Calories in Context

The Paleo Manifesto, Pt. II: Weak Evidence for the Hunter-gatherer Way

Posted on April 24, 2012 by decline104

Opening Comments

Welcome back, everyone, for part 2 of my Paleo critique. If you are just joining me I highly suggest going back and reading last week’s article before proceeding. However, for those of you who are lazy, in the interest of time I will copy and paste my concluding remarks from last week, here, so that we’re all caught up.

“Not only do Paleo advocates follow a rigid diet based on loose assumptions of ancestral food patterns (which they’re wrong about in the first place), but they also make adjustments to their philosophy where they see fit, even if it deviates from their core principles. To me it just sounds like an excuse to impose one’s own views about nutrition on others.”

Now that we’ve got that out of the way, I would like to pick up this week by looking at the limited research that compares the Paleo diet to some more traditional diets on various metabolic risk factors and satiety. Now, before we begin, I would like everyone to remember: the point of the Paleo diet is not the ratios of protein, carbohydrate, and fat. Paleo nuts could care less about strict dietary ratios. Rather, the Paleo diet is about the types of foods that can and cannot make up those proportions. If you have to, refer back to the list of ‘foods to consume’ and ‘foods to avoid’ in last week’s article.This is important when reviewing the literature on Paleolithic diets because there must be compelling evidence that it is the food choices of the Paleo diet that are beneficial to health and not the ratios of those foods. This is, in fact, the primary focus of today’s discussion. That being said,I will start by going in order from the earliest to the most recent study, and then I’ll try to tie things up and make some final comments about Paleo diets in general.

Lindeberg et al. 2007

In one of the first studies looking at Paleolithic diets, researchers Lindeberg et al. saw that a Paleolithic diet improved glucose tolerance more than a Mediterranean-like diet in individuals with ischemic heart disease and impaired glucose tolerance [1]. This, however, is not surprising given that the Paleo group consumed fewer calories (450kcals less) and significantly fewer carbohydrates (CHO) than the Mediterranean group.

Above, I’ve provided a screen shot of the daily intakes of CHO between the two diet-groups (Paleo is the left column, Mediterranean is the right column). As you can see, the Paleo group consumed about 97g (or 42%) fewer carbohydrates than the Mediterranean group. On the other hand, the protein content between the groups did not differ by any significant degree (90g vs. 89g), nor did the fat content (42g vs. 50g). However, the failure to account for equal macronutrition between the two groups makes it hard to determine the actual impact of the Paleo food choices rather than just having an ideal ratio of protein to CHO. In fact, a substantial amount of research done by Donald Layman, at the University of Illinois at Urbana-Champaign, shows that having a higher protein to CHO (PRO:CHO) ratio helps to improve glucose homeostasis in individuals, especially during weight loss [2-6]. What’s more, Layman’s subjects were definitely not eating a Paleolithic diet!

Frassetto et al. 2009

In the next study, Frassetto et al. saw that compared to usual dietary habits, a Paleolithic-style diet improved glucose tolerance, insulin sensitivity, blood pressure, and lipid profiles, independent of weight loss, in nine sedentary, overweight subjects [7]. Again, the results are not surprising given the poor, prior dietary habits of the participants. Below, the screenshot clearly shows that the usual intakes of subjects were higher in saturated fats, cholesterol, and sodium, while being lower in mono- and polyunsaturated fats, protein, and some other micronutrients.

Also, if you look closely, you will see that protein is almost twice as high while on the Paleo diet, therefore increasing the PRO:CHO ratio and possibly explaining the reason for the improved glucose tolerance. However, the small sample size and failing to control for macronutrition (again) makes this a weak study and still leaves us questioning whether or not excluding grains, dairy and sugars truly is optimal for human health, rather than just eating less CHO and more protein.

Jönsson et al. 2009

Jönsson et al. examined the effects of a Paleolithic diet on glycemic control and several risk factors for cardiovascular disease (CVD) over a 3-month period in patients with type 2 diabetes [8]. They found that the Paleo diet was superior to a traditional diabetic diet for improving glycemic control and CVD risk factors. Like the previous two studies, the results, again, are not surprising given the greater reduction in calories (300kcals less) and CHO (71g less) in the Paleo group compared to the control. Furthermore, the protein content of the diet was 4% higher in the Paleo group compared to the control (24% and 20%, respectively), again, altering the PRO:CHO ratio. Anyone else seeing a pattern here?

Similarities & Failures

As you can see, the failure for each study to accurately control for overall calories and macronutrient composition between diet groups – specifically protein and CHO – makes it hard to conclusively say that a hunter-gatherer style diet – i.e. one devoid of post-agricultural foods – is truly superior for human health. Stronger study protocols would have had control groups with matching macronutrition equal to that of the Paleo group’s diet. That way, any differing results seen between the two groups could be attributed to the food choices and nothing else. However, given their failures to do so, not much can be concluded from the aforementioned studies other than having more protein and less CHO seems to be beneficial in terms of certain metabolic risk factors, specifically glucose/insulin homeostasis. Still, the question remains whether or not the specific types of CHO, proteins, and fats – as strictly recommended by the Paleo diet – are superior for human health when compared to more conventional diets. Obviously, switching to a diet that automatically restricts entire food groups high in CHO is an easy way to both cut calories and reduce overall CHO intake, the point is that the source of CHO may not matter more so than the overall amount of CHO in the diet. Therefore, Paleolithic nutrition may not be driving force for the results given certain confounding factors such as the PRO:CHO ratio in the diet and the greater reduction in overall caloric intake. Until better studies are conducted, the Paleo diet and its benefits on health markers is still speculative and nothing more.

Now, there is still one study left which I have yet to talk about, however, this study deals more with satiety rather than metabolic risk factors. Either way, it still has its implications for weight loss/control and overall health and therefore should not be discarded in today’s discussion.

Jönsson et al. 2010

The last study we will look at found that a Paleolithic-style diet was more satiating per calorie than a Mediterranean diet in 29 subjects with ischemic heart disease [9]. As you might remember from my previous article on beverages and satiety, satiety simply means fullness. On average, participants in the Paleo group consumed about 435 fewer calories than the Mediterranean group. Furthermore – as shown below – the protein content of both diets was similar (92g vs. 88g) even though the percentages of protein in the diets were significantly different (27% Paleo vs. 20% Mediterranean).

You will also notice the 82g difference in CHO intake between the two groups. Taken together, this drastically increases the PRO:CHO ratio, essentially making the Paleo diet nothing more than a low-CHO diet. To quote the authors themselves;

“The Paleolithic diet in this study plays out as a low-carbohydrate diet, and the term effects on weight loss from low-carbohydrate diets suggesting greater satiety could be the controlling factor behind the greater satiating effect of the Paleolithic diet in this study.”

This is important because there is accumulating evidence that diets higher in percentages of protein are more satiating than those with lower percentages protein, in both short-term and longer-term studies [3-5, 10-16]. Furthermore, another aspect of the Paleo diet was that it was considerably higher in fruit intake compared to that of the Mediterranean group (513g/day vs. 262g/day, respectively). In a study that produced a validated satiety index of commonly consumed foods, researchers saw that fruit was the most satiating food, even edging out that of protein-rich foods, as a group [17]. Therefore, given the ad libitum nature of the study – simply meaning they ate at their leisure – as well as the differences in diet protocols, it is not surprising that the diet with the higher PRO:CHO ratio and higher in fruit was more satiating than the diet that was lower in both.

Summary

So, to wrap things up, it seems that the benefits of a Paleo diet – i.e. a diet without starches, sugars and dairy – are still left up to debate. In no way did the studies above provide any insight into whether or not Paleo recommendations are better than just having a lower-carbohydrate diet with higher percentages of protein (at least in sedentary/health compromised populations). A much stronger set of studies would have had control groups with isocaloric diets and equal levels of PRO, CHO, and fats that vary only in the types of foods that comprise those ratios. Until then, the beneficial aspects of the Paleo diet are still theoretical and not much more. Obviously, eating a diet lower in refined grains and processed products will be much healthier than one that is higher in those types of foods. However, to dogmatically restrict entire food groups which CAN and DO offer health benefits is nothing more than someone imposing their own flawed views of nutrition on others. What ever happened to moderation? My suggestions are to eat a well-rounded and balanced diet, which is diverse in the amounts and types of foods you consume, in order to maximize the benefits from each source. Dichotomous thinking about nutrition always leads to more bad than good, remember that.

References

1. Lindeberg S, Jönsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjöström K, Ahrén B. A Paleolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischemic heart disease. Diabetologia 2007;50:1795-1807.

2. Layman DK, Clifton P, Gannon MC, Krauss RM, Nuttall FQ. Protein in optimal health: heart disease and type 2 diabetes. Am J Clin Nutr. 2008;87(5):1571S-1575S.

3. Layman DK. Dietary guidelines should reflect new understandings about adult protein needs. Nutr Metab. 2009;6:12.

4. Layman DK, Baum JI. Dietary protein impact on glycemic control during weight loss. J Nutr. 2004;134(4):968S-73S.

5. Layman DK, Boileau RA, Erickson DJ, Painter JE, Shiue H, Sather C, Christou DD. A reduced ratio of carbohydrate to protein improves body composition and blood lipid profiles during weight loss in adult women. J Nutr. 2003;133(2):411-7.

6. Layman DK, Shiue H, Sather C, Erickson DJ, Baum J. Increased dietary protein modifies glucose homeostasis in adult women during weight loss. J Nutr. 2003;133(2):405-10.

7. Frassetto LA, Schloetter M, Mietus-Snyder M, Morris RC, Sebastian A. Metabolic and physiologic improvements from consuming a Paleolithic, hunter-gatherer type diet. Eur J Clin Nutr. 2009;63:947-955.

8. Jönsson T, Granfeldt Y, Ahrén B, Branell UC, Pålsson G, Hansson A, Söderström M, Lindeberg S. Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study. Cadriovasc Diabetol. 2009;8:35.

9. Jönsson T, Granfeldt Y, Erlanson-Albertson C, Ahrén B, Lindeberg S. A Paleolithic diet is more satiating per calorie than a Mediterranean-like diet in individuals with ischemic heart disease. Nutr Metab. 2010;7:85.

10. Halton TL, Hu FB. The effects of high protein diets on thermogenesis, satiety and weight loss: a critical review. J Am Coll Nutr. 2004;23(5):373-85.

11. Veldhorst M, Smeets A, Soenen S, et al. Protein-induced satiety: effects and mechanisms of different proteins. Physiol Behav. 2008;94(2):300-7.

12. Westerterp-Plantenga MS. Protein intake and energy balance. Regul Pept. 2008;149(1-3):67-9.

13. Lejeune MP, Westerterp KR, Adam TC, Luscombe-Marsh ND, Westerterp-Plantenga MS. Ghrelin and glucagon-like peptide 1 concentrations, 24-hr satiety, and energy and substrate metabolism during a high-protein diet and measured in a respiration chamber. Am J Clin Nutr. 2006;83(1):89-94.

14. Smeets AJ, Soenen S, Luscombe-Marsh ND, Ueland Ø, Westerterp-Plantenga MS. Energy-expenditure, satiety, and plasma ghrelin, glucagon-like peptide 1, and peptide tyrosine-tyrosine concentrations following a single high-protein lunch. J Nutr. 2008;138(4):698-702.

15. Keller U. Dietary proteins in obesity and in diabetes. Int J Vitam Nutr Res. 2011;81(2-3):125-133.

16. Westerterp-Pantenga MS, Nieuwenhuizen A, Tomé D, Soenen S, Westertetp KR. Dietary protein, weight loss, and weight maintenance. Annu Rev Nutr. 2009;29:29-41.

17. Holt SHA, Miller JC, Petocz P, Farmakalidis E. A satiety index of common foods. Eur J Clin Nutr. 1995;49:675-690.

Posted in Diets | 9 Comments

The Paleo Manifesto, Pt. I: Idiot Ideology

Posted on April 24, 2012 by decline104

Opening Comments

In keeping with the theme of evolution and nutrition, today’s article is going to be the first installment of a two-part series on the Paleo diet (also called hunter-gatherer, Stone-Age, or ancestral dieting). Even if you are not familiar with Paleolithic nutrition per se, you most likely are familiar with Atkins, The Zone, or South Beach, which are essentially less-strict versions of ancestral eating. However, given their differences, we won’t concern ourselves with them and will therefore just stick to looking at Paleo. Part 1 will solely place emphasis on the Paleo diet and some of the inherent biases/contradictions it contains. Part 2 will strictly be reserved for a research review on the literature supporting the Paleo diet, wherein I will make some final comments and sum things up. My goal for today is to show you all why Paleo is a flawed and inflexible diet system comprised of ideologues who cement themselves in assumptions while blindly disregarding scientific literature that opposes their own views about nutrition. So, without further ado, let’s begin by taking a look at what Paleolithic nutrition actually is.

Enter Paleo: Society’s Stone-Age Solution

In essence, the Paleolithic period – some 2-million years ago – marked the start of humanity, most notably, with the advent of stone tools in order to facilitate food consumption. During this time period, it is assumed that grain and sugar consumption (other than fruit) was virtually nonexistent, maybe except for occasional honey here and there. Taking this into account, Paleo dieters believe that the Paleolithic “style” of eating – i.e. a diet devoid of grains, starches, sugar and dairy – is best suited to our current genetics because we have changed little – if at all – since the emergence of agriculture and its products some 5,000-10,000 years ago. To quote Dr. Loren Cordain – “the world’s leading expert on Paleolithic diets” – directly from his book, The Paleo Diet:

“Literally, we are Stone Agers living in the Space Age; our dietary needs are the same as theirs. “

It is from this rationale that Paleo fanatics believe that obesity, diabetes and the other “diseases of civilization” are caused from the consumption of grains – or as they like to call them, “the double-edge sword of humanity” – because these diseases were not a problem back then when grains were unavailable. However, today, both an overabundance of grains and diseases are available. Therefore, no post-agricultural foods are to be consumed because they somehow contradict our genetic disposition. As extremist as this is, many people are taken in by this philosophy because it does offer a very logical explanation for the current health crisis we are now witnessing. What most Paleo nuts choose toforget is that we also did not evolve with television, computer, cars, etc. that lowers our energy expenditure and potentially leads to weight gain and certain diseases when combined with poor dietary habits. Yet, most of them continue to use these things on a daily basis; hypocrisy? I’ll let you decide. That’s another article for another time; today’s focus is strictly nutrition.

Now, I have to say that I am in agreement with the idea that a diet which is full of McDonald’s, Dunkin’ Donuts, and other processed foods is not the healthiest diet to consume; no argument there. However, if you’re trying to debate that oatmeal, milk and a little bit of sugar here and there are bad for me, then Ihave a problem. But, before I get ahead of myself, let’s see if we can actually quantify what a “caveman” actually ate all those years back.

What did a Caveman Actually Eat?

In a few words: we can’t be sure and probably never will. However, even crazier than the people themselves are their claims that they, the Paleo proponents, actually know what a caveman ate. In one of the first papers talking explicitly about Paleolithic nutrition, authors Eaton and Konner provided some general ranges for the types of food sources a person might have eaten back then based off of some more recent hunter-gatherer societies which lasted into the late 20^th Century [1]. Although this serves as a rough estimate for Paleolithic nutrition, one must keep in mind that a hunter-gatherer culture living in the 1960’s is extremely different from that of a Paleolithic society living hundreds of thousands of years ago. Any suppositions made from these observations are purely speculative and far from conclusive. Nevertheless, using these contemporary hunter-gatherer societies (living mainly inland and in semi-tropical climates), Eaton and Konner saw that anywhere from 20-50% of their diet was obtained from meat and anywhere from 50-80% of their diet came from vegetation. However, populations in artic regions – like that of the Eskimos – derive as little as 10% of their diet from plant-based sources. Therefore, if my calculations serve me right, the ranges of nutrients potentially run anywhere from 20-90% meat-based and anywhere from 10-80% plant-based. To me it seems as though there was not one single hunter-gatherer-type diet. In fact, a well-written review by evolutionary archaeologist, John Gowlett [2], argues that in no way there could have been only one “Stone-Age diet.” This is due to various geographical limitations, such as food variety and climactic changes, which would require various nutritional adaptations to be undertaken in order to survive in a given region. Therefore it can be determined that humans did not evolve eating any one type of diet, but rather an all-encompassing and extremely varied diet that would allow for adaptive survival given their geographic location/conditions. This is exactly what was seen in our more recent hunter-gatherer proxies. But does that stop the Paleo zealots from prescribing strict nutritional guidelines?

Paleo’s Take on Hunter-gatherer Nutrition

Led by Dr. Loren Cordain – who, to his credit is published in a multitude of peer-reviewed journals – the Paleo diet is characterized by two food-lists; foods you can/should eat, and foods you should avoid at all costs (lest you not fear for your own health and well-being). Boiling it down even further, foods to consume and avoid are provided below, along with picture for those who are visually inclined.

You’ll notice they have a pretty rigid set of dietary guidelines. Furthermore, if you’ve ever read Cordain’s book (The Paleo Diet), you would have noticed some percentages for protein, carbs and fats (pg. 11) . In fact, they all fall well within the ranges noted earlier. However, like I already mentioned, we don’t know what a caveman ate! Providing your own dietary ratios for macronutrients is nothing more than using a blank slate with which to project your own views about diet composition. Disobey these dietary dogmas and I assume it’s like Scott Pilgrim vs. the World when the Vegan Police come and take Todd’s vegan powers after drinking a latte made with half and half. Well, maybe not that bad, but you’d probably be ostracized on some level.

Now, it’s pretty obvious that grains are to be wholly excluded from the diet. Again, this is due to the fact that grains were not (presumed to be) consumed prior to the agricultural revolution some 10,000 years ago. However, in 2009 and 2010, two papers were published that showed grains were indeed part of Paleolithic nutrition some 30,000 years ago [3], going as far back as 105,000 years ago [4]. To quote one of the authors directly [4];

“A large assembly of starch granules has been retrieved from the surfaces of Middle Stone Age tools from Mozambique, showing that early Homo Sapiens relied on grass seeds starting at least 105,000 years ago, including those of sorghum grasses.”

Even if you believe that 10,000 years is not enough time for genetic adaptation to occur, it would be hard to argue that 105,000 years isn’t either. Not only do these findings undermine the diet’s protocols, but they also illuminate the inherent weaknesses contained within the diet prescription itself: Paleo dieters have no idea what a Paleolithic man ate! Therefore, one cannot prescribe a diet based on assumptions that are not fully substantiated in scientific literature. Otherwise, as I already stated, you are using a blank slate with which to project your own ideological views about nutrition. Another perfect example of this is Cordain’s other book, The Paleo Diet for Athletes. To quote the text directly:

“Perhaps the most important refinement made to my original Paleo Diet was [the] recognition that consumption of starches and simple sugars was necessary and useful only during exercise and the immediate post-exercise period.” (pg. 6)

So wait, now Cordaine is advocating for starch and sugar consumption? Even when his entire manifesto was built around the notion that grains and starches are evil and should never be consumed? As you can see, Paleo fanatics make exceptions only where they see fit, all the while still calling it Paleo, even when it deviates from their core principles. I like to call it Paleo Plus! All the benefits of Paleo, plus the benefits of the things they say we’re not biologically meant to consume. You truly can have your cake and eat it too! Not that they would…

It’s not ALL bad, though

Now that we’ve pointed out a few of the biases and contradictions contained within the diet’s ideology, I think it’s only fair to point out some of the benefits that a Paleo diet can offer…and then some of the benefits from foods Paleo dieters choose to avoid. You didn’t think I would let them off the hook that easily did you? Nothing Paleo zealots do make any logical sense.

Benefits of the Paleo Diet

Based on what we just saw, going Paleo primarily consists of lean meats, seafood (with an emphasis on omega-3s), fruits, vegetables, and various nuts and seeds which also contain some “heart-healthy” fats. As a nutrition student, I would be lying if I said I disliked any diet that advocated for such a healthful array of foods. In fact, the scientific literature supporting the benefits of said food types runs the gamut. Fruit and vegetable consumption is consistently associated with reduced risk of coronary heart disease [5, 6], stroke [7, 8], type II diabetes [9, 10], and even some types of cancers [11-14]. Similarly, omega-3 consumption (either via supplementation or fatty-fish consumption) has been shown to reduce certain cardio-metabolic risk factors [15] as well as incidences of many chronic inflammatory diseases such as IBD, cancer, rheumatoid arthritis and Alzheimer’s [16]. There is even starting to be some strong evidence for the use of omega-3s, specifically EPA, in the treatment of depression [17]. Lastly, nuts have been implicated in the improvement of cholesterol levels, oxidative stress, blood pressure, inflammation and other cardiovascular risk factors [18, 19]. Ideology aside, the literature seems to support the basis of Paleo, but what about the foods they don’t consume?

Paleo Dieters are Missing Out!

Although the foundation of Paleo is bolstered by scientific literature that confirms the plethora of health benefits to be expected when one eats fruits, vegetables, nuts and lean sources of meat, what the Paleo extremists seem to be flat-out ignoring are the health benefits from foods they’re excluding – nay, unjustifiably denouncing!

Benefits of Paleo-banned foods

In the interest of time I’ll stick to the major food groups noted on the ‘avoid’ side of the above Paleo manifesto, those being grains, legumes, and dairy. Starting with grains and legumes, whole grains have been associated with having protective effects against the development of type 2 diabetes [20], coronary heart disease [21, 22], and stroke [22] while both are associated with improvements in glucose, lipid and lipoprotein metabolism in both healthy and diabetic populations [20]. Furthermore, in a recently published review looking at 135 studies on refined grains – namely breads, pastas, rice and cereals – it was shown that there was no association between refined grain consumption and an increase in disease risk, even when 50% of grain consumption came from refined grain products [23]. So, at the very worst, there’s no ill effect of refined grain consumption, as long as it doesn’t comprise the majority of your diet. At best, you get all of the above-mentioned health benefits from whole-grains and legumes. Paleo zealots, however, just look the other way.

Dairy is the next food group exiled on account of its relatively recent inception. Dairy products weren’t introduced until about 5,000 years ago, which is, according to Paleo dieters, well-after human evolution (as if it were some event in time rather than a fluid process which still continues to this day). Therefore, dairy is denounced just the same—that is, unless you’re former NFL lineman, John Welbourn or Paleo advocate and author, Robb White, who both follow a Paleo + Dairy regimen (or as Alan Aragon so eloquently put it, “A Paleo-when-convenient doctrine.”) Regardless of individual inconsistencies, the Paleo dogma clearly states which side of the isle it’s on with complete disregard to evidence pointing the other way. For instance, dairy has been shown time and time again to be a major factor in the maintenance of bone health due to the ample amounts of protein, calcium and other minerals present in milk that help regulate and comprise human bone [24-27]. To quote a recent study on dairy [28];

“[Al]though it is possible to meet calcium intake recommendations without consuming dairy foods, calcium replacement foods are not a nutritionally equivalent substitute for dairy foods and consumption of a calcium-equivalent amount of some non-dairy foods is unrealistic.”

In fact, a study—which we will look at next week—that compared a Paleo diet to a traditional diabetic diet saw that calcium was significantly lower (~50% less) in the group adhering to a Paleolithic diet [29]. Furthermore, there has been accumulating data to suggest that dietary calcium further improves weight loss/management [30-32] and is responsible for up to 50% of the anti-obesity effects of dairy [32].

Those seeking to add muscle would most certainly benefit from the consumption of dairy products due to its shown effects on strength and muscle gains when combined with resistance training [33-37]. Moreover, a fractional component of milk protein, whey, is commonly used in supplements and has been shown to enhance muscle hypertrophy and recovery from heavy lifting, as well as decreasing muscle damage and soreness [38]. It has even been argued to be the “ideal” protein source for stimulating muscle protein synthesis [39]. Lastly, whey protein is even implicated as also having anti-obesity effects, complementing those of calcium [32]. This, in part, seems to be due to the high content of the amino acid Leucine seen in whey protein. Obviously a good case can be made for not adhering to a Paleo diet due to the quantitative benefits offered by the foods that are not eaten – in reality, decried – by Paleo dieters.

Summary

So, as you can see, there are some pretty stark contradictions within the Paleo way of eating. Not only do Paleo advocates follow a rigid diet based on loose assumptions of ancestral food patterns (which they’re wrong about in the first place), but they also make adjustments to their philosophy where they see fit, even if it deviates from their core principles. To me it just sounds like an excuse to impose one’s own views about nutrition on others. Next week we’ll take actually take a look at some studies that support Paleo diets and see whether or not Paleo lives up to all the hype, regardless of how flawed its ideology is. So until then, keep enjoying your oatmeal and protein shakes. I sure know I will!

References

1. Eaton SB, Konner M. Paleolithic nutrition: a consideration of its nature and current implications. NEJM 1985;312(5):283-289.

2. Gowlett JAJ. What actually was the stone age diet? J Nutr Environ Med. 2003;13(3):143-147.

3. Ravedin A, Aranguren B, Becattini R, et al. Thirty thousand-year-old evidence of plant food processing. PNAS 2010;107(44):18815-18819.

4. Mercader J. Mozambican grass seed consumption during the middle stone age. Science 2009;326:1680-1683.

5. Dauchet L, Amouyel P, Hercberg S, Dallongeville J. Fruit and vegetable consumption and risk of coronary heart disease: a meta-analysis of cohort studies. J Nutr. 2006;136(10):2588-93.

6. He FJ, Nowson CA, Lucas M, MacGregor GA. Increased consumption of fruit and vegetables is related to a reduced risk of coronary heart disease: meta-analysis of cohort studies. J Hum Hypertens. 2007;21(9):717-28.

7. Dauchet L, Amouyel P, Dallongeville J. Fruit and vegetable consumption and risk of stroke: a meta-analysis of cohort studies. Neurology 2005;65(8):1193-7.

8. He FJ, Nowson CA, MacGregor GA. Fruit and vegetable consumption and stroke: meta-analysis of cohort studies. Lancet 2006;367(9507):320-6.

9. Carter P, Gray LJ, Troughton J, Khunti K, Davies MJ. Fruit and vegetable intake and incidence of type 2 diabetes mellitus: systematic review and meta-analysis. BMJ 2010;341:c4229

11. Gandini S, Merzenich H, Robertson C, Boyle P. Meta-analysis of studies on breast cancer and diet: the role of fruit and vegetable consumption and the intake of associated micronutrients. Eur J Cancer 2000;36(5):636-46.

12. Conway DI. Each portion of fruit or vegetable consumed halves the risk of oral cancer. Evid Based Dent. 2007;8(1):19-20.

13. Pavia M, Pileggi C, Nobile CG, Angelillo IF. Association between fruit and vegetable consumption and oral cancer: a meta-analysis of observational studies. Am J Clin Nutr. 2006;83(5):1126-34.

14. Riboli E, Norat T. Epidemiological evidence of the protective effect of fruit and vegetables on cancer risk. Am J Clin Nutr. 2003;78(3 Suppl):559S-569S.

15. Abeywardena MY, Patten GS. Role of ω3 Longchain polyunsaturated fatty acids in reducing cardio-metabolic risk factors. Endocr Metab Immune Disord Drug Targets 2011;11(3):232-46.

16. Wall R, Ross RP, Fitzgerald GF, Stanton C. Fatty acids from fish: the anti-inflammatory potential of long-chain omega-3 fatty acids. Nutr Rev. 2010;68(5):280-289.

17. EPA but not DHA appears to be responsible for the efficacy of omega-3 long chain polyunsaturated fatty acid supplementation in depression: evidence from a meta-analysis of randomized controlled trials. J Am Coll Nutr. 2009;28(5):525-42.

18. Ros E, Tapsell LC, Sabate J. Nuts and berries for heart health. Curr Atheroscler Rep. 2010;12(6):397-406.

19. Ros E. Health benefits of nut consumption. Nutrients 2010;2(7):652-82.

20. Venn BJ, Mann JI. Cereal grains, legumes and diabetes. Eur J Clin Nutr. 2004;58:1443-1461.

21. Kelly SA, Summerbell CD, Brynes A, Whittaker V, Frost G. Wholegrain cereals for coronary heart disease. Cochrane Database Syst Rev. 2007;(2):CD005051

22. Flight I, Clifton P. Cereal grains and legumes in the prevention of coronary heart disease and stroke: a review of the literature. Eur J Clin Nutr. 2006;60(10):1145-59.

23. Williams PG. Evaluation of the evidence between consumption of refined grains and health outcomes. Nutr Rev. 2011;70(2):80-99.

24. Heaney RP. Dairy and bone health. J Am Coll Nutr. 2009;28(Suppl 1):82S-90S.

25. Huth PJ, DiRienzo DB, Miller GD. Major scientific advances with dairy foods in nutrition and health. J Dairy Sci. 2006;89(4):1207-21.

26. Protein and calcium: antagonists or synergists? Am J Clin Nutr. 2002;75(4):609-610.

27. Heaney RP. Calcium, dairy products and osteoporosis. J Am Coll Nutr. 2000;19(2 Suppl):83S-99S.

28. Fulgoni VL 3rd, Keast DR, Auestad N, Quann EE. Nutrients from dairy foods are difficult to replace in diets of Americans: food pattern modeling and an analysis of the National Health and Nutrition Examination Survey 2003-2006. Nutr Res. 2011;31(10):759-65.

29. Jonsson T, Granfeldt Y, Ahren B, Branell UC, et al. Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study. Cardiovasc Diabetol. 2009;8:35.

30. Van Loan M. The role of dairy foods and dietary calcium in weight management. J Am Coll Nutr. 2009;28(Suppl 1):120S-9S.

31. Faghih Sh, Abadi AR, Hedayati M, Kimiagar SM. Comparison of the effects of cows’ milk, fortified soy milk, and calcium supplement on weight and fat loss in premenopausal overweight and obese women. Nutr Metab Cardiovasv Dis. 2011;21(7):499-503.

32. Zemel MB. Proposed role of calcium and dairy food components in weight management and metabolic health. Phys Sportsmed. 2009;37(2):29-39.

33. Hartman JW, Tang JE, Wilkinson SB, Tarnopolsky MA, Lawrence RL, Fullerton AV, Phillips SM. Consumption of fat-free fluid milk after resistance exercise promotes greater lean mass accretion than does consumption of soy or carbohydrate in young, novice, male weightlifters. Am J Clin Nutr. 2007;86(2):373-81.

34. Josse AR, Tang JE, Tarnopolsky MA, Phillips SM. Body composition and strength changes in women with milk and resistance exercise. Med Sci Sports Exerc. 2010;42(6):1122-30.

35. Tipton KD, Elliot TA, Cree MG, Wolf SE, Sanford AP, Wolfe RR. Ingestion of casein and whey proteins result in muscle anabolism after resistance exercise. Med Sci Sports Exerc. 2004;36(12):2073-81.

36. Kammer L, Ding Z, Wang B, Hara D, Liao YH, Ivy JL. Cereal and nonfat milk support muscle recovery following exercise. J Int Soc Sports Nutr. 2009;6:11.

37. Phillips SM, Hartman JW, Wilkinson SB. Dietary protein to support anabolism with resistance exercise in young men. J Am Coll Nutr. 2005;24(2):134S-139S.

38. Hulmi JJ, Lockwood CM, Stout JR. Effect of protein/essential amino acids and resistance training on skeletal muscle hypertrophy: a case for whey protein. Nutr Metab. 2010;7:51.

39. Phillips SM. The science of muscle hypertrophy: making dietary protein count. Proc Nutr Soc. 2011:70(1):100-3.

Posted in Diets | 10 Comments

Liquid Calories and Weight Gain: Are Sodas Really To Blame? – ARTICLE REVIEW

Posted on April 24, 2012 by decline104

Beverage consumption, appetite, and energy intake: what did you expect?

Bridget A. Cassady, Robert V. Considine, and Richard D. Mattes. Am J Clin Nutr. 2012;95(3):587-93.

PubMed: http://www.ncbi.nlm.nih.gov/pubmed/22258267

BACKGROUND:

Beverage consumption is implicated in the overweight/obesity epidemic through the weaker energy compensation response it elicits compared with solid food forms. However, plausible mechanisms are not documented.

OBJECTIVE:

This study assessed the cognitive and sensory contributions of differential postingestive responses to energy- and macronutrient-matched liquid (in beverage form) and solid food forms and identifies physiologic processes that may account for them.

DESIGN:

Fifty-two healthy adults [mean ± SD age: 24.7 ± 5.5 y; BMI (in kg/m(2)): 26.3 ± 6.3] completed this randomized, 4-arm crossover study. Participants consumed oral liquid and solid preloads that they perceived, through cognitive manipulation, to be liquid or solid in their stomach (ie, oral liquid/perceived gastric liquid, oral liquid/perceived gastric solid, oral solid/perceived gastric liquid, or oral solid/perceived gastric solid). However, all preloads were designed to present a liquid gastric challenge. Appetite, gastric-emptying and orocecal transit times, and selected endocrine responses were monitored for the following 4 h; total energy intake was also recorded.

RESULTS:

Oral-liquid and perceived gastric-liquid preloads elicited greater postprandial hunger and lower fullness sensations, more rapid gastric-emptying and orocecal transit times, attenuated insulin and glucagon-like peptide 1 release, and lower ghrelin suppression than did responses after oral-solid and perceived gastric-solid treatments (all P < 0.05). Faster gastric-emptying times were significantly associated with greater energy intake after consumption of perceived gastric-liquid preloads (P < 0.05). Energy intake was greater on days when perceived gastric-liquid preloads were consumed than when perceived gastric solids were consumed (2311 ± 95 compared with 1897 ± 72 kcal, P = 0.007).

CONCLUSIONS:

These data document sensory and cognitive effects of food form on ingestive behavior and identify physical and endocrine variables that may account for the low satiety value of beverages. They are consistent with findings that clear, energy-yielding beverages pose a particular risk for positive energy balance. This study was registered at clinicaltrials.gov as NCT01070199.

Opening Comments

Today’s topic is one of much intrigue and debate, particularly because of liquid calories being implicated in today’s obesity epidemic. It is no secret that we drink more soft drinks today than we did 50 years ago [1], but simply saying that soft drinks cause obesity is flat out foolish, for reasons I will make explicit in a little bit. What merely started as a short article review quickly turned into more of an in-depth research review, but I promise it is well worth the read. So without much further ado, let’s delve in!

…But right after a quick announcement

Sorry, but before I get into today’s topic, I need to make myself perfectly clear from the very start. Because this topic somewhat overlaps with the “Great High-fructose Corn Syrup (HFCS) Debate,” the distinction between the two topics must be made now before I have people misquoting me later on. Got it? Good.

The Distinction

I believe I made myself pretty clear two months ago when I argued that HFCS is not the cause obesity. Obesity is a multi-factorial condition, meaning that it has many causes, and therefore picking one factor out of a whole host of other collinear factors (such as reduced physical activity, high-calorie foods, and greater caloric intake overall) is foolish and forms the basis of a very weak argument. HOWEVER, over the years there has been a lot of research done on the non-satiating (not filling) effects of liquid calories (i.e. soda, juices, sports drinks and the like (which commonly use HFCS as a sweetener)) and how they make us consume more food than solid foods do. The idea that the energy from caloric beverages, as opposed to solid foods, is poorly compensated for is not a new concept [2-6]. In fact, the topic has been studied as early as the late 1970’s and continues to this day.

A substantial amount of the literature suggests that liquid calories are not efficiently compensated for by physiologic responses in the brain and therefore do not cause us to reduce food intake as much as a solid foods do [7]. This is important because it draws the distinction between beverages and solid foods and their subsequent effects on appetite and potential weight gain. One of the more interesting studies (given the upcoming Easter season), conducted by DiMeglio and Mattes in 2000 [8], observed the effects of 450kcals of either soda or jelly beans on subsequent food intake over the course of the day. It was shown that people who consumed the jelly beans slightly decreased their food intake over the course of the day while the soda group not only ate as much as they usually did but actually ate slightly more. This study implies that, not only are liquid calories inferior to solid calories in terms of compensating food intake, but also that it doesn’t matter which sweetener is used but rather the vehicle in which that sweetener is added to (i.e. solid or liquid). Re-read that sentence if you have to. Therefore, HFCS (or any sweetener for that matter) in a beverage (like soda) would not have the same effect on appetite and food intake as HFCS in a solid product would. That’s, at least, what the research is looking like thus far, although I do have some reservations which will be made evident later on. But, before I get ahead of myself, let’s get back to the paper at hand.

As I was saying, it looks like beverages seem to be inferior to solid foods when it comes to appetite and food intake, however, a specific mechanism for why we can’t compensate for liquid calories as well as we do for solid calories is the question which today’s article tries to answer. Also, an extremely interesting (and historical) paper, written by Georgy A. Bray and Barry M. Popkin, on why we can’t compensate for liquid calories can be found here for those who are interested. The authors essentially claim that our ancestors did not drink anything other than water and breast-milk, the latter which is only important for babies, for most their human evolution and therefore did not evolve a physiologic mechanism to compensate for liquid calories. It’s a very easy read if you’re so inclined. However, let’s get back to today’s article and see why liquid calories might not be compensated for as well as solid calories are.

The Study

Today’s article essentially looks at the same exact outcomes that previous studies have looked at (i.e. satiety and subsequent food intake); however this study throws a whole other factor into the mix, which is the human mind. Here, the researchers wanted to see how perceptions of beverages and solid foods would (if at all) influence metabolism, satiety, and subsequent food intake. This is extremely interesting because it asserts that we can essentially control how full we are and how well we digest liquids based solely off of how we perceive a food’s effect in our body regardless of its physical state. I know crazy, right? This concept actually falls perfectly in line with the thinking that people eat less at dinner after they have soup. In fact, it has been consistently observed in acute studies that people consume fewer calories from a meal after the ingestion of soup [9-14]. Moreover, in a recent study done with children aged 3-5 years, similar effects were shown when the children received a small portion of tomato soup right before lunch [15]. However, the actual mechanism for why soups – and not other liquids – induce satiety has never been accurately identified, although today’s study may provide some insight.

Participants (n = 52) were exposed to 4 separate experimental conditions with a wash-out period between each protocol. The 4 conditions were; liquid-liquid, liquid-solid, solid-liquid, and solid-solid. The liquid-liquid (L-L) condition meant that subjects were given a caloric beverage and were told it would remain liquid in their stomach. The liquid-solid (L-S) condition was the same exact beverage however they were told that the beverage would turn to a solid in their stomach (when in fact it was the same beverage as the L-L). The solid-liquid (S-L) treatment was a gelatin cube in which participants were told would turn to liquid in their stomachs, and the solid-solid (S-S) treatment was the same exact cube aside from being told it would remain a solid in participant’s stomachs.

After ingestion of the beverages or cubes subjects were told to rate their satiety every half hour for a total of 4 hours. Also, breath tests and blood samples were taken to measure the rate of digestion of the beverage or cube and the concentrations of certain hormones associated with hunger and satiety. At the end of 4 hours they were each given a plate of macaroni and cheese and were told to eat until they felt full.

The Results

Subjects who were told that the liquid solution would remain a liquid in their stomach (L-L) digested it faster than those who thought the beverage would turn into a solid in their stomach (L-S). This happened even though it was, again, the exact same liquid beverage. The only difference was what the researchers told them would happen. Furthermore, receiving the L-L beverage made people rank their satiety as being much lower than when given the L-S beverage, also causing them to eat more calories (~130kcals more) when given a meal 4 hours later.

Similarly, those who believed an isocaloric gelatin (solid) cube would turn into a liquid in their stomach (S-L) digested the cube much faster than those who thought the same cube would remain solid in their stomach (S-S). Just as before, when subjects received a food they though would be liquid in their stomachs, they ranked their satiety as being much lower than when given a food they thought would remain solid in their stomachs. Also, the S-S cube resulted in the least amount of calories eaten from the plate of macaroni across all treatments.

Overall, the L-L and L-S beverages were digested faster than the S-L and S-S cubes (as seen by breath tests), adding to the literature that transit time of a liquid through the GI tract may also play a role in perceived satiety (faster transit = lower satiety) [16-18]. However, to quote the authors;

“The findings indicate that the mere expectation that a food will be in one form or another in the [GI] tract produces behavioral and physiologic responses likely to contribute to lower satiety effects and weaker dietary compensation after beverage ingestion.”

Simply put, just by thinking a food or beverage will act a certain way in your stomach actually dictates how you will digest that food and how full you will actually feel regardless of the physical state that food or beverage is actually in. This lends credence to research involving soup. Soups are predominantly liquids (yes there are some vegetables in some of them) yet most people perceive them to be foods (solids). Having soup before a meal could reduce hunger and improve satiety based solely on our perceptions of that soup – i.e. that it will make us feel full because we think it’s a solid-food rather than a liquid one. However, whether or not this is relevant towards the obesity epidemic is something I will talk about in a little bit.

To go back and further expand upon the blood samples/measurements, I should also note that ghrelin, a hormone related directly to hunger, was seen to be higher after the L-L and L-S beverages compared to the S-L and S-S cubes, correlating strongly to the higher perceived hunger seen in the participants after they consumed the liquid solutions. Again, just to reiterate, there were no differences between the beverages besides what the researchers told the participants. The same goes for the solid cubes, which, I might add, also turned to liquid in the stomach and therefore weren’t much different from the liquid solutions aside from the participants having to masticate.

Still, even though the solutions and cubes were essentially all identical people’s perceptions dictated their physiologic responses which made them feel more or less full. This led participants to eat more or less food 4 hours later when given a meal. Pretty profound results, if I say so myself.

My Thoughts

One thing to consider – and this is the one caveat I will stress when looking at satiety papers dealing with liquid calories – is the time delay seen between the administration of the liquids/cubes and the subsequent meal which was given 4 hours later. Most studies which show similar results use similar protocols when administering a meal [19-21]. However, given that the pre-loads were not administered in close proximity to the meal (like the soup studies I mentioned earlier) we don’t know if the results would have been different had the meal been given sooner. A lot of other studies show that liquid calories in fact do cause people to reduce caloric intake, although these studies used fairly large pre-loads (>600mL) and gave the meal close to immediately afterwards (0-30 minutes) [22]. Due to the differences used in the time between pre-load and the meal, it makes it hard to argue one way or the other without taking into context the way in which the liquid is consumed. To quote the authors of a well-written review on liquid calories and failed satiety [22];

“The controversy regarding liquid foods and the supposed failure of satiety may be resolved if we consider the time elapsed between the [beverage] and the [meal]… Whether energy is provided in liquid or solid form may be less important than the timing of intake and the context in which it is consumed.”

Application/Relevance with Regards to the Obesity Epidemic

Although this study is extremely interesting and truly shows the power of the mind over physiology, I do not see how the results relate much to the obesity epidemic at hand. No one in their right mind thinks soda or juice would turn into a solid in their stomach. Therefore, it’s pretty safe to say that people’s perceptions of commonly consumed beverages (unlike soups) won’t change anytime soon. Consequently, the results seen here are purely academic and are nonetheless irrelevant to normal human consumption of beverages, which right now are sodas, juices, sports drinks and the like which potentially cause us to eat more. That is unless companies start marketing a liquid-solid soda or something similar to those Shot-Blocs made by Clif® that will stay as a solid in the stomach. Maybe then people would start reducing their calories throughout the day, however, I doubt that will happen. So, in the end, the results are cool but not extremely relevant given common perceptions of sodas and juices which are the main supposed culprits in today’s epidemic.

Summary

So, are liquid calories to blame for the obesity epidemic? Well, the preponderance of studies, including this one, which similarly deliver a meal 2-4 hours after the pre-load, seem to suggest that liquid calories may be involved. Due to the fact that sodas and sugar-sweetened beverages (SSB) aren’t soups, nor will they ever be perceived as foods (solids in the stomach), it seems that they may be a contributor to the obesity epidemic, although they are by no means THE CAUSE. I cannot stress this enough. Obesity is a multi-faceted problem and no one factor will ever be seen as the root-cause. Certain factors may contribute while others may seem to help, however, in the end it comes down to what we put in and what we put out. My personal views, habits, and opinions on sodas are as follows:

1. I don’t particularly like soda, but I defend the right to sell/drink it. Just don’t be a lazy bum and you can enjoy the occasional sugar-sweetened beverage (SSB) every now and again. Even if soda did cause you to increase caloric intake (aside from it being a source of calories itself), if your energy expenditure (exercise) is still more than what you put in, soda will never cause you to gain weight.

2. I myself do not drink SSBs (Hell, I don’t even put sugar in my coffee). I was not raised in a household where we drank soda or juice and I believe SSBs displace calories I could easily get from better food sources.

3. Lastly, if you absolutely MUST have soda, switch to diet. Even if you do eat as much as you would have, you still get the soda without the added calories and can maintain caloric balance.

I will end with noting that I did not talk much about alcohol, an extremely popular beverage among the US population and one which does offer calories. Being a college student myself I would be lying if I said undergraduates don’t consume alcohol. That being said, it seems that alcohol, too, does not offer a compensatory response for energy intake, leading to greater consumption even when alcohol is given immediately (30 minutes or less) before the meal [23-25]. Although it would make sense that drinkers would be heavier than non-drinkers due to the lack of caloric compensation, this appears not to be the case [26, 27]. Possible reasons for why drinkers are not heavier than non-drinkers could be due to the fact that people who have higher alcohol intakes might also have higher levels of physical activity on those days (see statement 1 above) [28].

So no matter what you choose to drink, remember that SSBs and the like ARE calories and you might not get the same satiating power you would get from a solid food, causing you to consume more later on. On the whole, anything you could derive from a soda (which is essentially just sugar) you could equally (if not beneficially) obtain from a better food source. I’d leave it at that.

References

1. Economic Research Service, USDA. Food availability data. Updated February 1, 2011.

2. Pliner PL. Effect of liquid versus solid preloads on eating behavior of obese and normal persons. Physiol Behav 1973;11:285-290.

3. Malagelada JR, Go VLW, Summerskill WHJ. Differential gastric, pancreatic, and biliary responses to solid-liquid or homogenous meals. Dig Dis Sci 1979;24:101-110.

4. Kissileff HR, Klingsberg G, Van Itallie T. Universal eating monitor for continuous recording of solid or liquid consumption in man. Am J Physiol 1980;238:R14-R22.

5. Jordan HA, Levitz LS, Utgoff KL, Lee HL. Role of food characteristics in behavioral change and weight loss. JADA 1981;79:24-29.

6. Mustad VA, Jonnalagadda SS, Smutko SA, Pelkman CL, Rolls BJ, Behr SR, Pearson TA, Kris-Etherton PM. Comparative lipid and lipoprotein responses to solid-food diets and defined liquid-formula diets. Am J Clin Nutr 1999;70:839-846.

7. Mattes RD. Fluid energy – where’s the problem? JADA 2006;106(12):1956-61.

8. DiMeglio DP, Mattes RD. Liquid versus solid carbohydrate: effects on food intake and body weight. Int J Obes Relat Metab Disord 2000;24:795-800.

9. Rolls BJ, Federoff IC, Guthrie JF, Laster LJ. Foods with different satiating effects in humans. Appetite 1990;15:115-126.

10. Jordan HA, Levitz LS, Utgoff KL, Lee HL. Role of food characteristics in behavioral change in weight loss. JADA 1981;79:24-29.

11. Kissileff HR. Effects of physical state (liquid-solid) of foods on food intake: Procedural and substantive contributions. Am J Clin Nutr 1985;42:956-965.

12. Rolls BJ, Bells EA, Thorwart ML. Water incorporated into food but not served with a food decreases energy intake in lean women. Am J Clin Nutr 1999;70:448-455.

13. Mattes RD. Soup and satiety. Physiol Behav 2005;83:739-747.

14. Flood JE, Rolls BJ. Soup preloads in a variety of forms reduce meal energy intake. Appetite 2007;48:626-634.

15. Spill MK, Birch LL, Roe LS, Rolls BJ. Serving large portions of vegetable soup at the start of a meal affected children’s energy and vegetable intake. Appetite 2011;57(1):213-9.

16. Jian R, Ducrot F, Najean Y, Cortot A, Modigliani R. Effect of alcohol on gastric empting of an ordinary meal in man. Gut 1983;24:A363.

17. Marciani L, Gowland PA, Spiller RC, Manoj P, Moore RJ, Young P, Fillery-Travis AJ. Effect of meal viscosity and nutrients on satiety, intragastric dilution, and emptying assessed by MRI. Am J Physiol Gastrointest Liver Physiol 2001:280(6):G1227-33.

18. Marciani L, Gowland PA, Spiller RC, Manoj P, Moore RJ, Young P, Al-Sahab S, Bush D, Wright J, Fillery-Travis AJ. Gastric response to increased meal viscosity assessed by echo-planar magnetic resonance imaging in humans. J Nutr 2000;130(1):122-7.

19. Mattes RD. Dietary compensation by humans for supplemental energy provided as ethanol or carbohydrates in fluids. Physiol Behav 1996;59:179-187.

20. Drewnowski A, Massien C, Louis-Sylvestre J, Fricker J, Chapelot D, Apfelbaum M. The effects of aspartame versus sucralose on motivational ratings, taste preferences ad energy intakes in obese and lean women. Int J Obes Relat Metab Disord 1994;18:570-578.

21. De Graaf C, Hulshof T, Weststrate JA, Jas P. Short-term effects of different amounts of protein, fats, and carbohydrates on satiety. Am J Clin Nutr 1992;55:33-38.

22. Almiron-Roig E, Chen Y, Drewnowski A. Liquid calories and the failure of satiety: how good is the evidence? Obesity 2003;4:201-212.

23. Westerterp-Plantenga MS, Verwegen CRT. The appetizing effect of an aperitif in overweight and normal-weight humans. Am J Clin Nutr 1999;69:205-212.

24. Heatherington MM, Cameron F, Wallis DJ, Pirie LM. Stimulation of appetite by alcohol. Physiol Behav 2001;74:283-289.

25. Poppitt SD, Eckhardt JW, McGonagle J, Murgatroyd PR, Prentice AM. Short-term effects of alcohol consumption on appetite and energy intake. Physiol Behav 1996;60:1063-1070.

26. Alcohol consumption, nutrient intake and relative body weight among US adults. Am J Clin Nutr 1985;42(2):289-295.

27. Colditz GA, Giovannucci E, Rimm EB, Stampfer MJ, Rosner B, Speizer FB, Gordis E, Willett WC. Alcohol intake in relation to diet and obesity in women and men. Am J Clin Nutr 1991;54(1):49-55.

28. Westerterp KR, Meijer EP, Goris AH, Kester AD. Alcohol energy intake and habitual physical activity in older adults. Br J Nutr 2004;91(1):149-52.

Posted in Reviews | 3 Comments

Want to lose more weight? Eat your carbs at night! – ARTICLE REVIEW

Posted on April 24, 2012 by decline104

Greater weight loss and hormonal changes after 6 months diet with carbohydrates eaten mostly at dinner.

Sigal Sofer, Abraham Eliraz, Sara Kaplan, Hillary Voet, Gershon Fink, Tzadok Kima and Zecharia Madar. Obesity 19(10):2006-14, 2011.

PubMed: http://www.ncbi.nlm.nih.gov/pubmed/21475137

ABSTRACT. This study was designed to investigate the effect of a low-calorie diet with carbohydrates eaten mostly at dinner on anthropometric, hunger/satiety, biochemical, and inflammatory parameters. Hormonal secretions were also evaluated. Seventy-eight police officers (BMI >30) were randomly assigned to experimental (carbohydrates eaten mostly at dinner) or control weight loss diets for 6 months. On day 0, 7, 90, and 180 blood samples and hunger scores were collected every 4 h from 0800 to 2000 hours. Anthropometric measurements were collected throughout the study. Greater weight loss, abdominal circumference, and body fat mass reductions were observed in the experimental diet in comparison to controls. Hunger scores were lower and greater improvements in fasting glucose, average daily insulin concentrations, and homeostasis model assessment for insulin resistance (HOMA(IR)), T-cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels were observed in comparison to controls. The experimental diet modified daily leptin and adiponectin concentrations compared to those observed at baseline and to a control diet. A simple dietary manipulation of carbohydrate distribution appears to have additional benefits when compared to a conventional weight loss diet in individuals suffering from obesity. It might also be beneficial for individuals suffering from insulin resistance and the metabolic syndrome. Further research is required to confirm and clarify the mechanisms by which this relatively simple diet approach enhances satiety, leads to better anthropometric outcomes, and achieves improved metabolic response, compared to a more conventional dietary approach.

Opening Comments

Today’s review actually ties in quite nicely with my first post about fat gain and carbohydrates and the myths that surround them. A lot of fitness enthusiasts are, what I like to call, “Carbophobics,” meaning that they fear carbohydrates and/or sugars. This is, in part, due to a gross misunderstanding of how insulin works in the body and how it stores carbohydrate. For this reason alone some extremists severely limit their carb intake for fear of fat gain, while others limit sugars (which are wrongly perceived as having a greater affinity to be stored as fat), and a good handful of people even go so far as to forbid carbs past some arbitrary time of day. This typically occurs sometime in the late afternoon/early evening, which segues nicely into today’s topic.

As you may have already read (skimmed?), the article that I will be speaking about involves carbohydrates and weight loss, but more specifically, carbohydrates being consumed at dinner time causing greater weight loss than carbohydrates spread throughout the day. This is a relatively novel concept in terms of a structured weight loss diet, however, a similar diet plan has been studied before, mainly in Muslim populations which participate in Ramadan, a month-long religious observation where people refrain from food and drink during daylight hours and then consume some form of enriched-carbohydrate dinner at night. Along a similar vein, the researchers of this article discuss how manipulating carbohydrate intake during a hypocaloric diet might have greater beneficial effects on obesity, certain metabolic markers associated with diabetes (insulin sensitivity, fasting glucose, lipid profile), and overall satiety than does a traditional low-calorie diet where carbs are spread out over the course of the day (breakfast, lunch, dinner).

Their rationale is based on eating in accordance with the natural diurnal (daytime) rhythms of certain hormones in the body (namely insulin, leptin, and adiponectin) which deal with metabolism, hunger and satiety. I won’t go into too much detail, but in theory, if you can control the way these hormones act on your body throughout the day you can curb your hunger and lose more weight and essentially adhere to a diet more so than someone who is fighting their hormonal physiology on a standard diet. In this manner, you can diet longer and lose even more weight… hypothetically. This is exactly what this study sought to examine. Sounds good, right? Well, some of you out there might not buy it at all (carbophobes), while others may take it for gospel and eliminate their daytime carbs right off the bat. I, on the other hand, would rather take a more sound/sensible approach and see how they conducted this study before I go jumping to conclusions.

The Study

The study was conducted in Israel with a cohort of 78 relatively healthy police officers, between the ages of 25-55, and who had a BMI > 30 (overweight). 39 officers were randomly assigned to the control group (i.e. carbs throughout the day), while the remaining 39 officers were part of the experimental group (i.e. carbs for dinner). Randomization essentially eliminates any differences seen between the groups and makes them equal across all variables. From this any results can be seen as a direct relation to the experimental procedure.

The researchers (unlike the last study I talked about) controlled for calories, so that each group received the same amount of calories (1,300-1,500kcals/person) as well as macronutrient composition (20% protein, 30-35% fats, and 45-50% carbohydrates). This amounted to roughly 65-75g protein, 43-50g fats, and 163-188g carbohydrate for each group participant. The participants also filled out forms, periodically throughout the study, which ranked their hunger and satiety on a scale from 1-10, 1 being starving and 10 being devastatingly full. Finally, researchers took blood samples (also periodically throughout the study) to measure certain health markers such as insulin resistance and fasting glucose (which are indicative of metabolic syndrome and diabetes), as well as lipid profile (cholesterol, and triglycerides) and certain hormones (leptin and adiponectin, which are known to regulate hunger and satiety). This was all done at day 0 (baseline), day 7, day 90, and finally at day 180. The participants were also met by a personal dietitian every 1-3 weeks to make sure the diet was adhered to. Those who failed to comply with the diet were thrown out of the study.

By the end of the study the researchers saw that both groups lost significant amounts of weight and both improved upon their health markers, however, the group who received the majority of their carbohydrates at dinner lost more weight and had better health markers than the group who ate carbs throughout the day. Most notably, the experimental group had lower insulin concentrations and lower fasting glucose levels, (meaning they were moving farther away from becoming diabetic). They also improved upon their levels of adiponectin, a hormone which is involved in lowering insulin levels. Probably the most important finding of the study was that the group who received their carbs later in the day reported feeling less hungry and more satiated than the control group. In fact, the experimental group actually felt FULLER as study went on, while the control group got hungrier over the 6 month period. If you’ve ever tried to lose weight for any significant period of time you know that this usually is NOT the case. Even more interesting was the finding that not one of the experimental group participants had preoccupied thoughts about food, whereas one-third of the control group did by 6 months. Again, this is something else not common during dieting.

Summary

So, what can explain these results? The researchers believe, as I pointed out in the beginning, that by eating in accordance with the natural diurnal rhythms of certain hormones in the body, one can actually take advantage of these hormonal “windows of opportunity” and curb appetite while losing more weight. This is, in part, due to being able to keep leptin elevated during the day, telling the brain not to eat and to increase energy expenditure. However, as measured through blood sampling, leptin concentrations weren’t much different between the two groups throughout the study, so it is hard to explain why the experimental group felt fuller and was more satiated at 6 months.

The other question, as to why the experimental group became less insulin resistant than the control group, could be explained by the experimental diet keeping insulin release lower throughout the day, allowing adiponectin concentrations to be higher than the control group’s levels. As the authors point out, when insulin is high adiponectin is low, therefore negating the effects of adiponectin. Adiponectin is known to play a role in energy metabolism, specifically with carbs and fats, and helps to lower these concentrations in the body, causing one to be less insulin resistant (i.e. not diabetic). As seen with blood sampling, the experimental group’s concentrations of adiponectin were much higher than the control groups’ levels, possibly explaining the reason for having better insulin and fasting glucose levels.

So, would I go so far as to say that everyone should consume carbs at night rather than throughout the day? Well, maybe if you’re dieting and have had problems adhering to diets in the past. The evidence seems to suggest better satiety which may help you to eek out a couple more weeks or so of dieting. Also, most people like to go out with friends to dinner, so going carb-free throughout the day and saving your carbs for the evening may be more realistic and help you better adhere to your diet when faced with social gatherings. Personally, I would have liked to have seen the study completed up to 1 year. Many studies see very different results in diet protocols past the 6 month point, so it’s hard to say what would happen in the long-run. Also, I wish there was a third and fourth group with a carb-load in the morning only and carb-load at lunch only. Perhaps it doesn’t matter when the carbs are being consumed as long as it only happens once throughout the day?

If you’re overweight or obese and are looking to improve insulin sensitivity, this diet might be a better approach than a traditional weight loss diet. However, exercise has a strong effect on insulin sensitivity, so a traditional diet coupled with a solid exercise plan may be just as good. This was something not talked about by the authors. My thoughts are that this is a great study with a novel approach to losing weight, however, more studies need to be done in order to confirm or deny that dinner is ONLY time in which the carbs can be consumed to yield this result. So for now, as long as you’re healthy and you’re exercising and eating correctly I see no need to eat your carbs at dinner-time only.

Posted in Reviews | 3 Comments

Amino Acid Supplementation – ARTICLE REVIEW

Posted on April 24, 2012 by decline104

Exogenous amino acids stimulate human muscle anabolism without interfering with response to mixed meal ingestion.

Douglass Paddon-Jones, Melinda Sheffield-Moore, Asle Aarsland, Robert R. Wolfe, and Arny A. Ferrando

Am J Physiol Endocrinol Metab 228: E761-E767, 2005.

PubMed: http://www.ncbi.nlm.nih.gov/pubmed/15572657

ABSTRACT. We sought to determine whether ingestion of a between-meal supplement containing 30 g of carbohydrate and 15 g of essential amino acids (CAA) altered the metabolic response to a nutritionally mixed meal in healthy, recreationally active male volunteers. A control group (CON; n = 6, 38 +/- 8 yr, 86 +/- 10 kg, 179 +/- 3 cm) received a liquid mixed meal [protein, 23.4 +/- 1.0 g (essential amino acids, 14.7 +/- 0.7 g); carbohydrate, 126.6 +/- 4.0 g; fat, 30.3 +/- 2.8 g] every 5 h (0830, 1330, 1830). The experimental group (SUP; n = 7, 36 +/- 10 yr, 87 +/- 12 kg, 180 +/- 3 cm) consumed the same meals but, in addition, were given CAA supplements (1100, 1600, 2100). Net phenylalanine balance (NB) and fractional synthetic rate (FSR) were calculated during a 16-h primed constant infusion of L-[ring-2H5] phenylalanine. Ingestion of a combination of CAA supplements and meals resulted in a greater mixed muscle FSR than ingestion of the meals alone (SUP, 0.099 +/- 0.008; CON, 0.076 +/- 0.005%/h; P < 0.05). Both groups experienced an improvement in NB after the morning (SUP, -2.2 +/- 3.3; CON, -1.5 +/- 3.5 nmol x min(-1) x 100 ml leg volume(-1)) and evening meals (SUP, -9.7 +/- 4.3; CON, -6.7 +/- 4.1 nmol x min(-1) x 100 ml leg volume(-1)). NB after CAA ingestion was significantly greater than after the meals, with values of 40.2 +/- 8.5 nmol x min(-1) x 100 ml leg volume(-1). These data indicate that CAA supplementation produces a greater anabolic effect than ingestion of intact protein but does not interfere with the normal metabolic response to a meal.

Opening Comments

Today’s objective is two-fold. The first objective is to outline for everyone how to critically analyze and interpret a scientific paper using a specific example (i.e. the study above). The second objective is to simply give my interpretation of the paper provided and the reasoning behind my interpretation. You are free to disagree, but if so, please provide evidence as to why. That being said, we can now move on.

Today’s paper is not new. In fact, it was published back in 2005 by a group of researchers from the University of Texas and Shriner’s Hospital for Children in Galveston, TX, but I like the topic so much, because amino acids (AA) are becoming such a growing presence in the gym and among athletic communities, alike. This group has put out plenty of other papers on amino acids and muscle protein synthesis and I suggest looking them up and digging through the literature if you’re interested. I will not talk much about those papers because that will not be my focus today, but rather I will analyze this paper and see if their conclusions are sound and if any recommendations can be made from this paper. I will, however, disclose some information right now, being, that anyone who makes a recommendation from one paper is foolish, so essentially no recommendations can be made, however implications can, and even those are shaky without a body of literature. So let’s continue.

The Abstract

As provided above, the abstract is meant to supply the reader with (almost) everything he/she needs to know about the study. There is a brief 1-2 sentence opening describing why the study is important, and it then continues with the methods and procedures, any salient results, and finally their conclusions based off of the results. Simply reading an abstract doesn’t give you all of the information needed, because their might be some methodological flaws or inherit bias built into the study, and therefore the entire text is needed to fully critique and analyze the findings. The above paper is freely available online and I highly suggest finding it and reading along as you read.

The Introduction

The introduction is meant to describe to the reader WHY the paper is important. It may also illuminate some previous research that was done which prompted this study and it may even provide some statistics to show you how important the problem is and why this study is important to help alleviate that problem. Today’s paper does just that. The authors open with the rationale (reasoning) for why AA supplements should be used, and the specific requirements that a supplement must have in order to be effective. They also allude to some previous research which prompted this study to be done. They finish with their objectives for the study, which were to examine the effects of an AA and carbohydrate (CHO) supplement on muscle protein synthesis (MPS) when given between meals. This is essentially only relevant for certain populations looking to maximize muscle gains. A study like this can provide some critical insight into how to treat older populations who are at risk for sarcopenia, which simply means losing muscle as one ages, or in clinical settings where people are in extreme catabolic states and desperately need to hang on to whatever lean tissue they have. The final population is the athletic community who wish to maximize muscle gains. I will essentially be speaking directly to the latter.

Materials and Methods

The next section is probably one of the most important (and potentially boring) sections of the paper. A result is only as good as the method used to produce that result. Remember that. This means that you might get a great result, but if the method (or protocol) used to find that result was poor then those findings come into question. Now, let us use that rationale and apply it to this section of this paper.

The researchers had 13 (n = 13) healthy, physically active males between the ages of 28-48 participate in the 16-hr, in-lab study. Seven (7) of them were assigned to the supplement (SUP) group and the remaining six (6) were the placebo or control (CON) group. The control group is meant to be used almost as a baseline, so that any differences seen between the two groups can be solely attributed to the supplement given to the treatment group. Simply put, every condition is the same for each group EXCEPT the supplement given to the SUP group. Easy enough.

Once admitted to the facility where they would be studied, the participant’s caloric requirements were established using the Harris-Benedict equation (~2,600kcals each). From here, each participant’s total caloric intake was split evenly over 3 mixed-meals (breakfast, lunch, dinner) with 59%, 27%, and 14% of calories coming from CHO, FAT, and PRO, respectively (This means each group got the same percentage of carb, fat and protein given their caloric requirements). This amounted to about 380g CHO, 93g FAT, and 70g PRO for each participant. In addition to the 3 meals, the SUP group was given an AA supplement containing 30g sucrose, and 15g essential amino acids (EAA) dissolved in a diet, calorie-free beverage, regardless of caloric requirements. The CON group received only the diet beverage. The supplement was given after each meal i.e. three times throughout the study protocol to each of the seven SUP group members.

Throughout the study blood samples were taken periodically and a continuous infusion of stable isotope phenylalanine was administered in order to measure muscle protein synthesis (MPS) as well as the rate of that synthesis.

The Results

The second most important section of the paper is the results. The results tell you whether or not the experimental condition worked or didn’t work. This either proves or disproves the hypothesis.

The most salient results of this study were as follows:

The meals plus the EAA+CHO supplement resulted in a greater anabolic response than just the meals alone.
The rate of MPS in the SUP group was ~25% greater than the CON group.

Simply put, the SUP group had a greater anabolic response from the supplement, and their rate of MPS was greater than the CON group. The rest of the results are listed in the abstract above. I merely listed the most relevant ones to my discussion.

The Discussion

This is the part where the authors take their results and try to explain them. They might also relate their findings to other previous findings that were seen in other studies done elsewhere. This is also the chance for the authors to reflect on the strengths and weaknesses of the paper wherein suggestions can be made for future studies. Sometimes a separate section, conclusions can also be made in the discussion. This is essentially their interpretation of the results which can be accepted or doubted by the reader. Here is where I will give my interpretations of the findings. As I stated earlier, feel free to agree or disagree, but make sure to back it up. I will refer you to my very first post back in January as to why I believe this.

My Interpretations

At first glance, one might argue that an amino acid supplement taken in between meals indeed works to enhance MPS and that taking an EAA supplement will surely increase muscle synthesis (especially bodybuilders and muscle-hungry gym-goers that only care about increasing muscle mass). However, let us backtrack and take a look at the study protocols again before we go jumping to conclusions.

First-off, this is a short-term study (16-hrs) and tells us nothing about consistent, long-term AA supplementation.

Secondly, and more importantly, the researchers used protein intakes which are DRASTICALLY lower than what many bodybuilders or other athletes consume on a daily basis. In this study, all participants consumed a paltry 70g of protein/day spread over their 3 meals (~23g per meal). In my opinion, 70g is not sufficient enough protein for the athletic population trying to build muscle, so the results cannot accurately be applied to this population who most definitely do consume enough protein. Furthermore, even with the EAA+ CHO supplement, the SUP group only amounted to 115g total protein which is barely adequate to begin with, which brings me to my next and final point.

The final major flaw of this study was that the SUP group’s total caloric intake, as caused by the supplement, was greater than the CON group due to the extra 45g EAA and 90g of CHO (~540kcals). This amounted to ~2,600kcals for the CON group and ~3,150kcals for the SUP group. Again, the two group’s diet conditions were so different that it’s hard to say that the supplement is what caused the results. It could have just been virtue of eating 500+kcals over the SUP group’s baseline needs. Had the researchers controlled for kcals the study would have been much better. Usually during studies using micronutrients this isn’t an issue because vitamins and minerals do not supply calories. However, this study seemed to neglect controlling for calories, and to me this was the biggest flaw.

In conclusion, the aforementioned are all confounding factors which bring the final results into question. Does this mean that taking an amino acid supplement won’t help increase MPS for the athlete/bodybuilder looking increase his/her muscle mass? Well, it’s hard to say. Given adequate protein intake (definitely one above the intakes seen in the study), adequate calories, and a solid training protocol it’s nearly impossible to argue that this study answers the question at hand. There are just too many confounding factors and weaknesses in the study which make it useless when put into context of the athletic population who most likely cover all their dietary needs to begin with. A much better study would have used adequate protein intakes and would have controlled for calories.

Summing it up

As you can see, it’s not good enough to only read the abstract. There are many components of a research paper besides the results and conclusions. It is up to you to dig through the literature, recognize potential flaws and bias, and make your own decisions given the data. As I just showed you, something may seem great at first glance, but once you start picking it apart and analyzing the details you may realize the results aren’t as applicable or as relevant as you thought. Which brings me back to the insistent and unrelenting theme of my Blog, and that is context. It is IMPERATIVE to keep things in context, because without context, results mean nothing.

Posted in Protein, Reviews, Supplements | Leave a comment

Other Novel Forms of Creatine: A Brief Follow-up Commentary

Posted on April 24, 2012 by decline104

Opening Comments

So just a little while ago I did a little digging around on BB.com to see the Top 10 Selling Products, just to see what people were spending their hard-earned money on, and without naming the product, I found one that really make me laugh. I found it EXTREMELY relevant, given my topic yesterday about creatine; because this company’s new pre-workout formulation is probably just a huge waste of money. Literally, their advertisement goes as follows;

“Contains 5 novel creatine sources – No creatine monohydrate.”

Moreover, right on the bottle it mentions, “5 novel creatine analogs,” which simply means, creatine equivalents, more or less. Now, this is supposed to persuade the consumer that this product is better than other pre-workout supplements which contain boring old plain creatine monohydrate, because the analogs are better used by the body and will help you get bigger. However, there has been little research done on these newer creatine forms whereas creatine monohydrate has been proven time and time again to be an effective ergogenic aid (see article below). However, given the flashy label, awesome adjectives, and muscular bodybuilders who are endorsed by the company, who could resist such an appealing product??

The Ingredients

As are most things, a dietary product is only as good as what’s inside, and sadly enough, this product is nothing but a way to produce expensive urine. If you’re shelling out $36+ for this crap, I feel sorry for you. To the left, I’ve provided a nice screen shot of this product’s “novel” ingredients. The rest of the label is much, much longer. As you can see, the “Proprietary Blend,” which is just a fancy way of saying, “a bunch of stuff thrown together,” is made up of Di-Creatine-Malic Acid, Creatine-Sodium Phosphate, Creatinol-O-Phosphate-Malic Acid, Creatine Ethyl Ester HCl, and Creatine-Alpha-Aminobutyric Acid (Creatine AAB). We’ve already discussed CEE in depth, so I won’t bore you to death with that again, however the rest of these creatine analogs do deserve some scientific scrutiny, and that’s exactly what I’m going to do.

Creatine Forms

Below is essentially the same little chart I showed yesterday but altered to include the ingredients listed in the product above (except Creatinol-O-Phosphate). Again, the chart shows different creatine forms and their respective % of creatine in relation to creatine monohydrate [1].

So far, looking at the chart, it looks like EACH AND EVERY ONE of the creatine analogs contains LESS creatine than regular old creatine monohydrate. Already this product looks like a scam, however let’s continue, because, even though they may have less creatine per unit, they might be more bioavailable… although I doubt that’s the case.

Creatine Characteristics

In my last article I talked a lot about solubility, stability, and bioavailability and how CM differed from CEE in those respects. Like I said, I am not going to bore you with CEE again (we know it is crap), but I will touch upon the other creatine analogs briefly. If you haven’t read my previous article, I suggest doing so now.

Solubility

Essentially each one of the creatine analogs is a creatine salt (except Creatinol-O-Phosphate), meaning that it is a creatine molecule with an acid attached. This basically allows the creatine to become more soluble by lowering the pH of the liquid. If you remember from yesterday, creatine is more soluble in warmer water or liquids with a lower pH. The solubility factor goes to the creatine salts (except Creatinol-O-Phosphate); however we know how to easily correct this for CM without the added costs.

Stability

To reiterate yesterday’s comments; the lower the pH of the liquid, the greater the extent of creatine’s degradation (in addition to solubility) to creatinine. One might accurately say that this is irrelevant because we’re not leaving the solution sitting around long enough to allow the creatine salts to degrade. However, the stomach environment is acidic and these newer forms of creatine are less stable than monohydrate in acidic environments [1] and could definitely degrade to creatinine before they even reach circulation (CEE definitely does). To date there are no studies comparing these (specific) newer creatine analogs to CM, however, these analogs do contain less creatine than CM and it can be assumed that given their reduced stability in the stomach, they would offer no benefit over regular CM.

Bioavailability

There is one study I’m aware of that does compare creatine monohydrate to an effervescent creatine (tricreatine citrate) abbreviated TCC, on total body creatine retention [2]. 16 males were assigned to consume either a placebo (dextrose), creatine monohydrate, CM + dextrose, or TCC + dextrose supplement. It turns out that the CM + dextrose group had the highest levels of creatine retention (muscle stores), retaining about 80% of the ingested supplement. The regular creatine monohydrate without dextrose and the TCC + dextrose retained about 61 and 63% creatine, respectively, meaning, that even with the added dextrose, TCC was no better than CM alone, but was inferior to CM + dextrose. In addition, TCC contains about 66% creatine, which is more than more the creatine analogs contain within NO Xplode. Although hard to generalize, it can be assumed that these salts add no additional benefit over CM either. More research is needed to make definitive conclusions, however.

Creatinol-O-Phosphate (COP)

So you may have noticed that so far I haven’t really mentioned COP. Well, it is for the fact that I pretty much grouped all the other creatine compounds together, and COP doesn’t really match up with them. COP is less soluble than CM; that much I did point out. However, there was evidence back in the late 70’s that COP could be a precursor to creatine within the body due to increased levels of creatinine in the urine of patients taking COP [3]. The creatine, however, just degrades to creatinine through normal processes and probably does not contribute to creatine stores. In other words, they’re trying to sell you on a cool name rather than definitive research.

Save Your Money

Again, it all comes down to what people will buy. If you put enough flashy adjectives on a bottle and get a huge muscular IFBB pro to endorse your product then you can pretty much watch the cash flow in. This product comes from one of the bigger supplement companies out there, so I am positive there are plenty of people consuming this pre-workout supplement. Please, do yourself a favor and buy something that’s actually been shown to work. Too easily we get caught up in the flashy advertisement and can’t see past (or through) the BS. And for what, an extra rep at the gym you could have easily gotten if you focused more on your diet and training protocol than buying the newest and enhanced pre-workout formula? I’ll leave it at that.

References

1. Jager R, Purpura M, Shao A, Inoue T, Kreider RB. Analysis of the efficacy, safety, and regulatory status of novel forms of creatine. Amino Acids 2011;40:1369-1383.

2. Greenwood M, Kreider RB, Earnest C, Rasmussen C, Almada A. Differences in creatine retention among three nutritional formulations of oral creatine supplements. J Exerc Physiol 2003;Online 6:37-43.

3. Melloni GF, Minoja GM, Lureti GF, Merlo L, Pamparana F, Brusoni B. Acute clinical tolerance of creatinol-O-phosphate. Arzneimittelforschung 1979;29(9A):1477-1479.

Posted in Supplements | Leave a comment

Creatine Monohydrate vs. Creatine Ethyl Ester: Settling the Score!

Posted on April 24, 2012 by decline104

Opening Comments

A little over two weeks ago I gave a presentation to the Army ROTC cadets at Rutgers University, wherein I fielded some questions following the presentation. During that time I was asked the question of whether or not I thought creatine monohydrate was better than creatine ethyl ester in terms of its beneficial effects on weight training (increased strength, muscle size, etc.). This was not surprising given the growing popularity of newer versions of creatine that purport greater strength and muscle gains, etc. Due to various factors, creatine has taken many shapes and forms over the years, and in doing so, has become shrouded in controversy, mainly pertaining to the effectiveness and ergogenic (performance enhancing) capabilities between traditional monohydrate and these other alternate forms.

Without going into my answer just yet, I thought this question would be a great topic for my blog, and is indeed the focus of today’s article. First I will discuss what creatine actually is and how’s it made in the body, along with some of the claims and research behind creatine monohydrate’s characteristics. Then I will get into what creatine ethyl ester (CEE) is and the claims surrounding its potential (non-existent?) benefits over regular creatine monohydrate (CM). Many are under the impression that these newer forms of creatine are better… but are they, and in particular, is CEE?

Creatine 101: a Primer on Creatine Metabolism [1]

So, what is creatine? Well, for starters, creatine is not some dangerous steroid that many uneducated individuals make it out to be, if only half joking. Creatine nutrient found naturally in food sources such as fish and meat and is synthesized daily in all humans and other mammals. Its primary role is to help regenerate ATP (the body’s energy currency) from ADP during intense exercise. Unfortunately it’s only used during shorts bouts of physical exertion i.e. sprints and lifting weights (sorry endurance crowd). There has even been some evidence for the use of creatine in clinical settings, specifically for the use of treating various muscle myopathies and cardiac diseases. That however, is way beyond the scope of today’s focus.

Creatine is synthesized every day from three amino acids, namely glycine, arginine, and methionine. The process starts in the kidney with arginine and methionine, wherein the two amino acids react to form guanidino acetic acid (GAA). GAA then moves to the liver where it is then methylated to become creatine. It’s as simple as that. The newly formed creatine then makes it way to skeletal muscle wherein a phosphate (P) is added, making creatine phosphate. It is this phosphate group (P) which gets added back on to ADP (adenosine DI phosphate) to yield ATP (adenosine TRI phosphate) and essentially increase the ability for the muscle to do more work. The more Creatine phosphate one has, the greater the potential to phosphorylate ADP back to ATP and increase work capacity. In fact, supplementing with creatine (~20g/day for 5 days) has been shown to increase muscle creatine stores (both total and creatine phosphate) by anywhere from 15-40% [2-4], thus proving its potential for ergogenic capabilities.

Now, you may also be wondering why we constantly make new creatine? Well, it is for the simple, yet important, fact that creatine is spontaneously degraded to creatinine in muscle tissue and excreted in the urine. Therefore dietary intake and synthesis make up the majority of our creatine stores (and supplementation to some extent for those using it). The more muscle mass you have, the greater your creatine stores can be, as well as the more you excrete in your urine as creatinine (it’s a two way street). Obviously, vegans and vegetarians would have lower creatine stores than omnivores who regularly consume meat and fish. They (vegetarians and vegans) also excrete less. Vegetarians and vegans would be prime candidates for creatine supplementation due to existing low levels.

Creatine in the Market Place

As a supplement, creatine was introduced in the early 1990’s as creatine monohydrate (CM). It has actually been studied as early as the mid-1920’s but didn’t catch on as a dietary supplement until the past 20+years. CM is the form of creatine found in fish and meats. Shortly after its introduction, newer versions of creatine were introduced to the market, trying to appeal to consumers by promoting their better solubility, stability, bioavailability, and performance enhancing capabilities (ergogenic capacity). Who could resist!? Although partially true, these claims are not substantiated by research and are nothing more than playing at every man’s weakness… and that’s the desire to get stronger (ironic).

So what is the research behind creatine monohydrate that has makes it such a popular supplement, and where are the claims for other versions, specifically creating ethyl ester, going wrong? Time to look into the research and start tallying up the points!

The Research

Solubility [5]

It just so turns out that creatine monohydrate is relatively poor at mixing with water (solubilizing). If any of you have ever added a tsp. (~5g) to your shaker, you know well that the powder does not dissolve and that you’re most likely going to get a couple granules left in your mouth. But so what, just a small price to pay for strength, right? That’s my view anyway. In fact, it would take about a liter of cold water (~40°F) just to dissolve that tsp. of creatine, and who in their right mind would chug a liter of cold water half an hour or so before they lift? Probably not many, however, if you just use warmer water (~70°F) you will increase the solubility, reduce the actual amount of water needed, and boom, dissolve your creatine! You can also just lower the pH (put some lemon juice in your water) and this will also increase the solubility. This gave rise to some liquid versions of creatine which are not effective, reasons for which I explain shortly.

Stability

Along a similar vein, stability is a major factor among creatine properties. Interestingly enough, it has been showed that dry CM being stored at temperatures as high as 140°F had no significant signs of creatinine until 3.5 years later! [6] Pretty good shelf life for such harsh conditions. However, unlike its dry form, CM is not very stable in solution (liquid) and therefore degrades to its inactive form (creatinine) more easily [7]. As long as you drink it immediately there is neither harm nor waste. Only after a few days of being mixed will it start to degrade, and the lower the pH of the liquid, the faster the conversion to creatinine [7-9], therefore mixing it with water (pH ~7) won’t degrade it much at all. And even if you use warmer water or drink it with lemon juice in your own home there will be minimal conversion, if any, as long as you consume it immediately thereafter and don’t leave it sitting around for hours or days on end.

So where does CEE fit into all of this? Well, it just so happens that CEE is even LESS stable in acidic environments (like the stomach for instance) than CM due to the added ethyl group. In fact, this added ethyl group actually accelerates the breakdown of CEE to creatinine [10], and moreover, researchers Giese and Lecher (2009) [11] concluded that under normal physiological conditions CEE is primarily broken down to creatinine and that it most likely contains no ergogenic effect when used as a supplement. They actually went as far as to call it a PRO-nutrient for creatinine rather than creatine. This is the total OPPOSITE of what the companies are claiming! So far it’s not looking good for CEE. But perhaps you’re still not yet convinced.

CM – 1, CEE – 0

Bioavailability

Another important factor of creatine supplementation is bioavailability. This simply means how well the body can 1) absorb and 2) use creatine after ingestion. First off, absorption of CM is nearly 100% [12] (Awesome!), and there is even some evidence that taking it with carbohydrate, protein, or both, or other various compounds like beta-alanine and HMB enhance creatine’s uptake into skeletal muscle [13-15]. However, looking directly at CM vs. CEE [16] it was shown that CEE increased serum (bloodstream) creatinine levels significantly in subjects taking the supplement. For those who don’t follow, that means they were just pissing it out instead of taking it up in the muscle. Also, creatine levels in the muscle for the CEE group were not significantly different than those in the PLACEBO group, i.e. the group not receiving ANY creatine AT ALL. This isn’t to say they didn’t have more; they just didn’t have much more. CM, however, WAS significantly different from the placebo and DID NOT show a significant increase in serum creatinine levels. Simply put, they were able to absorb AND use the creatine. Which brings me to a point that drives me absolutely CRAZY when I (seldom) go into GNC, and that is when the sales rep tries to sell me on the fact that some new form of creatine doesn’t cause water retention. Water retention is a side effect (if you will) of CM [1], but it also lets you know that it’s working. Of course there’s no water weight with CEE, you’re pissing most of it out! However, the same study did see that people who were taking CEE still gained some water weight, albeit less than the CM group… Hmmm, I wonder why?

CM – 2, CEE – 0

Creatine Forms

On a more interesting note, creatine ethyl ester actually contains LESS creatine than creatine monohydrate. Here’s a table of some creatine forms and their respective % of creatine in relation to CM [5]. Just something I found interesting. Companies try to sell a product that is inherently less creatine, for more money. It makes no sense.

CM – 3, CEE – 0

Creatine and Performance

Again, looking at the aforementioned CEE study by Spillane and co. [16], they also looked at actual performance outcomes during the study, which included indices of strength, training adaptations and fat free mass. To this date, this is the only study to do so (CM vs. CEE in this manner), making it very difficult to generalize. Nonetheless, subjects in the CEE group did not experience any additional gains in strength (1RM for bench press), body mass, muscle mass, or sprint performance (Wingate Test) over the CM group or placebo group. In addition, the CM group scored highest in all of those categories, although it was not statistically significant. I should note, however, that this study was conducted in untrained individuals, so any gains that were seen were most likely due to the training protocol and not the supplementation per se. Further studies in weight trained populations are needed to confirm or deny these findings. Either way, in this untrained population, CEE afforded no additional benefits over CM or the placebo.

CM – 4, CEE – 0

Given the accumulation of data thus far in addition to the findings of this study [16] it’s not looking good for CEE. Conversely, studies looking at CM, as an ergogenic aid, are well established and relatively consistent [17-25]. Without getting into too much detail, CM works, and works consistently well, contributing to the fact of why it’s so widely studied and so widely used. I’ll leave you to do some reading in your spare time. The references are always found below. And even if you don’t believe CM works well, it’s safe to assume it works a hell of a lot better than CEE. And it’s probably safer too (no extra creatinine floating around in the bloodstream).

CM – 5, CEE – 0

Final Score

In the end, after tallying up all the points, creatine monohydrate wins, hands down. Surprised anyone? There were no additional benefits to consuming CEE over CM, and in all actuality, there weren’t ANY noticeable benefits from CEE whatsoever… unless you’re in the business of selling CEE. Then in that case, you’re laughing all the way to the bank.

Moral of the story, save your money, buy something that works (and is cheaper!), and try avoiding sensational claims that promise things that seem too good to be true, because, well, they usually are. Given CM’s outstanding track record and ability to remain stable over long periods of time, I would buy CM in bulk, keep it proper stored at temperatures under 140°F (that’s sarcasm), and reap the benefits of CM for years to come. I know I do!

References

1. Wyss M, Kaddurrah-Daouk R. Creatine and creatinine metabolism. Physiol Rev 2000;80(3):1107-213.

2. Kreider RB. Creatine supplementation in exercise and sport. In: J. Driskell, I. Wolinsky (eds). Energy-yielding Macronutrients and Energy Metabolism in Sports Nutrition. CRC Press LLC, Boca Raton, FL, 1999, pp. 213-242.

3. Kreider R. Creatine supplementation: Analysis of ergogenic value, medical safety, and concern. J Exerc Physiol 1998;Online 1:7-18.

4. Williams MH, Kreider R, Branch JD. In: Creatine: The Power Supplement. Human Kinetics Publishers, Champaign, IL, 1999.

5. Jager R, Purpura M, Shao A, Inoue T, Kreider RB. Analysis of the efficacy, safety, and regulatory status of novel forms of creatine. Amino Acids 2011;40:1369-1383.

6. Jager R. The use of creatine monohydrate in sports nutrition. 2003, Freising, Germany.

7. Howard AN, Harris RC. Compositions containing creatine. 1999, US Patent.

8. Cannon JG, Orencole SF, Fielding RA, Meydani M, Meydani SN, Fiatarone MA, Blumberg JB, Evans WJ. Acute phase response in exercise: interaction of age and vitamin E on neutrophils and muscle enzyme release. 1990 Am J Physiol 259 (6 Pt 2):R1214-R1219.

9. Dash AK, Mo Y, Pyne A. Solid-state properties of creatine monohydrate. J Pharm Sci 2002;91(3):708-718.

10. Child R, Tallon MJ. Creatine ethyl ester rapidly degrades to creatinine in stomach acid. Paper presented at the ISSN 4^th Annual Meeting, Las Vegas, Nevada, June 12, 2007.

11. Giese MW, Lecher CS. Non-enzymatic cyclization of creatine ethyl ester to creatinine. Biochem Biophys Res Commun 2009;388(2):252-5.

12. Deldicque L, Decombaz J, Zbinden Foncea H, Vuichoud J, Poortmans JR, Francaux M. Kinetics of creatine ingested as a food ingredient. Eur J Appl Physiol 2008;102(2):133-143.

13. Cribb PJ, Williams AD, Hayes A. A creatine-protein-carbohydrate supplement enhances responses to resistance training. Med Sci Sports Exerc 2007;39(11):1960-1968.

14. Hoffman J, Ratamess N, Kang J, Mangine G, Faigenbaum A, Stout J. Effect of creatine and beta-alanine supplementation on performance and endocrine responses in strength/power athletes. J Sport Nutri Exerc Metab 2006;16(4):430-446.

15. Jowko E, Ostaszewski P, Jank M, Sacharuk J, Zieniewicz A, Wilczak J, Nissen S. Creatine and beta-hydroxy-beta-methylbutyrate (HMB) additively increase lean body mass and muscle strength during a weight training program. Nutrition 2001;17(7-8):558-566.

16. Spillane M, Schoch R, Cooke M, Harvey T, Greenwood M, Kreider R, Willoughby DS. The effects of creatine ethyl ester supplementation combined with heavy resistance training on body composition, muscle performance, and serum and muscle creatine levels. J Int Soc Sports Nutr 2009;6:6 (14 pages).

17. Greenhaff P. Creatine supplementation and implications for exercise performance. In: Jeudendrop A, Brouns M, Brouns F (eds) Advances in training in nutrition for endurance sports. Novartis Nutrition Research Unit, Maasticht.

18. Kraemer WJ, Volek JS. Creatine supplementation. Its role in human performance. 1999 Clin Sports Med 1999;18(3):651-666.

19. Kreider RB. Effects of creatine supplementation on performance and training adaptations. Mol Cell Biochem 2003;244(1-2):89-94.

20. Cribb PJ, Hayes A. Effects of supplement timing and resistance exercise on skeletal muscle hypertrophy. Med Sci Sports Exerc 2006;38(11):1918-1925.

21. Kreider RB, Ferreira M, Wilson M, Grindstaff P, Plisk S, Reinardy J, Cantler E, Almada AL. Effects of creatine supplementation on body composition, strength, and sprint performance. Med Sci Sports Exerc 1998;30(1):73-82.

22. Volek JS, Kraemer WJ, Bush JA, Boetes M, Incledon T, Clark KL, Lynch JM. Creatine supplementation enhances muscular performance during high-intensity resistance exercise. J Am Diet Assoc 1997;97(7):765-770.

23. Volek JS, Duncan ND, et al. Performance and muscle fiber adaptations to creatine supplementation and heavy resistance training. Med Sci Sports Exerc 1999;31(8)1147-1156.

24. Willoughby DS, Rosene J. Effects of oral creatine and resistance training on myosin heavy chain expression. Med Sci Sports Exerc 33(10):1674-1681.

25. Willoughby DS, Rosene J. Effects of oral creatine and resistance training on myogenic regulatory factor expression. Med Sci Sports Exerc 35(6):923-929.

Posted in Supplements | 4 Comments

High-fructose Corn Syrup: Obesogenic Evil or Dietary Scapegoat, Part 2

Posted on April 24, 2012 by decline104

Opening Comments

Welcome back for part 2 of the great HFCS debate. Before I begin, I’d like to briefly recap last week’s arguments (for those who may have missed it) by simply copying and pasting my concluding remarks:

In summary, energy from added sugars, namely HFCS, is higher now than it was in 1970, but it increased at a slower rate than that of other macronutrients in proportion to our total caloric intake. Also, availability of HFCS has also been on the decline since 1999 yet obesity prevalence still continued to rise. Finally, total energy has not been driven up disproportionally by HFCS, but rather the diet as a whole. Simply stated; we’re eating more of EVERYTHING.

So, now that we’re all caught up, we can all agree that increased consumption of HFCS doesn’t prove a thing and we can now move on to today’s focus, which I’m just going to jump right into. Basically there needs to be a compelling and convincing argument that HFCS is indeed different from sucrose (which we’ve already seen really isn’t the case, at least not compositionally) and is uniquely obesogenic, meaning that it causes you to gain weight more so than sucrose could. In lieu of this theory there has been a surge of studies within the past couple of decades on fructose and HFCS. These studies help to provide a biological rationale (mechanism) for why our increased consumption is potentially causing obesity. Much of these studies, however, are based on rodent data and/or studies which involve HUGE doses of fructose (some without accompanying glucose) that are irrelevant to normal human consumption patterns. Although these types of studies provide insight to certain, albeit rarely used, biochemical pathways, and in doing so show us the harms of massive quantities of fructose, my retort is that what nutrient in massive excess WON’T cause adverse effects? Abuse anything well enough and of course you’re going to see detrimental outcomes. That being said, let us begin.

Fructose Metabolism

A common argument when talking about HFCS and obesity is that fructose metabolism is markedly different from that of glucose, and fructose strongly favors fat synthesis, otherwise known as de novo lipogenesis (DNL), a topic I covered in depth a couple of weeks ago. Although the metabolism of fructose is indeed different than that of glucose metabolism, this argument holds PLENTY of water.

First off, upon fructose consumption (which I will say right now, almost NEVER happens devoid of glucose consumption) most of it (~50%) is either oxidized in the liver [1] or is converted to glucose and is then oxidized by other tissues in the body [2]. Either way you look at it, almost half of what you consume is immediately oxidized to CO2 (i.e. not stored as fat). The rest of the fructose is either; 1) converted and stored as liver glycogen (~17%) [3]; 2) converted and released as lactate (~25%) [4-6]; or 3) converted into fatty acids by way of DNL (~8%). However, as you can see, DNL is not a major pathway, as shown by various studies [7-9], and most likely does not contribute to any appreciable gain in body fat (see previous article on DNL).

This, however, is not to say that studies don’t exist where appreciable levels of plasma triglycerides (fat floating around in the blood stream) were made from fructose. There are two that I know of: one was in a hamster study, which is irrelevant because the pathway that was seen in hamsters hasn’t been found in humans yet, and the other was done in humans about 12 years ago. Here a group of researchers saw that a group of healthy males who were fed diets containing fructose increased their plasma triglycerides by 32% [10]. The diet, however, contained 17% of total calories as fructose. Even looking at estimated fructose intake from 1999, when fructose and HFCS consumption were THE HIGHEST THEY HAD EVER BEEN, fructose only accounted for ~8% of total kcals. And it can easily be assumed that this number is lower today due to reduced consumption since that time (see previous HFCS article). Therefore this study is irrelevant to what normal people usually eat. And just to stress the point, if you do the calculations, 17% of today’s kcal intake (which is ~2,700kcals) is about 460kcals. That equates to ~115g of fructose alone. You would have to consume nearly 2 liters of soda a day in order to get that much fructose. Which brings me to the point I will continue to stress within everything I write on this site; and that is context.

Context!!!

Without context, research means nothing. The fact of the matter is that we’re talking about the effects of HFCS within NORMAL consumption patterns. No one in their right mind consumes almost a fifth of their calories as fructose (be it from HFCS or any other sources). And sure, maybe you do know someone who drinks a 2-liter bottle of Coke a day, but my guess is that they’ve probably got a whole host of other things going on rather than JUST fructose consumption (i.e. sedentary behavior, other poor dietary habits, poor sleep/wake cycle, etc.). Moving on.

Fructose and its Effects on Insulin, Leptin and Subsequent Food Intake

The next huge argument surrounding HFCS and obesity is fructose’s effects (or lack thereof) on insulin and subsequently, leptin. Insulin, as many of you may know, is a storage hormone released by the pancreas in response to a rise in glucose concentration in the bloodstream. As I suspect, most of you don’t know what leptin is, so long story short, leptin is a hormone, stimulated by insulin, which tells the brain to stop eating and increase metabolism (double awesome!). Based on this principle, many researchers believe that, because fructose has such a minimal effect on insulin release, there is no leptin response and therefore no satiety signals on which the brain can act. Simply put; fructose may have no effect on appetite suppression.

No insulin = no leptin = keep on eating. But is this true?

Well, indeed the glycemic index, and therefore the insulin response, of fructose is much (about fivefold) less than that of glucose [11], but this isn’t to say that fructose doesn’t have any insulin response when consumed. If you remember, I mentioned earlier that fructose is converted into glucose in the body. This conversion requires the use of insulin in order to take up the newly formed glucose. So, in fact, there is a small amount of insulin released in response to actual fructose consumption.

But when do you EVER eat fructose by itself? Probably never. It’s nearly impossible to do unless you go to a health food store and buy a bag of fructose powder… and then only eat that. So yea, probably not likely. And let’s not forget, we’re talking about HFCS and not just fructose. If you remember the nice little table I provided last week, you should know that HFCS is nearly HALF glucose! Glucose DOES stimulate insulin, glucose DOES affect leptin. How easily we forget. So the better question would be; is HFCS any different from sucrose at stimulating insulin and leptin?

It just so happens that there is a couple of studies which show just that. A number of then show that not only do sucrose and HFCS BOTH elicit a leptin response, but they also have appetite suppressing effects [12-16]. Let me say that again. They were shown to actually SUPRESS participant’s appetites. How’s that for throwing a wrench into the gears?

And, if we want to take the original argument and pin fructose against glucose, it was shown that when looking at fructose solutions and glucose solutions given before a meal, studies show either NO DIFFERENCE in caloric intake between the two solutions, or a LESSER intake for people who consumed pure fructose before eating a meal [17-21]. There is one study which does show a greater consumption of food after consuming a fructose solution, however, this study had participants consume roughly 30% of their calories as pure fructose [5]. Now remember, just above we talked about how much 17% of total kcals is… now double that! These people were drinking almost 4-liters worth of soda a day. Now I ask you again, how relevant is that to NORMAL human consumption?

Fructose and Thermogenesis

Just to drive the point home, there happen to be a handful of human studies that saw higher levels of thermogenesis (energy expenditure, not fat storage) in men and women, as well as in obese women, after a mixed meal with 75g of carbs coming SOLELY from a fructose solution compared to another meal with 75g of glucose. In other words, there was higher carbohydrate OXIDATION (burning) and higher thermic effect of food (TEF) when fructose is given as the only carbohydrate source [1, 22-25]. This again shows that even high amounts of fructose might not get deposited as triglyceride, at least not in the short term.

Conclusions

Now I know I sound like a soda company’s wet dream right now, but it is my firm belief that, as a future dietitian and advocate for nutrition, we must not succumb to misinformation. We must learn how to accurately and effectively discern the relevant from the irrelevant. My goal over the past two weeks has been to show you all that certain views persist even in the face of solid research saying the exact opposite. HFCS doesn’t make people fat, food does, along with physical inactivity and a whole host of other factors. Trying to use HFCS as a scapegoat isn’t justified as far as I’m concerned. So with that being said, I will leave you all with some key points, taken directly from a paper written by metabolic researcher Dr. Geoffrey Livesey [26], who in my mind is the voice of reason needed within a world of fructose (mainly HFCS) hysteria. If you have never heard of him, I suggest you look him up; he is a world renowned metabolism expert. A few of his Key Points from said paper (not in any particular order) are as follows:

Moderate doses of fructose have neutral or diametrically opposite effects to those expected for very high or excessive fructose intakes and show evidence of improved glycemic control.
There is reason to believe that modest fructose ingestion could be beneficial for public health, whereas excess intake would be a risk to health. Practical application will depend on future research.
Epidemiological studies are difficult to interpret. The roles of [glycemic load] and other factors collinear with fructose intake need to be examined.
Intervention studies using humans use fructose at doses that are excessive compared with amounts generally eaten by adults; such are not interpretable for purposed of public health policy in adult nutrition.
Animal studies often use doses of fructose in excess of what humans would normally consume and so have a high potential to mislead about the public health aspects of fructose.

References

1. Tappy L, Randin JP, Felber JP, Chiolero R, Simonson DC, Jequier E, DeFronzo RA. Comparison of thermogenic effect of fructose and glucose in humans. Am J Physiol Endocrinol Metab 1986;250:E718-E724.

2. Delarue J, Normand S, Pachiaudi C, Beylot M, Lamisse F, Riou JP. The contribution of naturally labeled 13C fructose to glucose appearance in humans. Diabetologia 1993;36:338-345.

3. Nilsson LH, Hultman E. Liver and muscle glycogen in man after glucose and fructose infusion. Scan J Clin Lab Invest 1974;33:5-10.

4. Burns SP, Murphy HC, Iles RA, Bailey RA, Cohen RD. Hepatic intralobular mapping of fructose metabolism in the rat liver. Biochem J 2000;349:539-545.

5. Teff KL, Elliot SS, Tschop M, Kieffer TJ, Rader D, Heinman M, Townsend RR, Keim NL, D’Alessio DA, Havel PJ. Dietary fructose reduces circulating insulin and leptin, attenuated postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab 2004;2963-2972

6. Tounian P, Schneiter P, Henry S, Jequier E, Tappy L. Effects of infused fructose on endogenous glucose production. Am J Physiol Endocrinol Metab 1994;267:E710-E717.

7. Chong MF, Fielding BA, Frayn KN. Mechanisms for the acute effect of fructose on postprandial lipemia. Arthritis Rheum 2008;59:109-118.

8. McDevitt RM, Bott SJ, Harding M, Coward WA, Bluck LJ, Prentice AM. De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women. Am J Clin Nutri 2001;74:369-377.

9. Parks EJ, Skokan LE, Timlin MT, Dingfelder CS. Dietary sugars stimulate fatty acid synthesis in adults. J Nutr 2008;138:1039-1046.

10. Bantle JP, Raatz SK, Thomas W, Georgopolous A. Effects of dietary fructose on plasma lipids in healthy subjects. Am J Clin Nutr 2000;72:1128-34.

11. Foster-Powell K, Miller JB. International tables of glycemic index. Am J Clin Nutr 1995;62:871S-890S.

12. Stanhope KL, Griffen SC, Bair BR, Swarbrick MM, Keim NL, Havel PJ. Twenty-four-hour endocrine and metabolic profiles following consumption of high fructose corn sysrup-, corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. Am J Clin Nutr 2008; 87:1194-203.

13. Soenen S, Westerterp-Plantenga MS. No differences in satiety or energy intake after high-fructose corn syrup, sucrose, or milk preloads. Am J Clin Nutr 2007; 86:1586-94.

14. Melanson KJ, Zukley L, Lowndes J, Nguyen V, Angelopoulos TJ, Rippe JM. Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on apetite in normal-weight women. Nutrition 2007; 23: 103-112.

15. Monsivais P, Perrigue MM, Drewnowski A. Sugars and satiety: does the type of sweetener make a difference? Am J Clin Nutr 2007; 86: 116-23.

16. Melanson KJ, Angelopoulos TJ, Nguyen V, Zukley L, Lowndes J, Rippe A. High-fructose corn syrup, energy intake, and appetite regulation. Am J Clin Nutr 2008; 88(suppl): 1738S-44S.

17. Spitzer L, Rodin J. Effects of fructose and glucose preloads on subsequent food intake. Appetite 1987 Apr;8(2):135-45.

18. Rodin J, Reed D, Jamner L. Metabolic effects of fructose and glucose: implications for food intake. Am J Clin Nutr 1988 Apr;47(4):683–9.

19. Rodin J. Comparative effects of fructose, aspartame, glucose and water preloads on calorie and macronutrient intake. Am J Clin Nutr 1990;51:428–35.

20. Rodin J. Effects of pure sugar versus mixed starch fructose loads on food intake. Appetite 1991;17:213–9.

21. Moran TH. Fructose and satiety. J Nutr. 2009 Jun;139(6):1253S-1256S. Epub 2009 Apr 29.

22. Schwarz JM, Schutz Y, Piolino V, Schneider H, Felber JP, Jequier E. Thermogenesis in obese women: effect of fructose vs. glucose added to a meal. Am J Physiol. 1992; 262: 394-401.

23. Schwarz JM, Schutz Y, Froidevaux F, Acheson KJ, Jeanprêtre N, Schneider H, Felber JP, Jéquier E. Thermogenesis in men and women induced by fructose vs. glucose added to a meal. Am J Clin Nutr ; 49(4): 667-74.

24. Simonson DC, Tappy L, Jequier E, Felber JP, DeFronzo RA. Normalization of carbohydrate-induced thermogenesis by fructose in insulin-resistant states. Am J Physiol 1988; 254: 201-7.

25. Blaak EE, Saris WH. Postprandial thermogenesis and substrate utilization after ingestion of different dietary carbohydrates. Metabolism: clinical and experimental 1996; 45: 1235-42.

26. Livesy G. Fructose ingestion: dose-dependent responses in health research. J Nutr 2009 Jun;139(6):1246S-1252S.

Posted in Carbohydrate, Misc. | 4 Comments

High-fructose Corn Syrup: Obesogenic Evil or Dietary Scapegoat, Part I

Posted on April 24, 2012 by decline104

High-fructose Corn Syrup: Obesogenic Evil or Dietary Scapegoat, Part I

Today’s topic is probably one of my favorite topics, partly because it’s so controversial and partly because there is so much research behind it (epidemiological and lab-based), which makes it fun to draw conclusions. Over the years, high-fructose corn syrup has gained so much attention ever since its introduction into the food supply in the late 1960’s, largely in part to HFCS’s increased availability and consumption since that time, as well as similar rising trends in obesity. Many have tried to relate the two data sets to make the case that it is indeed HFCS that is causing this weight gain, but this just simply isn’t the case when you look at direct data from laboratory studies. Because this topic is so misconstrued and unfounded I will be devoting not one, but TWO articles to the topic of HFCS. Today will just be devoted to looking at the history behind HFCS, its introduction into the US food supply, and lastly, obesity trends, HFCS consumption trends (as well as total caloric intake trends) and the implications between the two. For part 2 I will delve into the more sciency articles and support why I believe HFCS is perfectly fine to consume. Let’s get to it, shall we?

HFCS: How it’s Made, and when it was introduced

HFCS is made by the isomerization of glucose to fructose in corn sugar. This is just a fancy way of saying that the glucose in corn syrup is flipped (via the enzyme isomerase) so that it becomes fructose. If you look up the chemical structure of the two monosaccharides you’ll notice they’re just mirror images of each other; seems safe enough. Many believe that because HFCS is largely in part a processed food then that makes it less healthy (or more harmful). In fact, if you want to really get into manufacturing processes I suggest you look up how normal sugar is processed and then make your case.

HFCS was first introduced into the food supply in 1967 as HFCS-42. As the ending number indicates, HFCS-42 is 42% fructose. Not until 1977 was HFCS-55 introduced, which is now the predominant version used (and is the sole sweetener used in soda). In total, HFCS (55 and 42) makes up about 42% of caloric sweetener availability in the United States [1], with the rest coming from sources such as sucrose (table sugar), honey, glucose, fructose, and other, less popular sweeteners.

HFCS composition

It’s commonly thought that HFCS is ‘high’ in fructose, which is actually far from the truth. First off, there is no definition for what high is, and second off, if we are using sucrose as the reference sweetener, than HFCS, on average, has about 5% more fructose. That’s not a whole hell of lot more, nor is it particularly ‘high’. Below I’ve provided a nice table so that you can visually see the similarities and differences between popular sweeteners and their contributions to fructose intake, because after all, that’s what it’s all about; fructose intake.

As you can see, HFCS is not really all that high in fructose, and in some cases, it’s actually quite ‘low’. The next thing you’ll recognize is that HFCS- 55 is not that different in composition from sucrose or honey, both of which humans have been consuming for quite some time now. So does this little bit of extra fructose REALLY make such a huge difference in terms of weight gain? Some seem to think so, while others (like myself) seem to think not.

Obesity Trends in the US: 1976-2010

It’s no secret that Americans are getting fatter. You’ve all seen the CDC color changing America that goes from a nice shade of blue to a deep orange and dark red country. If that’s not a symbol of our deteriorating health status, I don’t know what is. In fact, there was an article in the NY Times just the other day asserting that airlines will be increasing their seat sizes in order to accommodate larger passengers. Now, this is not something that hasn’t been done before (because it has with train seats), but it definitely symbolizes the severity of today’s weight status in America and proves that there is something going terribly wrong with our either our metabolic machinery or our lifestyles. I tend to thinks it’s a combination of both despite others trying to make causation out of correlation as you’ll see very shortly. Actually, I don’t think our metabolic machinery is messed up at all, but rather, we’re just abusing it.

So, without getting into too much detail, the prevalence of obesity has increased since 1976 (right around when HFCS made its way onto the scene) to the point where upwards of 68% of all Americans are either overweight or obese [2]. In terms of obesity alone, the most recent CDC data estimates over 33% of adults ages 20-74 with another 17% of children and adolescents ages 2-19 are obese [2, 3]. This wouldn’t be such a problem if obesity wasn’t related to diseases such as Type II Diabetes, cardiovascular disease, coronary heart disease, hypertension, various types of hyperlipidemias, and some forms of cancer, but unfortunately it is. Not to mention the draining costs of healthcare paid by innocent citizens like you and me. So why pin this all on one macronutrient in the spectrum of everyone’s dietary consumption and lifestyle choices? There must be some compelling data to make this assertion, right?

HFCS Consumption Trends: 1967-2010

Coincidentally (and conveniently), HFCS consumption closely mimics obesity trends over the past 40 years, causing many to assume HFCS has played a significant role in obesity’s increase by disproportionally driving up caloric intake [4]. Today, HFCS consumption has increased greater than 100-fold since the 1970’s and contributes to ~132kcals/day/person (~19g fructose) [4]. Using the United States Department of Agriculture data set [1] we can see that HFCS availability (not consumption) went from 0g/day to about 92g/day in 2000, while total caloric sweeteners increased from 166g/day to 218g/day. However, since 1999 (when HFCS consumption peaked), there has been a steady decline in HFCS consumption [5] while obesity rates continued to rise [1, 2]. It should also be noted that, within the same time frame, total calories increased nearly 25% from about 2,170kcals in 1970 to 2,700kcals in 2005 [6]. Yea, it was HFCS and not the extra 530kcals a day that were causing people to gain weight! And, in actuality, HFCS consumption, as a percentage of total kcals, actually decreased over time, meaning, that as our caloric intake increased, HFCS decreased as part of that intake while other macronutrients like fats and flour/cereal products increased [5]. Simply put, HFCS did not drive up caloric intake, but rather other foods such as flour/cereal products and fats did.

HFCS Intake by Quintiles

The rest of what I will present today really sets the stage for where the studies which support HFCS causing obesity fall apart, wherein I’ll pick up again next week. Simply put, it’s from this information that makes the research relevant or not, and I will explain why. Judging from the data presented by the CSFII and USDA charts and interpreted by Bray et al. [4, 6-7], the lowest 20% of HFCS consumers only take in about 2% of their total energy (kcals) as HFCS, while the highest 20% take in about 11% of total energy as HFCS. On average, about 7% of the Nation’s total energy intake comes from HFCS. This, however, is based on the average 2,000kcal diet. Remember earlier that I said caloric intake increased by 24% since 1970 and is hovering around 2,700kcals. This REALLY makes consumption of highest quintile (these are the top 20% of people who consume HFCS), only about 8% and the National average about 5%. By using the recommended 2,000kcal diet instead of actual caloric intake, Bray and colleagues make HFCS consumption artificially high. This misrepresents the data and does a disservice to science. I would ask you to keep in mind these numbers, because a lot of what we will look at next week is based on research that administers either HFCS of fructose in doses that exceed the highest 20% of US consumption!!! So before I get ahead of myself let’s wrap up what I’ve gone over so far today.

Summary

I hope so far you’re on the same page as me and can see that even though HFCS consumption has increased over the years, it is nothing compared to overall caloric intake which is a MUCH better indicator of weight gain. Next week I hope to show you why all the studies that paint HFCS as bad are virtually irrelevant to normal consumption patterns and even some research that suggests higher fructose intake might even be beneficial.

References

1. Puttnam, JJ, Allshouse, JE. Food consumption, prices and expenditures: 1976-97. United States Department of Agriculture Research Service statistical bulletin no. 965, April 1999. Washington DC; US Government Printing Office, 1999.

2. Flegal, KM, Carroll, MD, Ogden, CL, Curtin, LR. Prevalence and Trends in Obesity Among US Adults, 1999-2008. The Journal of the American Medical Association. 2010;303(3):235-241.

3. Odgen, CL, Carroll, MD. Prevalence of Obesity Among Children and Adolescents: United States, Trends 1963-1965 through 2007-2008. Center for Disease Control and Prevention. 2010.

4. Bray GA., Nielson, SJ., Popkin, BM. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. The American Journal of Clinical Nutrition. 2004;79:537-43.

5. Economic Research Service, USDA. Loss-Adjusted Food Availability Data. Updated Feb 27, 2009.

6. White, JS. Misconceptions about high-fructose corn syrup: is it uniquely responsible for obesity, reactive dicarbonyl compounds, and advanced glycation endproducts? The Journal of Nutrition. 2009;139:1219-27.

7. Tippet, KS, Cypel, YS. Design and operation: the Continuing Survey of Food Intakes by Individuals and the Diet and Health Knowledge Survey, 1994-96. Continuing Survey of Food Intakes by Individuals 1994-96, Nationwide Food Surveys report no. 96-1. Beltsville, MD: US Department of Agriculture, Agriculture Research Service, 1998.

8. United States Department of Agriculture, Agriculture Research Service. Design and Operation: the Continuing Survey of Food Intakes by Individuals and the Diet and Health Knowledge Survey 1994-196 and 1998. Beltsville, MD: US Department of Agriculture, Agriculture Research Service, 2000.

Posted in Carbohydrate, Misc. | Leave a comment

Carbohydrates: Dietary Pariah

Posted on April 24, 2012 by decline104

The Claim

Perhaps the greatest misconception I’ve encountered over my times spent in the gym – and believe me, there are many – is that you can’t eat carbs past a certain time because they’ll get stored as body fat due to insulin being released. The funny part is that most of these guys, despite believing this dogma, try to induce the biggest insulin spike possible post-workout to drive carbs into the muscle (as glycogen). Along a similar vein, I want to look at this question of carbohydrate and fat storage and try to answer the question of carbs being stored as fat in adipose tissue. I think the low-carb craze (Atkins for example, there are many others), along with perceptions of low-carb diets being popularized by dieting bodybuilders who are known for ridiculous low levels of body fat, have contributed significantly to this mindset, and it needs to be unraveled. And don’t get me wrong, low-carb diets have their time and place. However, the misconception that carbs get stored as body fat and are the reason you should do low-carb is a completely misguided assumption.

The Facts

First off, can dietary carbohydrate even be stored as body fat? The quick and easy answer is yes, they absolutely can. However, the more pertinent question is, do they get stored as body fat, and to what extent? The fact of the matter is that although we have the ability to store dietary carbohydrate as body fat, our body’s capacity for doing so is very limited [1]. This process is called de novo lipogenesis (DNL), and luckily for us it doesn’t contribute greatly to our fat stores.

Carbohydrate Storage

So what’s the alternative? Well, our body has a wonderful storage form of carbohydrate called glycogen. Once we ingest a meal containing carbohydrate our levels of blood glucose increase causing the beta-cells of the pancreas to sense this increase and release insulin (a storage hormone) to clear the bloodstream of glucose (gym-rats you were right about one thing). In doing so a majority of the glucose is shuttled off to muscle tissue where it is converted to glycogen and stored for future use while some goes directly into glycolysis for immediate use. Any active tissue that can use glucose most likely will (save the heart which runs on a mixture of fatty acids, glucose and ketone bodies to some extent) while shutting down the body’s ability to make its own glucose (gluconeogenesis). The remaining glucose (if any depending on the meal size) is stored as glycogen in the liver. I should note that some of the glucose is also delivered to the brain where it is oxidized completely to CO2 (~120g/day for a normal, well fed person).

It is right about at this point where it gets a little tricky. If glycogen stores are full and the body is oxidizing carbohydrate as best it can (which actually increases as consumption increases), then yes, some carbohydrate will go to glycerol-3-phospate (G3P) and synthesized into triglyceride (our body’s storage form of fat) [2]. But, like I pointed out, this is limited and in most cases doesn’t exceed fatty acid oxidation.

The Research

As promised, what I’ve said thus far is supported by a number of studies which show that storing triglyceride made from carbohydrate is not the major pathway for carbohydrates in the human body [1, 3], even under conditions of excess calories from carbohydrate given in conjunction with a mixed diet [4-6]. It should be recognized that these studies used indirect calorimetry (a measure of heat production via CO2) which does not measure DNL directly, but rather Net DNL (synthesis – oxidation). Either way, NDNL exceeded lipolysis only after 5 days of overeating (175% daily kcal needs). This is probably not very realistic (or comfortable) for most people to do, unless you’re consciously eating almost twice as much as you need.

Furthermore, short-term studies looking at a single meal excessively high in carbohydrate (500g or about 2,000kcals from carbs alone!) were not shown to significantly contribute to fat gain after 24 hours [7, 8]. In fact, glycogen storage was seen as the primary fate of the excess carbohydrate, with stores increasing up to 1kg (or 2.2lbs for the metrically challenged)! Again, these studies used indirect calorimetry, but the theme remains the same: DNL < oxidation.

Studies using more accurate measure, such as stable isotopes have found limited DNL in subjects consuming very low-fats diets (high carbohydrate), but lipogenesis again did not exceed oxidation and contributed insignificantly to body fat stores [9, 10]. Even using more accurate measures yielded similar results. And because normal “Western Diets” are not typically very low in fat, DNL is probably not very active in most people under normal dietary consumption patterns anyway.

The Conclusion

So although DNL in fact does exist as a pathway in the human body, it doesn’t exist to any significant extent that you should label carbohydrates as “bad,” or fat promoting, or worse yet, exclude them past some arbitrary time. The fact of the matter is that any fat gain from DNL is likely to be trivial at best and shouldn’t worry you in the least.

References

1. Hellerstein, MK., Schwarz, JM., Neese, RA. Regulation of hepatic de novo lipogenesis in humans. Annu Rev Nutr 1996;16:523-557.

2. Labayen I, Forga L, Martinez JA. Nutrient oxidation and metabolic rate as affects by meals containing different proportions of carbohydrate and fat in healthy young women. Eur J Nutr. 1999;38(3):158-66.

3. Hellerstein, MK. De novo lipogenesis in humans: metabolic and regulatory aspects. Eur J Clin Nutr 1999;53(1):S53-65.

4. Minehira K, Vega N, Vidal H, Acheson K, Tappy L. Effect of carbohydrate overfeeding on whole body macronutrient metabolism and expression of lipogenic enzymes in adipose tisue of lean and overweight humans. Int J Obes Relat Metab Disord. 2004;28(10):1291-8.

5. Hellerstein, MK. Synthesis of fat in response to alterations in diet: insights from new stable isotope methodologies. Lipids 1996;31:S117-25.

6. Schwarz, JM, Neese, RA., Hellerstein, MK., et al. Short-term alterations in carbohydrate energy intake in humans: striking effects on hepatic glucose production, de novo lipogenesis, lipolysis and whole-body fuel selection. J Clin Invest 1995;96:2735–43.

7. Acheson, KJ., Schutz, Y., Bessard, T., et al. Nutritional influences on lipogenesis and thermogenesis after a carbohydrate meal. Am J Physiol 1982;246:E62–70.

8. Acheson, KJ., Flatt, JP., Jequier E. Glycogen synthesis versus lipogenesis after a 500-g carbohydrate meal. Metabolism 1982;31:1234–40

9. Hudgins LC, Hellerstein M, Neese R, et al. Human fatty acid synthesis is stimulated by a eucaloric low fat, high carbohydrate diet. J Clin Invest 1996;97:2081–91.

10. Hudgins LC, Seidman CE, Diakun J, Hirsch J. Human fatty acid synthesis is reduced after the substitution of dietary starch for sugar. Am J Clin Nutr 1998;67:631–9.

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