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.

What's Worse for Your Body Composition & Liver Health? 10g of Sugar from Coke or the Same 10g From Cookies? Plus: Liquid Sucrose is Harder on the Liver Than Fructose

Hard do believe, but the 10g from coke may actually do more harm than the same amount from cookies.

If you want to scare me away from a discussion about the "fat problems" the US and large parts of Europe are struggling with, you just have to repeat Taubs'ian statements such as "if we had not eaten carbohydrates all the mess wouldn't have happened."

It's certainly true that the exorbitant and mislead carbohydrate intake and the psyochological consequences ("Fat is bad, isn't it?") of the "low fat" decades from the 1970-1990s is part of the problem, but when we look closer, it's not as simple as to say "we don't eat enough fat".

As Yvonne Ritze and her colleagues from the University of Hohenheim, the Technische Universität München, and the Interdisciplinary Obesity Center in Rorschach (Switzerland) write in their latest paper in PLoS One, it's rather the unhealthy conglomerate of "changes in dietary and eating behavior such as preferring sugar-sweetened beverages and sugar-rich processed food, in addition to a sedentary life style", which is to blame form the "sharp rise in obesity" (Ritze. 2014).

Learn more about alternatives to sugar sweetened beverages 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?

Artif. Sweetened Foods Good, Not Bad for Fat Loss.

In said paper, Ritze and her colleagues present data from rodent and human experiments they conducted which highlight the fact the "form of sugar intake (liquid versus solid) is presumably more important than the type of sugar" (Ritze. 2014), when it comes to its ability to disturb our appetite regulation, increase the fat accumulation in the liver and promote the development of type II diabetes.

In mice, Ritze et al. observe a liquid high-sucrose diet caused an enhancement of total caloric intake which was not comparable to the effects the solid variety of the high sucrose diet had.

Figure 1: Diet (left) and energy (right) intake in the five diet groups (Ritze. 2014)

Over the course of the experiment (8 weeks), the female C57BL/6 mice (Janvier, Saint Berthevin Cedex, France) had been feed on one out of the following five ad-libitum (=eat as much as you want to) diets:

• Group 1 (controls, C) received water and mouse breeding (MZ)-diet (standard diet from Sniff, Soest, Germany) containing 10% (g/g) sugars. 
• Groups 2 (fructose liquid, Fl) and 3 (sucrose liquid, Sl) received water supplemented with fructose or sucrose at 30% (vol/vol), respectively, and enriched MZ-diet to compensate for reduced food uptake. 
• Groups 4 (fructose solid, Fs) and 5 (sucrose solid, Ss) received water and the high-fructose or -sucrose diet containing 65% (g/g) sugars, which equals the sugar amount per day that mice ingested when offered sugar water at 30%. 

Every two weeks the mice were placed in metabolic cages for 24 h, to which they had been acclimatized before. The mice were weighed, their food intake and feces analyzed and their body composition quantified; and what the scientists found was:

1. The sugar intake in groups 2-4 was significantly higher than in group 1 - obviously a simple and necessary consequence of the composition of the diet
2. The mice on the liquid diets consumed significantly more energy, sugar, liquid and food - distinct evidence that the rodent equivalent of sugar-sweetened beverages leads to overeating
3. The fructose diets were not by any means worse than the sucrose diets - an observation that confirms what I have been preaching to the choir: The fructose bashing as "lustig" (engl. "funny") as some experts believe it was, is based on a shortsighted prejudice
4. The weight increase in the solid high-sucrose groups was small compared to that of the mice in groups 2 & 3 who were fed sucrose or fructose in their water - this is the logical consequence of the increased energy intake
5. When the scientists compared the obesogenic effects (weight gain per food intake) of the diets, they found a significant difference between the liquid and solid sugars but not the sugar types - more evidence we cannot simply blame everything on fructose
6. Interestingly, all four high sugar-diets caused an increase in blood glucose and in tendency some increase in liver weight, which was more pronounced if the sugars were administered in solid form.

In addition, Ritze et al. found a strong increase in GLUT2 mRNA expression (Fl = about 90 fold;  P < 0.001; Sl = about 160 fold; P < 0.001) when sugars were dissolved in drinking water compared to the control mice - again more pronounced in the sucrose vs. fructose group. Compared to the 90x & 160x increase in the liquid groups, the likewise significan increase of ileal GLUT2 mRNA expression (P < 0.05) in the solid high sugar groups 4 & 5 was almost negligible.

"Similar results were obtained for GLUT5 mRNA expression. Comparing sugar form and type we showed a significant difference between liquid and solid sugar form for GLUT2 and GLUT5 (P < 0.001) as well as a significant difference of sugar type (fructose versus sucrose) for GLUT5 (P < 0.05) within the different dietetic groups." (Ritze. 2014)

Whether these difference in glucose transporter activity are actually relevant (they would simply speed up the uptake of glucose / fructose) is questionable.

Is absorption speed all that matters?

Figure 2: Suspiciously similar changes in glut-2 & 5 expression in the two groups fed liquid diets (top) and obese vs. lean human (bottom)

The fact that Ritze et al. observed them when they compared the GLUT2 and GLUT5 expression in obese and lean human subjects, as well, is yet quite telling. In the end, it may thus in fact all be about "speed" and the question "How fast is the sugar trickling into your body?"

Whether the speed of the sugar influx is also responsible for the slightly up-regulated ghrelin mRNA levels in mice who were fed the liquid diet compared to the solid diet (P < 0.05) is something, I cannot tell. What I can tell you though is that (a) elevated or rather not appropriately reduced ghrelin levels after a meal are characteristic of obese vs. lean humans, too (Le Roux. 2005) and that (b) there was once again no difference between fructose and sucrose diet.

Did you ever notice that none of the "fructose is bad studies" was conducted with a solid diet? The fructose was always provided on top of a solid diet with the liquid, just like the the surcose and fructose in the diet at hand. And if we are honest, it does not look like fructose was by any means significantly worse than simple sugar (which obviously is a 1:1 glucose : fructose mixture).

Figure 3: Effect of high-sugar diets on hepatic lipid accumulation. Concentrations of triglycerides in the liver (A), and liver to body ratio (B) were detected. Portal endotoxin (C), and Oil Red O staining showing fat accumulation in the liver (D) are shown

Now, what certainly comes as a surprise is the fact that it's not the liquid fructose group which had the highest liver fat concentrations, but rather the group that received the equivalent of sugar (=sucrose) sweetened beverages in their diets (see Figure 3, A). Accordingly, the Oil Red O staining in Figure 3, D is most significant in the Sl (=sucrose liquid) diet group.

The endotoxin concentration in the portal vein (see Figure 3, C), on the other hand, are the highest (yet not significantly elevated!) in the fructose groups. In conjunction with the relatively low triglyceride levels in the liver this goes against a theory by Bergheim et al. which revolves around the idea that fructose induced changes in the gut microbiome would lead to an increased endotoximia (this is true) and consequent fatty liver disease (this is at least less severe that with sucrose in the study at hand).

Bottom line: Let's get away from the "fructose vs. the rest of the world" discussion and focus on those "foods" that contain significant amounts of fructose. If you click on "foods highest in fructose" on nutritiondata.com, you will obviously find "pops, sodas, and soft drinks" on the first three ranks. And while they do have a high fructose concentration (29.8g per 200ml serving), the study at hand should remind you of another thing they have in common... ha? Yeah! Right, they are liquid fast absorbing and a real stressor for your liver.

Figure 4: Replacing SSBs or juices with water or artificially sweetened beverages has identical beneficial effects on the weight trajectory of adults (Pan. 2013) - Even low fat milk would have you gain less body weight!

I am far from suggesting that after blaming fructose for everything, we should now start blaming liquid foods for everything, but the results Ritze et al. present in their latest paper do in fact "provide evidence that liquid versus solid high-sugar diets differentially modulate feeding behavior, distinct intestinal sugar transporters and weight regulating hormones" and may thus be "a critical component for the development of obesity and fatty liver disease", not just in mice, but also in humans, where Ritze et al. found "similar enhanced sugar transporter regulation within the small intestine as in liquid high-sugar diet fed mice" and previous studies suggest that simply replacing energy containing drinks with water will inhibit or at least slow down long-term weight gain (Pan. 2013)

Reference:

• Bergheim, Ina, et al. "Antibiotics protect against fructose-induced hepatic lipid accumulation in mice: role of endotoxin." Journal of hepatology 48.6 (2008): 983-992. 
• Le Roux, C. W., et al. "Postprandial plasma ghrelin is suppressed proportional to meal calorie content in normal-weight but not obese subjects." The Journal of Clinical Endocrinology & Metabolism 90.2 (2005): 1068-1071. 
• Pan, An, et al. "Changes in water and beverage intake and long-term weight changes: results from three prospective cohort studies." International journal of obesity 37.10 (2013): 1378-1385. 
• Ritze, Yvonne, et al. "Effect of High Sugar Intake on Glucose Transporter and Weight Regulating Hormones in Mice and Humans." PloS one 9.7 (2014): e101702.

Sugar Sweetened Beverages, Bottled Water & the Obesity Epidemic: Evidence, Counter-Evidence & Scapegoatism

SSBs worse than an obesity pill?

It is a given fact that neither I nor any sane researcher is going to debate the over-consumption of sugar sweetened beverages are part of the reasons why we are fat. The way they are currently portrayed as the worst invention since trans fats, could however fire back on us. You do just have to look how willingly the oil refiners are bashing the corn refiners, how the fruit "juice" industry claims that their "healthy 100% fruit juices were less obesogenic" than a coke (which is clearly not the case) and how consumers are standing in the line at their local fast-food outlet thinking about taking the diet coke with their menu to be able to have an additional "healthy fruit smoothie" as a dessert.

I had all that in the back of my head already, when I hit on a related "Pro v Con Debate" in the early views (articles that are not yet available in the print edition) of the Obesity Reviews and thought that you might be interest in some of the arguments F.B. Hu and K.A. Kaiser et al. are presenting in their "debate" (in fact we are talking about to separate position papers) on the "Role of sugar sweetened beverages in Obesity", as well.

Point: Sugar sweetened beverages, obesity & diabetes - Scientist says the evidence is there

(Hu. 2013) I would assume that the vast majority of you is not going to have to be convinced by rational or irrational arguments that sugar sweetened beverages will increase your risk of obesity and diabetes. Still, F.B. Hu, a scientists from the Departments of Nutrition and Epidemiology at the Harvard School of Public Health in Boston must have thought of the rest of the public and the bribed, ah... pardon "mislead" policy makers, when they compiled their latest paper with the tell-tale title "Resolved: there is sufficient scientific evidence that decreasing sugar-sweetened beverage consumption will reduce the prevalence of obesity and obesity-related diseases". According to Hu,

Figure 1: Relative risk of the development of obesity per increment of 10 risk alleles, according to intake of sugar-sweetened beverages; data based on the Nurses’ Health Study (NHS) and Health Professionals + follow up (HPFS), the Women’s Genome Health Study (WGHS) and the three cohorts together (Hu. 2013)

"Consumption of SSBs has increased markedly across the globe in recent decades, tracking closely with the growing burdens of obesity. These beverages are currently the largest source of added sugar intake and the top source of daily energy in the U.S. diet. The cumulative evidence from observational studies and experimental trials is sufficient to conclude that regular consumption of SSBs causes excess weight gain and these beverages are unique dietary con- tributors to obesity and T2D. Compelling evidence indicates that reducing SSBs will have significant impact on the prevalence of obesity and its related diseases, especially T2D. [...] Although reducing SSB consumption alone is unlikely to solve the obesity epidemic entirely, limiting intake of SSBs is one simple change that could have a measurable impact on weight control and prevention of T2D and other metabolic diseases" (Hu. 2013; my emphasis)

Hu also points to the "strong resistance from the beverage industry" and the few, but increasingly numerous  public policies and regulatory strategies to reduce intake of SSBs that are already in place or being developed. The importance of a grass-roots approach, on the other hand appears to escape him. After all, it often does not look like this, but in the end the US is still a free country: You don't have to drink Pepsi, Coke and Mountain Dew, folks and neither do your friends and family.

Counterpoint: Sugar sweetened beverages are bad - in theory, but what about the reality?

(Kaiser. 2013) Now that your conviction that sugar sweetened beverages are bad, has been confirmed. let's shake the evidence and take a peak at what K. A. Kaiser, J. M. Shikany. K. D. Keating and D. B. Allison have to say about the question whether reducing sugar-sweetened beverage consumption will reduce obesity and why they feel that "[The e]vidence supporting conjecture is strong, but evidence when testing effect is weak".

Theory vs. experimental evidence: In fact the theoretical slope of the line depicting the increase in weight gain due to the consumption sugar sweetened beverages is more than 10x steeper than the one that has been observed in scientific studies (see figure 3).

What is particularly interesting is that the theoretical prediction is accurate only in the lowest 10-15% of the SSB intakes investigated in the study, for the "real SSB junkies" the gab widens significantly.

Figure 2: Rise in obesity rates (round markers) and bottled water consumption (square markers) in the US (Kaiser. 2013)

If you take a look at the graph to the right (figure 2) you will notice right away: We can as well blame the obesity epidemic to the increase in bottled water consumption (or the decrease in tap water consumption?) - the epidemioloical "evidence" is conclusive!

This figure is yet not the only thing Kaiser at al. enlist to make you at least reconsider how conclusive the evidence of which Hu just argued that it is "there" actually is. The most important factors Kaiser, Shikany, Keating and Allison want to remind us of, when it comes to the interpretation and evaluation of the hitherto available studies are...

• the risk of bias -- Most scientists start out with the same conviction we do: "Sugar sweetened beverages make you fat!" Against that backround it is even more detrimental that  "some study designs failed to adequately isolate treatment effects from the attention researchers paid to some groups." (Kaiser. 2013) The researchers also point out that not all studies had an objective measure of participant compliance (returned containers, urinary sucralose measures) and did not report whether the people who accessed the effects were blinded as well (10 out of 15 studies did not). Publication bias, on the other hand, did not appear to be a factor to skew the results (Kaiser. 2013)
• missing / insufficient sensitivity analysis -- In their re-analysis the researchers found sign. differences in the obesogenic effects of SSBs on young vs. old, male vs. female and lean vs. obese participants, yet the majority of the studies does not accordingly differentiate the outcomes.
  

  

  Figure 3: Observed (30,34,40–42,62) versus theoretical (63) weight gain effect of mandatory sugar-sweetened beverage (SSB) consumption (Kaiser. 2013)

  "[...] we evaluated the overall summary effects by excluding the studies referenced above. The overall SMD for the added SSB studies (adults only) increased by 0.06 (to 0.34; 95% CI: 0.15 to 0.54). The overall SMD for the reduction of SSBs in children of all weight categories was reduced by 0.01 (to 0.07; 95% CI:  -0.01 to 0.15). The overall SMD for the reduction studies in children only who were overweight or obese at baseline increased by 0.05 (to 0.30; 95% CI: 0.13 to 0.46)." (Kaiser. 2013)

  The general heterogenity (all variables included) is yet not another contributor to significant changes in the study outcomes.
• data interpretation / analysis - The scientists suggest that analyzing only absolute weight / BMI levels is not an adequate measure and propose two different methods to evaluate the data
  
  1. Asking the question, whether a person that is in the "SSB" group would increase or decrease weight / BMI if he or she switched to the other group - This analysis yielded a +2% and +7% change of weight / BMI reduction.
  2. Using the correlation data as basis to calculate the explanatory value of SSB consumption - This analysis showed that only 1.92% of the variance in body weight or BMI change is explained by SSB consumption, for the variance weight reductions in persons of all weight categories the figure is a hilariously irrelevant 0.09%
  As you can see, looking at the data from a marginally different angle can easily make all the difference. 

I know what you are thinking now "but XY said..." or "but what about..." and obiously Kaiser et al. must also have thought about objections like these and added a brief adjunct to their paper in which they point towards three major reasons that explain why the influence of sugar sweetened beverages is perceived as larger than life by the public:

1. 

   Don't get me wrong, I love the "ads" of the NYC Dept. of Health & Mental Hygiene campaign against sugar sweetened beverages, and used it as title picture for a previous post on the fattening effects of SSBs, but they are part of the problem Kaiser et al. are pointing at in their paper. People will sit next to them think about the gym and say: "Well I drink diet coke, so I don't have to go to the gym today - after all sugar is the problem!"

   Emotion-raising language - Emotion-raising language has often been used in discussions of SSBs and obesity. Some authors have used words like ‘plague’, ‘toxic’, ‘hazardous’ (4,53) and ‘deadly’ when describing SSBs or the sugars they contain and have tried to promote perceived connections between SSB marketers and the worst behaviour of tobacco marketers . Although such words may help to advance an agenda, they do not educate or inform the public.
   
   Moreover, they likely raise emotions and impair logical reasoning. As Kersh and Morone wrote, ‘Scientific findings never carry the same political weight as does a villain threatening American youth.
   
   If critics successfully cast portions of the industry in this way, far-reaching politi- cal interventions are possible, even likely. When an industry becomes demonized, plausible counterarguments (privacy, civil liberties, property rights, and the observation that “everyone does it”) begin to totter.’
2. Distortion of scientific information - A second factor that has likely contributed to misperceptions in this area is the distortion of scientific information by some authors and commentators. [...] Clearly, such practices mislead and have likely contributed to misperceptions in the scientific and lay communities about the strength of the evidence regarding the proposition debated here.
3. The mere exposure effect - The final factor that we believe has led to the erroneous perception that the evidence showing that the proposition of this debate has been unequivocally proven is the ‘mere exposure effect.’
   
   The mere exposure effect is the label psychologists use for the phenomenon that the more a person is exposed to an idea, the more they come to like and accept it. As the Nobel Prize-winning economist Daniel Kahneman described, ‘A reliable way to make people believe in falsehood is frequent repetition, because familiarity is not easily distinguished from truth. Authoritarian institutions and marketers have always known this fact. But it was psychologists who discovered that you do not have to repeat the entire statement of a fact or idea to make it appear true’
   
   The number of articles on SSBs and obesity and the number of statements that SSBs are especially problematic in obesity are extraordinary, especially in comparison to the modest amount of probative data. Thus, opinions about SSBs may have been offered so often that these opinions have become accepted as fact by many in the scientific community, media and lay public.

I probably could quote addtional parts of the excellently written paper here, but I guess you are getting the notion and will be able to understand that neither my nor the scientists who wrote the original paper intend to support the position of the SSBs industry that have long realized that this war cannot be won on the scientific stage and have long focused all their efforts having their "lifestyle" drinks being marketed by the "cool and hip" celebrities, athletes and super models to the "wanna be cool and hip" normals.

---

Bottom line: I am well aware that some of you are now probably already dialing the Dr. Lustig's phone number or calling the blogosphere's vice police to accuse me of making a pact with the Coca Cola company.

You all know I am an opponent of the consumption all sugar & HFCS sweetened drinks and foods and well aware of the "fat consequences" (learn more), but overemphasizing the roles of SSBs or HFCS, is not going to help us solve the global obesity problem.

But let's be honest, you all know that I neither drink nor recommend anyone to drink sugar sweetened beverages. My interest is in understanding the contributions each and every of the myriad of dietary, behavioral, endocrine, paracrine, neurological, environmental, social, ... to the obesity epidemic and if you take a look the 1.92% explanatory value of SSBs consumption in terms of body weight and BMI, it is clear that sugar sweetened beverages are a major contributor to the obesity epidemic.

Still it is not warranted and would be a consequential mistake to expect that by taking them off the market the whole issue would be solved. We all know that this won't be the case and you just have to look at the non-existent long-term effects switching to diet sodas had on the waist lines of the obese to know that we have to do more than remove all sugar sweetened beverages from the displays of the supermarket.

Does this mean we should not tell people they are bad for them? Try to tax or ban them? No. What it does mean, though, is that the war against obesity is not a war against SSBs, only.

References:

• Hu FB. Resolved: there is sufficient scientific evidence that decreasing sugar-sweetened beverage consumption will reduce the prevalence of obesity and obesity-related diseases. Obes Rev. 2013 Jun 13.  
• Kaiser KA, Shikany JM, Keating KD, Allison DB. Will reducing sugar-sweetened beverage consumption reduce obesity? Evidence supporting conjecture is strong, but evidence when testing effect is weak. Obes Rev. 2013 Jun 7.

Sugar Addicted or Just Stressed Out? Study Investigates Modulatory Effects of Different Macronutrient Compositions on Serotonin in the Presence and Absence of Stress

Image 1: She has the reason she is so relaxed right in her hand... but does she know that sugar is no sustainable way of coping with stress unless you don't care that you thusly pave the way from from initial episodes of hypoglycemia over binges, to obesity and diabetes.

"Sugar addiction" is a recurring theme in the blogosphere and whether it exists or not and what potential causes and treatments might be is still a matter of a partly very emotional debate. If we go by the definition of "addiction", of which the venerable Oxford English Dictionary says that it was "a condition characterized by regular or poorly controlled use of a psychoactive substance despite adverse physical, psychological, or social consequences, often with the development of physiological tolerance and withdrawal symptoms", it would be, if we had prove that sugar is a "psychoactive" substance. After all, the "adverse physical, psychological, or social consequences", i.e. diabetes, obesity, eating disorders, isolation, depression etc., are too obvious to be argued away - and I don't have to tell you about the "withdrawal symptoms", do I? Or, could it be that this is all just in our brains? Well, according to a recently published study from the Neurochemistry and Biochemical Neuropharmacology Research Unit at the Department of Biochemistry of the University of Karachi in Pakistan (Moin. 2011), it actually is ;-)

A amino acidic tale of sugary binge eating and fat anorexia

In their study, which was unfortunately conducted on rodents, not humans (apparently decapitation of human subjects for research purposes is prohibited in Pakistan ;-), Samia Moin and his (or her?) colleagues tried to assess how different dietary macronutrient compositions effect the ability to cope with and the brain response to stress. To this ends the scientists fed 48 rodents with diets that contained either 1/3 sugar (sugar diet), 1/3 beef protein (protein diet) or 1/3 fat (fat diet) in addition to the standard rodent chow (normal diet). Unfortunately, they did not provide the specific macronutrient composition of the diets, so that I had to calculate the latter on my own. The results are depicted in figure 1 and are based on the assumption that the Pakistani "standard rodent chow" is identical to the one animals in US labs are fed ;-)

Figure 1: My calculation of the macronutrient composition of the experimental diets; the calculation is based on the "standard rodent diet" that is used in US labs, whether that was identical to the one the Pakistanis used, I cannot tell.

If you take a look at the macronutrient composition of the different diets, the inter-diet difference between the "normal" and the "sugar diet" ended up to be not so significant. I mean 58% vs. 72% of the calories from carbs? For me both would be high carb and thusly it should not really surprise you that of those 24 rats who had to endure 2h of immobilization stress the rats in the "normal" and "sugar" group showed a similar, yet for the "normal" diet 1-day postponed, stress response: They ate more!

Figure 2: Effect of repeated stress (2h immobilization) on food intake in the different groups (data calculated based on Moin. 2011)

If you look at the data in figure 2, it does yet become obvious that - at least within the study period - "more" has to be understood relative to an initial stress-induced decrease in food intake, which, and this is another interesting finding, was sustained at -44% (average over the 5-day period) in both the high fat and the high protein group.

The Pakistani perspective: "Carbohydrate help you cope with stress!"

From the perspective of the Pakistani scientists, this "restorative effect" of a high carbohydrate diet on stress-induced appetite may be a good thing, from the perspective of someone living in a society with an overabundance of both food and stress, it must however be consider a potential risk factor for obesity.

Figure 3: Changes in serotonin (5-HT), its metabolite 5-HIAA and its precursors in response to dietary intervention; the "normal" diet serves as a reference (data calculated based on Moin. 2011)

If we take a closer look at the diet induced changes in brain 5-HT (=serotonin), 5-HIAA (=main serotonin metabolite) and brain and serum tryptophan (=serotonin precursor) levels in figure 3, it becomes quite obvious that the changes in the macronutrient composition alone already "mess" with the serotonin metabolism. What stands out, here is that, contrary to the "sugar" and the "protein diet", the "fat diet" increases the amount of serotonin in the brains of the unstressed rats compared to the "normal" control by +20%.

Figure 4: Changes in serotonin (5-HT), its metabolite 5-HIAA and its precursors in response to stress in the different diet groups; data expressed relative to unstressed controls; only changes marked with an asterisk (*) are statistically significant, p < 0.05 (data calculated based on Moin. 2011)

A different picture emerges, though, when we take a look at the effects of combined macronutrient modulation and stress (cf. figure 4). Contrary to the changes in the "normal" and "sugar group" which (plasma tryptophan levels aside) lack statistical significance, we see a reduction serotonin metabolism (as indicated by reduced 5-HIAA levels) in both the "protein" and the "fat" diet and the serotonin level in the "protein" group was profoundly elevated in response to the 2h immobilization stress.

What implications do these 5HTs, 5-HIAAs and ABCDEFGs have?

From previous studies, we know for quite some time that high protein diets are associated with higher rates in stress-induced depression (Markus. 1998). Moreover a reduced 5-HIAA / 5-HT ratio in the brain has been identified as a characteristic feature of depression (Zangen. 1997). If we keep that in mind and take a final look at the data in figure 4 and figure 5, we would have to draw the following conclusions:

• a high sugar diet modulates the 5-HIAA / 5-HT in an "anti-depressive" way
   
• a high protein diet does not change the 5-HIAA / 5-HT ratio as long as there are no external stressors, when stress comes into play it is associated with a profound "pro-depressive" decrease in the 5-HIAA / 5-HT ratio
   
• a high fat diet induces a pro-depressive reduction in the 5-HIAA / 5-HT ratio in the absence of stress, but is associated with a less pronounced reduction in the 5-HIAA / 5-HT ratio in response to stress, when compared to a high protein diet

Now its up to you to tell me whether these neurotransmitter changes in a rodent study and the associated pro- and anti-depressive effects reflect the way you feel on different diets in the presence and absence of stress... and I suggest, whenever you feel good with the way you eat, discard all the information I have just given you and keep doing what works for you. Not just because you are no rat, but simply because we are all wired differently and this wiring may change overtime :-)