight) of foods and drinks, which resulted in an average EI of 694, 832, or 971 kJ/d at levels 1, 2, and 3, respectively. The artificial sweetener content of the intervention diet was 54% aspartame, 23% cyclamate, 22% acesulfame K, and 1% saccharin.

No low fat allowed: Some of the artificially sweetened products were low fat, so the subjects in the sweetener group were given additional butter or corn oil to keep the fat intake in the 2 intervention diets as similar as possible.

In the sucrose group, ~70% of the sucrose came from drinks (average: ~1.3 L/d), and ~30% came from solids foods. About 80% by weight of the supplements were beverages, and ~20% by weight were solid foods. The beverages consisted of several soft drinks and fruit juices, and the solid foods consisted of yogurt, marmalade, ice cream, and stewed fruit.

The products were handed to all participants at the University without informing them about the specific content of sucrose and artificial sweeteners in the supplemented products was unknown to the subjects - all thought, they were consuming products with artificial sweeteners. Otherwise, they were advised to to consume their habitual diet ad libitum. And guess what happened!?

Figure 1: Changes in body weight and fat mass (kg) and energy intake (in MJ) during breakfast, lunch and dinner measured on the one day all subjects had to spend in a metabolic ward (Sorensen.2014).

Yep, you already saw it, the sugar victims (sucrose sweetened products) got fat, while the subjects who had been supplied with artificially sweetened products saw small, bus significant improvements in their body composition without deliberately restricting their energy intake (Remember: all subjects thought that they were consuming zero calorie products).

The reason? Well, take a look at the left hand side of Figure 1. The subjects in the sucrose group did what some people claim would happen, if you consume artificially sweetened products: They ate more! Why? Well, because they were hungrier. Significantly hungrier; and that in spite of their 22% higher energy intake.

Figure 2: The satiety response at lunch was (non significantly) less sustained in the sucrose group (full circles) compared to the artificial sweetener group (open circles) during the subjects visit at the metabolic ward (Sorensen. 2014).

Especially after lunch, the satiety effects were significantly less sustained than in the artificial sweetener group (see Figure 2). What is interesting, though, is the fact that unlike its consequences and the perceived fullness and prospective food consumption (not shown in Figure 2), the satiety difference did not reach statistical significance.

Figure 3: 24h fatty acid oxidation after 10 weeks on diets with sucrose or artificially sweetened add-ons (Sorensen. 2014)

The data in Figure 1 did already tell you: The net effect of the satiety differences was a significantly higher energy intake (+22%) that was not fully compensated by the ca. 6% higher total 24h energy expenditure of the subjects in the sucrose group.

In concert with the reduced fatty acid oxidation rates (see Figure 3) the remaining energy surplus of approx. 1,000kcal (that's the mere mathematical difference of total 24h energy expenditure during the stay at the metabolic ward and the corresponding energy intake) was obviously more than enough to fatten the subjects up.

There is one impor- tant reason why I still recommend to be careful with any kind of sweetener (inclu- ding stevia) and that's the fact that they won't help people get rid of their extra-sweet tooth. A "tooth" which is in many cases the reason they ran into weight problems in the first place. And a tooth that is rather going to get more, not less sugar hungry if you are adding stevia, sucralose or aspartame to whatever foods you eat.

Putting the results into perspective: What this study does confirm is that artificially sweetened products can help average healthy non-dieting, non-overweight individuals lose weight. What it does not confirm is that artificially sweetened products will help obese people lose weight or ward off further weight gain in an ad libitum diet scenario such as the one at hand.

If we go one step further and extend our skepticism from a potential subject- to a potential duration-specific effect, we still don't know if the chronic consumption of artificially sweetened products wouldn't have negative effects on what some people call the "energy intake gauge". Or, put differently, whether the constant exposure to no-calorie foods with an extreme sweetness would not - in the long term - reduce the satiety the subjects in the artificial sweetener group obviously felt after consuming their diet products. If that was the case, the "energy deficit" would disappear and the short term benefits would eventually turn against you.

References: 

• Sørensen, Lone B., et al. "Sucrose compared with artificial sweeteners: a clinical intervention study of effects on energy intake, appetite, and energy expenditure after 10 wk of supplementation in overweight subjects." The American journal of clinical nutrition (2014): ajcn-081554.

Forgotten Dieting Aids: Choline, Carnitine, Caffeine and the Anti-Weight-Loss Plateau Effects of Sugar and Phosphates

I bet both Flex Wheeler (left) as well as Serge Nubret (right) still knew what choline is. Something you probably cannot say of many of today's gymrats.

In view of the fact that the brief "Oldie but Goldie" post on the efficiency of a stack of carnitine, choline and caffeine as a weight loss adjuvant on the SuppVersity Facebook Wall caught so much attention, I thought that especially those of you who have not yet "liked" the SuppVersity on Facebook and have thus missed this brief reminder of these "classic" fat loss helpers would appreciate if I devote a whole post to this issue as well as another "Oldie but Goldie", I came across recently: The anti-plateau effects of succrose (plain sugar) and phosphates during phases of (very) intense dieting.

ECA was yesterday and so was CCC ;-) 

Let's start with the CCC stack, though. In the year 2000, Hongu et al. published a paper describing a rodent experiment in which they were able to show that the combination of choline, carnitine and caffeine had similar beneficial effects on the body fat and leptin levels of sedentary rodents as exercise (Hongu. 2000).

Figure 1: Fat pad weight (in g) and serum glucose, lactate, triglycerides, free fatty acids and leptin levels expressed relative to sedentary rodents on standard chow (Hongu. 2000)

With statistically highly significant reductions in the weight of the epididymal, inguinal and perirenal fat tissue and corresponding decreases in leptin, the net fat (not simply weight!) loss the 7-wk-old male Sprague-Dawley rats exhibited in face of an unaltered basal energy intake at the end of the 5-weeks study period was yet so pronounced that the question, whether these results would be replicable and, more importantly, whether they could be reproduced in human beings should already be preying on your mind.

"So you are saying it's unlikely this will work in humans, right?"

For a follow up study, the scientists recruited 19 healthy non-obese women with no history of diabetes, or cardiovascular disease (18–54y; body weight, 47.5–92.7 kg; body mass index (BMI), 18.9–35.9kg/m²; body fat, 17.9–37.8%) and repeated the experiment (Hongu. 2003); yet with a slightly different design (see figure 2) that would allow the researchers to differentiate the individual effects of choline and carnitine - unfortunately, without the third "C", i.e. the caffeine.

Figure 2: Study design of the follow up human study three years later (Hongu. 2003).

In the absence of caffeine, the combination of choline and carnitine lost its congenial partner in crime, whose job it is to squeeze the lipids out of the fat cells (lipolysis). But that's not all, the dosages used in the human trial were also significantly lower than the human equivalents of those the rodents had coonsumed three years before (see infobox to the right of the next paragraph). With appropriately high doses, the caffeine may even not have been necessary to elicit the desired fat loss effects. What is unquestionable though is thatthe caffeine induced lipolysis would have amplified any existing effect, because you obviously need enough fatty acids to be transported to the mitochondria in order to make optimal use of the increase in oxidative capacity from the other "C"s in the CCC stack.

What we have here is not a fat loss study

What were the dosages of choline, carnitine and caffeine that were used in the studies? The human equivalent doses for the rodent study from 2000 were 98mg/kg choline, 52mg/kg carnitine and 1mg/kg caffeine. In the human study from 2003 the scientists used much lower dosages of 15mg/kg choline bitartrate and only 1mg/kg l-carnitine l-tartrate per day (!) no wonder the effects on the body composition were completely absent in the human trial.

Against that background the results of this follow up study are of greater theoretical than practical value for us, as they allow some insights into the underlying mechanisms which are responsible for the profound fat loss effects the researchers observed in the rodent trial. As far as this mechanism is concerned the researchers write in the discussion of their paper:

"The mild exercise routine enhanced fat utilization as energy substrate in both supplemented groups, but not in the placebo group [This went hand in hand with a 21–27%] loss of acylcarnitines in urine [that] has not been found in individuals subjected to low or high intensity exercise without supplement. [...] It may thus be argued that increased demand for energy by exercise in choline/carnitine-preloaded individuals increases rates of fatty acid oxidation, albeit incomplete, resulting in sustained loss of acyl groups in urine." (Hongu. 2003)

I willingly admit that this hardly sounds like an explanation, so let's briefly recap the main points.

Firstly, there is the increase in fat utilization in response to the ingestion of choline and carnitine. Secondly, therese there is the loss of acetylcarnitines, i.e. a complex of carnitine + the short-chain fatty acid acetyl in the urine of the women who participated in the study.

 "Choline promotes carnitine conservation and accretion by tissues that favor incomplete oxidation of fatty acids and disposal of fatty acid carbons in urine as acylcarnitines." (Hongu. 2003)

As the scientists point out, the reason for the latter is an incomplete oxidation of long(er)-chain fatty acids and the net result is a non-negligible loss of energy in the urine. With the addition of caffeine to the equation, the total amount of fat that is available for oxidation during exercise, but more importantly also at rest (not just during exercise) would have increased, the same would apply to the amount of fat that is shuttled into the mitochondria and the amount of fat that will leave the mitochondria only partially oxidized. And what happens if you use more stored fat and use it less efficiently? Correct! The fat depots on your hips, buttocks and abs and if you still have some, the nasty inter-organ fat will be gone faster than without the use of the "CCC" stack. Will it disappear magically overnight and without any dietary and lifestyle changes? Probably not overnight, but maybe over several weeks and months.

Add sugar & phosphate to ameliorate the downregulation of the metabolic rate on a diet

YoYo-Dieting or Constant Gluttony? What Happens During Weight Cycling? And Why Does Every Diet Make You Fatter? I have answered these and related questions in a previous blogpost, already (read more)

Sounds too good to be true? Well in a way it in fact is. After all, this requires a 100% constant food intake and presumes that your body does not adapt its caloric expenditure to achieve a new steady state. That the latter is not very realistic, is probably something many of you have already learned the hard way. after all, those new steady states are actually the underlying reasons of the nasty weight loss plateaus this 2nd part of today's SuppVersity post is dealing with.

"Sugar, orange juice, carrots, ..." does this ring a bell? Yeah, I see you have heard or read about this combination before on the Internet.  No idea yet? Well another hint, then: You usually complement those foods with egg shells, which are a good source of calcium, but not in the form of calcium phosphate, but rather as the simple white powdery calcium carnbonate and thus certainly not what the results of a 1996 study by Nazar et al. would suggest the sugars should be complemented with.

In the said study the results of which were published in the Journal of Physiology and Pharmacology 16 years ago, the researchers from the Polish Academy of Science write that the addition of a phosphate supplement containing non-disclosed amounts of calcium, potassium and sodium phosphate to a 1,000kcal, high viscose fiber diet ameliorated the diet induced reduction in basal metabolic rate in the 30 female overweight study participants (+15 / +19% depending on whether the supplement was taken from week 1-4 or week 5-8 of the 8-week dietary intervention). As Nazar et al. point out, the

"[p]hosphate supplementation ameliorated also a decrease in plasma triiodothyronine level and a decrease in thyroxine to triiodothyronine ratio. [While t]here were no differences between groups in the plasma insulin, catecholamine, growth hormone, cortisol and testosterone levels[,] plasma lipids or blood glucose concentration." (Nazar. 1996)

With the thyroid hormone concentration marking the only statistically significant hormonal difference between the supplementation and placebo phases of in the Nazar studies, the similarities to Dr. Ray Peat's previously alluded highly controversial "sugar for thyroid health protocol" should be obvious.

"Ok, but if it's phosphates instead of calcium, then it must be fat instead of sugar, right? "

Often a picture says more than 1000 words: Normal (left) and repeatedly hypoglycemic rodents (learn more about the obesogenic effects of hypoglycemia)

I bet the above question is now preying on the minds of some of you. "Sugar, really?" It may sound hilarious, but as I've pointed out several times before: An energy deficit, specifically a pronounced one, is a game changer. Things that would usually precipitate weight gain suddenly don't matter, when - at the end of the day - your body has used more energy than it has been able to acquire from the foods you  ate.

Unfortunately your body hates nothing more than having to fight to fulfill his acute energy demands by tapping into its body fat stores and will therefore after a couple of days start to save energy, this is particularly true, when your brain realizes that it's beloved glucose is becoming scarce and there is no abundance of ketone bodies to use instead.

Basically this is exactly the situation that arises on a HCG-like very low calorie (800kcal/day) high protein (95% protein, 4% fat, 1% carbohydrate) such as the one the obese women in a study by Hendler et al. were following at thne Yale Clinical Research Center in the late 1980s (Hendler. 1986). The exact study protocol was a bit complicated (and nonsensical ;-) with half of the patient starting out on what I would prefer to call a 'protein only' diet and not, as the scientists do a "high protein" diet, for 15 days followed by another 15 days on a "sucrose diet" with reversed macronutrient ratios, but identical energy content. The other half dieted for 15 days, only, on the sucrose regimen (I wonder why they did not switch those to the protein regimen afterwards...?!). And one miserable wretch "consumed the high-protein diet for 30 days to serve as a control for the sequential protein-sucrose diet"

HCG like dieting: Don't do this at home!

I guess, I don't have to mention that dietary interventions like these are meant to be used in clinical settings and in very obese individuals. So, don't be bamboozled by the 9kg of body weight the subjects lost within those 30 days and try something similarly stupid at home. Our interest in this study is merely related to the effects on the resting metabolic, which were (I will list the main effects and quote excerpts from the results):

• 

  Figure 3: Effect of the sequential protein-sucrose diet on resting metabolic rate (RMR), serum triiodothyronine (T3) and plasma norepinephrine concentra- tions (Hendler. 1986)

  significant reductions in resting metabolic rate during the protein phase: "After 15 days of the hypocaloric protein diet, resting metabolic rate decreased by 354 kcal/day, or 21 percent of control values (p < 0.01)"

• restorative effects of the sucrose diet in the subsequent 15 days: "Sucrose substitution significantly increased the resting metabolic rate (+228 kcal/day, p < 0.05) to values approaching those in the control period (p = NS)."

• metabolic shut-down in the poor wretch who followed the protein only diet for 30 days: "In contrast, the single patient given the protein diet continuously for 30 days showed a progressive decline in resting metabolic rate (2,165, 1,822, and 1,628 kilocalories per day at baseline and after 15 and 30 days of the protein diet, respectively)." 

• Plummeting levels of the active thyroid hormone T3 that were only partly restored in the sucrose phase: "Changes in serum triiodothyronine levels followed the pattern of diet-induced changes in resting metabolic rate. The serum triiodothyronine level fell by 41 percent (p < 0.02) after the protein diet and then rose (by 28 percent, p < 0.02) after sucrose substitution, reaching values intermediate between control and protein diet levels. 

• Significant correlations between the drop in T3 levels and the lowered metabolic rate: "There was a significant correlation between the changes in the serum triiodothyronine level and resting metabolic rate during the sequential diets (r = 0.701, p < 0.01).

• Only minimal signs of a reduced sympathetic tone in the protein phase, none in the succrose phase: "Supine norepinephrine concentrations were slightly, but not significantly, reduced by the protein diet (10 percent) and failed to change significantly when sucrose was substituted. 

• No correlation between epinephrine and the resting metabolic rate: "There was no correlation between changes in the supine norepinephrine concentration and resting metabolic rate."

Interestingly, no significant changes in any of the measured parameters, i.e. serum triiodothyronine (T3) levels, epinephrine and, most importantly, the reductions in metabolic rate were observed in the patients who followed the succrose diet.

---

 Does it make sense to eat carbs on a lean bulk as well, or will they just make you fat *scary sound*? Learn more in a previous SuppVersity post.

So what's the take home message, here? Don't worry, as I've already pointed out, I am neither suggesting that you should follow a pure sugar nor a 800kcal diet. And you can be sure that the negative effects on the resting metabolic rate are "diet dose depend" (meaning the harder and imbalanced you diet, the more pronounced they will be). What I am suggesting is that there is reason I keep repeating my mantra "you cannot live on protein alone", both here, as well as on the SuppVersity Science Round-Up. So if you insist on going on a "low carb diet" you better do it right and turn to a  high fat diet (<15% protein), use regular really high carb (including sugar!) refeeds or periods of normal high(-ish) carb intake to keep your metabolism chugging along nicely.

A final note on a possible CCC protocol: I actually did not want to write that down, but I know you will be asking anyways. Please keep in mind though, that I cannot tell you the optimal dose and that I have more than just second thoughts about taking high amounts of choline (see potential side effects next to the respective bullet point below).

• Max. (!) 3g choline: Take the choline (bitartrate or citrate, no funky GPC or similar junk) with meals split across the day, but refrain from taking the human equivalents (HED) from the rodent study, I suppose 3g could already make you smell like a fish. Watch out for potential side effects, such as cramps, nausea, vomiting, dizziness, high blood pressure, or acne-like skin rash. Stop the supplement immediately, if you experience any of those. Also make sure to get adequate amounts of potassium and magnesium.
• 3-5g of carnitine: Stick to the l-tartrate or regular form of carnitine. Take the carnitine in 3 doses best on empty (learn more about in the Amino Acids for Super Humans Series). 
• 200mg sevings of caffeine: Use the caffeine whenever you are fasted for at least 90min or before you are working out. Don't take more than 400mg, max. 600mg per day and - needless to say - don't take it before bed.

Again keep an eye on side effects and don't expect any miracles! This is a supplement to help you lose fat, not to make you lose fat.

Once you've got these fundamentals right you may want to consider adding in the CCC stack and a phosphate supplement to promote - not to induce - fat loss.



References:

• Hendler RG, Walesky M, Sherwin RS. Sucrose substitution in prevention and reversal of the fall in metabolic rate accompanying hypocaloric diets. Am J Med. 1986 Aug;81(2):280-4.
• Hongu N, Sachan DS. Caffeine, carnitine and choline supplementation of rats decreases body fat and serum leptin concentration as does exercise. J Nutr. 2000 Feb;130(2):152-7.
• Hongu N, Sachan DS. Carnitine and choline supplementation with exercise alter carnitine profiles, biochemical markers of fat metabolism and serum leptin concentration in healthy women. J Nutr. 2003 Jan;133(1):84-9.
• Nazar K, Kaciuba-Uściłko H, Szczepanik J, Zemba AW, Kruk B, Chwalbińska-Moneta J, Titow-Stupnicka E, Bicz B, Krotkiewski M. Phosphate supplementation prevents a decrease of triiodothyronine and increases resting metabolic rate during low energy diet. J Physiol Pharmacol. 1996 Jun;47(2):373-83.

Aspartame's Anti-Insulinogenic Effects During a Workout; Optimal Protein Intake on a Diet is Relative. Plus: Folate Fortification, Spirulia, Succinate, Sucrose, Pork Brain & the Low Cholesterol-Suicide Connection Reviewed!

Unbelievable: The results of the latest study from the University of Western Sidney appear to suggest that you could keep your insulin levels at bay, if you mixed your sugary intra-workout supplement with aspartame-laden diet coke instead of water! The mechanism that's behind this phenomenon does yet still have to be elucidated.

You may be surprised to see a long headline, a long post and a couple of bullet points: "Looks like On Short Notice, reads like On Short Notice, but is not published on Saturday? What's that?" The answer to this question is easy. Lot's of interesting stuff I have come across as of late! And while some of them, like the study on the marginal utility of higher protein intakes on a diet would actually deserve their own post, I decided to give you the "long(er) version of a short notice" in order not to miss any of them... and yes, this means there is going to be more than today's news on the unexpected anti-insulinogenic effects of aspartame, the only partly expected outcomes of the US folic acid fortification program, the aforementioned protein study, the usefulness of spirulina, succinate and sucrose supplements for athletes and physical culturists and some brainy insights into a possible connection between low cholesterol, depression and suicide risk in men and women... ah, ok I see, you are already reading the aspartame item - well, go for it!

• The astonishing anti-insulin effects of intra-workout aspartame consumption Meanwhile even bodybuilders who are injecting and "supplementing" with all sorts of unquestionably unhealthy stuff are so afraid of the hitherto still rather vaguely established pro-carcinogenic effects of aspartame that supplement companies place huge stickers on the boxes of their products saying "ASPARTAME FREE!" Now, I am pretty sure that a recently published study that was conducted by scientists from the School of Science and Health at the University of Western Sydney in Campbelltown, Australia (Siegler. 2012), won't do much about that, but you will probably have to agree that it is still remarkable, to say the least, that the co-administration of an artificial sweetener which has not produced any glucose, insulin or whatever response in previous trials (cf. "Sweeter than your tongue allows") would do that!?

  

  Figure 1: While the mechanism is still unknown and the results need to be repeated in a second experiment, there is no question that the drop in insulin during the workout (see arrow(s)) which occurred during the carbohydrate + aspartame trial in the presence of identical glucose ingestion and blood glucose levels warrants further investigations (based on Siegler. 2012)

  During the four trials, which were separated by 7-10 days of rest, the 9 healthy, recreationally active males (age: 22±2 years; height: 180±9 cm; weight: 78.6±8.5 kg; participating in regular physical exercise at least twice per week) who had volunteered for this (in the eyes of some aspartame extremists, probably unethical undertaking ;-) cycled fasted for 60 minutes in a climate controlled laboratory. The only difference between the four sessions was the "intra-workout nutrition" the participants were fed, with...
  

  1. carbohydrate - 2% maltodextrin and 5% sucrose (figure 1, C),
  2. carbs + aspartame - 0.04% aspartame with 2% maltodextrin and 5% sucrose (figure 1, CA),
  3. water - plain water, only (figure 1, W), and
  4. aspartame + malto - 0.04% aspartame with 2% maltodextrin (figure 1, A)

  As it is common practice in studies like this, "all participants were instructed to follow the same diet and training schedule for the three days prior to each experimental trial." (Siegler. 2012, my emphasis)
  The respective intra-workout beverages were to be consumed in boluses of 4ml/kg body weight before and at 15-minute intervals throughout the trial. For the CHO groups this summed up to a total carbohydrate intake of 104.4±11.3g per participant and did - probably not to your surprise - cause a corresponding increase in insulin levels... with one exception, however: the intraworkout period in the CHO + Aspartame group (figure 1, red), when the insulin level dropped, during the exercise sessions and bumped back up to the same level as in the carbs only control afterwards (see figure 1).
  As the researchers point out, we do not yet have a mechanistic explanation for this phenomenon... nor can we even be sure that this was not some sort of strange artifact, so that
  

  "the disparity between insulin levels [does not only] warrant further investigation with a larger cohort of clinically relevant subject populations (e.g. metabolic syndrome, diabetes, etc.) [, but must also] be considered when designing nutrition-based, exercise intervention studies [in the future]" (Siegler. 2012

  That this observation could actually have very practical implications, both, in view of its potentially compromising effects on blood glucose levels in diabetics, where any insulin blocking effect of aspartame would probably reduce the already compromised glucose uptake even more, as well as in view of the anti-lipolytic (=blocks the release of fat from the cells) of insulin during a workout, which could actually be blocked with a minuscule amount of aspartame ... but alas, until the results have been confirmed and the mechanism behind this effect has been elucidated, what we are doing here is more or less intellectual masturbation - nothing to feel bad about, but still not the real deal ;-)

• 

  Figure 2: This is what the USDA expected to happen - more folic acid in food = higher intake (here in the elderly) = lower homocysteine levels; the reality looked pretty different, though, at least in adolescents the folic acid intake went up, but the homocysteine levels did not go down; moreover the B12 levels have declined as well... how much of this is related to confounding factors still has to be elucidated, but as of now it does not seem as if the fortification program was the success the USDA wanted it to be (Mc Bride. 2007).

  US adolescents and their "healthy grains" are now folic acid fortified, but are they also healthier? According to a study that has just been published in the Journal of Public Health, the great idea to put another artificial vitamin into our the food chain and fortify "healthy" cereal-grain products with folic acid, was so "successful" that the average US teen (14y at the time the fortification program began, 18y now) does now have 16% higher folate and 14% higher B6 concentrations.
  Instead of the expected decrease in homocysteine levels, of which scientists still believe that it plays in imminently important role in the development of heart disease, its serum levels did likewise increase by 17%, while the serum concentrations of vitamin B₁₂ decreased by 11 % post-fortification. The additional ~118 μg folate/d the subjects ingested from the fortified food products, appeared to be particularly useless (or even detrimental?) for boys / young men whose total homocysteine (tHcy) levels increased by 24%  to a much greater extent than in the girls / young women.
  Honestly, I don't really know what to make of these results at the moment, ... at least nothing better than to shake my head over the hilariousness of trying to turn junk(-food) into (good) food by simply enriching it with artificial vitamins. On the other hand, I am happy that even Daniel A. Enquobahrie and his colleagues feel that it is "warranted to investigate the significance of these improvements in folate status on clinical outcomes, in the post-fortification era." (Enquobahrie. 2012) - and that not just because the fortification program did not produce the desired results, but also because the folic acid intake already started to exceed the RDA in many of the subjects. This, and the alarming decrease in B12 levels of which Katherine L. Tucker had cautioned in the 2007 interview with Judy Mc Bride, already, that "better diagnosis for B12 deficiency should be given high priority"(Mc Bride. 2007) do not "warrant", imho, they rather make it imperative to follow the effect of this "nationwide health program" very closely.

• 

  Figure 3: The principle of relativity for protein based body recompositioning diets - When it comes to weight los, the word "high" in high protein diets must always be seen in the context of habitual protein intake and to whom we are comparing our dieters; or put simply: The average SAD dieter benefits from every gram, the average bodybuilder will hardly benefit from the 7th whey shake.

  Effectiveness of high(er) protein diets for weight loss depends on spread / change vs. baseline not on total protein intake That's basically how you could summarize the conclusion of the latest review of the existing data on the influnece of (high) protein intakes on changes in body composition by John D. Bosse and his colleagues from the University of Utah. To find out whether either the protein change (=high protein diets are only effective when the change in protein intake from baseline to intervention is large enough) or the protein spread theory (=those dieters within a cohort with the highest protein intake will see the most beneficial changes in body comosition) could explain the different outcomes of previous studies best, the researches collected an impressive dataset comprising 51 peer-review studies the analysis of which yielded the following two main results (Bosse. 2012):
  1. The 35 successful dietary interventions had on average 58.4% higher average protein intakes than those trials in which the authors had not been able to observe an additional beneficial of going high protein over the standard calorical restriction approach
  2. The 17 successful (=greater anthropomorphic changes than with calorie restriction alone) of the 25 studies, where the baseline protein intake of the subjects was available, the increase in protein intake was 28.6% (if you ate 100g protein per day before, that would mean you would eat 128.6g while you are dieting), minimal increases in 4.7% range, on the other hand, did not provide any additional benefit over energy reduction, alone.
  Overall, the review does therefore support the original hypothesis of the researchers that there are certain thresholds which have to be surpassed before dieters will see any benefits from an increase in protein intake. This does yet also mean, that for someone who is already eating 200g of protein on a daily basis, the addition of a protein shake with 20g of protein is probably not going to make so much of a difference as it would be way below the 28.6% change in protein intake, the protein change theory would prescribe (see [2] in the list above). As a matter of fact going higher and higher (e.g. like eating 300g of protein per day), will, if anything stall, not propel your progress, after all, there will be too little room for other nutrients, when you are already getting the lions share of your daily energy intake from protein... and NO you cannot lose weight without being in a caloric deficit, even if that is not readily calculable by the idiotic "calories-in-vs-calories-out" equation.
• The BMJ Supplement Review says: Thumbs up for sucrose, thumbs down for succinate and undecided  for spirulina In installment #36 of the A-Z of Nutritional Supplement Supplements, a series dedicated to review the pros and cons of purported ergogenic aids, the authors conclude that ...

  

  Figure 4: In view of the fact that the TCA or citric acid cycle is one of the #1 aerobic source of cellular energy (APT) and succinate is one of its intermediates it makes sense that supplementation could improve exercise performance, but hitherto this has not been confirmed.

  • ...the studies on spirulina fail to "study well-trained individuals", to use appropriate standardization regimen with relevance for physical culturists and athletes, identify the active ingredients and their effect on the antioxidant status, of which the respective scientists speculate that it would be the underlying mechanism of the observed ergogenic effects on chronic low-intensity exercise regimen
  • ...the research on succinate (only) supplementation is basically non-existent and claims with respect to its permanence enhancing effects is mostly based on theoretical considerations about its role in the TCA cycle 
  • ...despite the general trend within our society, where the overconsumption of sucrose (table sugar) is one of the major offenders to public health, "there may be value in, or at least room for, its inclusion in sports products targeting the provision of carbohydrate fuel during exercise"
  Nothing exciting, but a realistic and educative analysis, which has all the classic elements you should keep in mind, whenever you try to find out whether a product is worth its money: What research is there? What are the results? Are the positive results significant for me as a person? And... in the case of succrose: Could the use of this ergogenic aid be an obstacle for another goal of mine? I mean, you can benefit from guzzling tons of sugary drinks during your workouts, but if "looking good naked" is your primary goal and your performance only a means to an end - it is probably not wise to do so ;-)

• 

  Figure 5: Suicide risk in psychiatric patients /w (SA) or w/out (PS) prev. suicide attempt and surgical control (SC) in lowest, 2nd and 3rd cmp. to highest quartiles (Olié. 2011)

  Can pork brain in milk tell us something about suicide? Those of you who are on the SuppVersity Facebook news RSS channel will already know the image on the right. I only saw it today, but as Mark mentioned on my Facebook wall, he has used it (the image not the brain) in lectures before... be that as it may, that reminded me of an older study on the highly significant correlation between cholesterol levels and suicide attempts Emilie Olié and her colleagues observed in a 2010 study on the reliability of serum cholesterol levels as a predictor of the suicide risk in 3207 subjects [510 patients with a history of suicidal attempts (SA), 275 patients with no history of suicidal attempts (PC), and 2422 surgical controls (SC); Olié. 2011].
  The exact mechanism for the highly significant increase in suicide risk, esp. among women with previous suicide attempts in the lowest (1st quartile) is still not fully elucidated, Olié et al reference previous studies which suggest that low serum cholesterol levels, a "potentialmarker of central nervous systemcholesterol", impair the serotoninergic activity and" increase impulsivity" and thus precipitate to severe depression and the tendency and ability to pot a premature end to your life.
  In view of the fact that this and similar results were derived exclusively from analysis of psychiatric patients and considering that the cholesterol levels in the SA group were already significantly lower that in the PC and SC control (178±36 mg/dL vs. 217±43 mg/dL and 219±52 mg/dL, respectively) we should be very wary of transferring these results 1:1 to the "normal" people. 

I guess this is enough for today. After all, news are not so different than protein, it's the relative intake that makes all the difference - in other words: If I keep flooding you with those awesome posts, you won't appreciate each and every of them the same way you do now... and we don't want that to happen, do we? 

References:

• Bosse JD, Dixon BM. Dietary protein in weight management: a review proposing protein spread and change theories. Nutr Metab (Lond). 2012 Sep 12;9(1):81.
• Enquobahrie DA, Feldman HA, Hoelscher DH, Steffen LM, Webber LS, Zive MM, Rimm EB, Stampfer MJ, Osganian SK. Serum homocysteine and folate concentrations among a US cohort of adolescents before and after folic acid fortification. Public Health Nutrition. 2012; 15: 1818-1826.
• Mc Bride. Foods To Be Fortified With Folic Acid. USDA ARS. News. February 7, 2007. < http://www.ars.usda.gov/is/ar/archive/jun97/folate0697.htm > retrieved on September 14, 2012.
• Olié E, Picot MC, Guillaume S, Abbar M, Courtet P. Measurement of total serum cholesterol in the evaluation of suicidal risk. J Affect Disord. 2011 Sep;133(1-2):234-8.
• Siegler J, Howell K, Vince R, Bray J, Towlson C, Peart D, Mellor D, Atkin S. Aspartame in conjunction with carbohydrate reduces insulin levels during endurance exercise. J Int Soc Sports Nutr. 2012 Aug 1;9(1):36.
• Zemski AJ, Quinlivan RM, Gibala M, Burke LM, Stear SJ, Castell LM. A-Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance: Part 36. Br J Sports Med. 2012 Sep;46(12):893-4. 

Fructose Epimer D-Psicose Could Be First Sweetener to Actively Promote Weight Loss: Reduced Weight Gain and Direct Inhibitory Effect on Adipocyte Maturation in Rodent + Reduced Postprandial Glucose & Insulin in Human Trial

Image 1: No, just a few grams of d-psicose won't turn these into a "health food", but it could help ameliorate the "damage"

Good news for everyone with a sweet tooth! Right after stevia has finally made it to the European market, the next 1/2 natural sweetener is at the ready. It's called d-psicose and it is a cousin of fructose that is yet only 70% as sweet as sucrose (fructose is +20% sweeter than sugar) but has only 0.3% of its energy content. In other words on a per calorie base it is 233x sweeter than sugar. That alone would however hardly justify an individual blogpost. What is yet exciting about this molecule is that a recently published rodent study does suggest that it can inhibit adipocyte maturation and thusly exerts direct anti-obesity effects.

The first sweetener that will actively help in weight loss?

In the course of a 12-week trial, a group of Sprague-dawley rats was initially fed up with the standard laboratory "high fat diet" that is essentially an identical twin of the standard American diet with 15.1% of the energy from protein, 38.8% from fats and 47.1% from carbohydrates. After four weeks the rodents were assigned to different groups, which were either switched over to a standard diet (14.7% protein, 9.4% fat, 76.9% carbohydrates) or were maintained on the energy-dense high fat diet. Each of the study arms had another 5 sub-groups the animals in which received, either

• normal (ND) or high fat (HF) diet without supplement (control),
• ND or HF + 5% sucrose (SU-5),
• ND or HF + 5% erythritol (ES-5),
• ND or HF + 2.5% d-psicose (DP-2.5), or
• ND or HF + 5% d-psicose (DP-5)

for another 52 days. The food intake and body weight of the animals was measured three times a week. At the end of the study, serum levels of total cholesterol (TC), triglycerides (TG), LDL-C and HDL-C were measured and biopsies were conducted to evaluate adipose tissue and liver weight.

Figure 1: Change in body weight, total food intake and feed efficiency (right axis) in the 2nd half of the study (data adapted from Chung. 2012)

As you can see in figure 1 there was a dose-dependent decrease in body weight gain, which left the rats in the HFD - ND-DP5 group, i.e. those animals who had been fattened up for 4 weeks and were then switched to a "normal" diet supplemented with 5% of d-psicose (with a food intake of ~20g per day, whit would be 1g per day, or in human terms ~ 0.3g/kg) at a final body weight level that was identical to the animals who had never been fat in the first place - and that despite a slightly higher food intake.

Could d-psicose be an ideal adjunct to your weight loss regimen?

In this context, it is important to note that the previously fattened rodents were already 23% "overweight". In other words, while the rodents on the normal diet kept gaining weight at a rate of 2.4-2.7g per day, the weight gain of the "fat" rodents in the ND-DP5 group was so profoundly ameliorated that they ended up at the same "normal" weight at the end of the study as the intially non-obese rodents on the standard diet. And even without the dietary switch, the addition of 5% d-psicose led to a profound (-50%) reduction in diet induced weight gain in the high fat group.

Figure 2: Total white adipose tissue (right axis, in g), epididymal, perirenal and retroperitoneal visceral fat (in g) in the different groups at the end of the post-fattening 52-day feeding period (data adapted from Chung. 2012)

And while the addition of the C-3 fructose epimer lead to a reduction in body fat in all animals, only the animals who had been switched to the high carb (=normal) diet, achieved body fat levels identical (2.5% d-psicose) and even below (5% d-psicose) those of the rats in the control group (cf. figure 2).

Lose weight, lose fat, but what about your liver?

Yet despite the fact the combined "weight loss effect" of the "normal" (=low fat) diet with supplemental d-psicose is thusly fundamentally different and unquestionably way more desirable than the "Half as Heavy, Twice as Fat" effect of the Atkins diet (cf. news from last Friday), the structural kinship of d-psicose and fructose raises the question if the former did induce similarly detrimental health effect on the liver as its notoriously sweet cousin.

Figure 3: Light image of liver tissue sections from ND, ND-SUS and ND-DP-5 groups (adapted from Chung. 2012)

The light image of liver tissue sections from the ND, the ND-SUS and the ND-DP-5 group does yet show that the dreaded NAFLD fatty deposition did not occur in the DP-5 group. The statistically significant increase in liver weight, on the other hand, is something the researchers attribute to increases in hepatic glycogen stores:

Our results [...] showed that ND-DP group tended to induce liver enlargement suggesting increased glycogen deposition in liver as extra-energy storage of d-psicose. However, HF-DP group did not show any difference compared to HF group. It is possible that HF diets containing relatively low carbohydrates [...] induced lower liver glycogen level masking the effects of d-psicose.

Moreover, previous long-term studies (12-18 months) by Yagi & Matsuo did not reveal any adverse side-effects in relation to the d-psicose induced increase in liver weight (Yagi. 2009).

Figure 4: Lipid profiles (triglycerides, LDL-C and HDL-C) at the end of the study period (data adapted from Chung. 2012)

The totally normal lipid profile (cf. figure 3), with lower triglyceride and cholesterol levels than the control group and identical total cholesterol to HDL-C (control: 1.73; DP5: 1.89) and LDL-C to HDL-C (control: 0.39; DP5: 0.39) ratios also supports the notion that, despite its "frutosian heritage", d-psicose is not promoter of diabesity and metabolic disease.

Bottom line: Promising, but more than one human study would be nice

Image 2: Sponge cakes made without addition, with fructose or with d-psicose (img courtesy of the Kagawa Industry Support Foundation)

If we add to that the results of a previous human trial, in which d-psicose administration reduced the postprandial glucose and insulin response following the ingestion of 75g of maltodextrin with 5g of d-psicose (Lida. 2008), and take into consideration that the incubation of pro-adipocytes with d-psicose led to a dose-dependent inhibition of adipocyte differentiation in the study at hand, the fructose epimer d-piscose could in fact turn out to be way more than just another artificial sweetener. And as you can see in image 2, the first practical applications, or should I say highly marketable "nutritional idiocies" are already on their way: Yummy sponge cakes ;-)

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.