FDA Flexes Muscle at DMAA – But Should We Even Care?

Opening Comments

Times may be tough, but people still want to get JACKED! That is, not unless the FDA (Food and Drug Administration) has something to say about it. Over the past couple of months things have really heated up over the use of 1,3-dimethylamylamine (commonly known as DMAA) in pre-workout supplements, most notably Jack3d and OxyElite Pro from USPLabs  – the poster boys, if you will, of the DMAA movement. This past April the FDA issued warning letters to ten manufacturers and distributors (USPLabs included) of dietary supplements that contain the “adulterated” ingredient because these companies have not submitted the required evidence to support the safety of their products. To quote Daniel Fabricant, the Director of FDA’s Dietary Supplement Program;

“Before marketing products containing DMAA, manufacturers and distributors have a responsibility under the law to provide evidence of the safety of their products. They haven’t done that and that makes the products adulterated.”

The law that Fabricant speaks of is the Dietary Supplement Health and Education Act of 1994 (DSHEA) which essentially states that, in order for DMAA to be legally sold as a dietary supplement, it must meet one of two requirements; DMAA must either be 1) a naturally occurring substance or 2) have documented history of use prior to 1994. Unfortunately, the evidence to support DMAA as meeting either of these requirements is undeniably scarce. In fact, the entire legitimacy of using DMAA as a dietary supplement hinges on a single study from a Chinese journal that does not exist anymore [1] and whose contents have currently come into question. Because I cannot access this journal article I cannot (and will not) comment on the legitimacy of the issue. Whether or not it’s legal will be left up to the courts to decide.  Rather, I will have to do the next best thing and look at some studies that directly analyze the efficacy and safety of DMAA (as Jack3d and OxyElite Pro) as a dietary supplement.

Unfortunately, all the studies that look at DMAA are from a single group of researchers down at the University of Memphis, TN, whose studies were funded by USPLabs and whose articles (4 out of 5) were published in a second rate journal (1 edition), the reputation of which is tenuous at best. That being said, let’s see if these studies lend any insight whatsoever into to whether or not DMAA is even safe and, more importantly, if Jack3d is even worth spending money on.

DMAA and its Effects on Blood Pressure

In one of the first studies looking at DMAA, researchers had 10 healthy, exercise-trained subjects (5 men, 5 women) ingest either 250 mg caffeine alone, 50mg DMAA alone, 75mg DMAA alone, 250mg caffeine + 50mg DMAA, or 250mg + 75mg DMAA on five different test days [2]. The addition of caffeine is due to the fact that DMAA is usually taken in conjunction with it (like in Jack3d and OxyElite Pro). In the paper there was no specification of a wash-out period between dosages, although the study was considered a randomized, double-blind, cross-over study. Like I said, tenuous.

Subjects ingested the capsules on an empty stomach in the morning following a 10-hour fast – not a likely scenario for most gym-goers, save maybe the few but growing number of intermittent fasters out there. After ingestion, heart rate (HR) and blood pressure (BP) – both systolic (SBP) and diastolic (DBP) – were measured every half hour for two hours, among other parameters that I will not discuss.

After the two hour study period, HR was not seen to be significantly altered by the ingestion of any of the capsules. In fact, HR actually slightly decreased in all protocols, but not enough that it couldn’t have been from procedural error. What was significant was the rise in SBP after the ingestion of 250mg caffeine + 50mg DMAA and 250mg caffeine + 75mg DMAA. SBP rose from ~119mm Hg in both conditions to about 132mm Hg and 141mm Hg, respectively (see table below).

Now, to put this into perspective, the American Heart Association classifies normal BP as being below 120/80 (see table below). Borderline hypertension is above 120/80, and Stage 1 hypertension is above 140/90, and so and so on. As you can see, subjects went from having fairly normal SBP (~119mm Hg) to either becoming Prehypertensive or Stage 1 Hypertensive within an hour!

However, one of the most interesting results of the study is that the effects of DMAA seem to be 1) dose-dependent and 2) exacerbated by caffeine. Therefore, taking greater quantities of both substances, especially in conjunction with one another, will potentially result in even higher levels of BP. The most common consequences of increased BP include stroke and congestive heart failure along with accelerated atherosclerosis, renal artery disease, and a whole laundry list of other comorbidities which can, and often do, result in death.

Conversely, DBP remained within normal ranges despite increasing by about 10mm Hg over the two hour study period. Nevertheless, overall BP was increased to levels deemed unacceptable by any health professional’s standards. What is most interesting is that even though SBP increased, HR did not, which means that either stroke volume or peripheral resistance was increased as a direct effect of DMAA in conjunction with caffeine. This simply means that the arterial walls of the blood vessels were constricted as a result of the supplementation – the exact opposite of what most gym-goers desire. The authors concluded that;

“[T]he vasoconstriction effect of [DMAA] is supported by Eli Lilly’s trademark application for Forthane™, which states “vasoconstrictor preparation.”

This is in reference to 1948 when DMAA was first introduced as an ingredient as part of a nasal inhaler for rhinitis by Eli Lilly & Co. By the 1970s, it had been removed from the market.

If you’re anything like me right now, you’re saying, “so what?” This is a single short-term study with little bearing on realistic, long-term patterns of Jack3d consumption. Moreover, this tells us nothing about the potential ergogenic effects of DMAA on resistance training. I mean, that’s the main reason it’s being sold/purchased!

Longer-term Observations using Jack3d

In a follow-up study by the same group, researchers looked at chronic (2-week) consumption of 2 servings per day of Jack3d and OxyElite Pro on the same aforementioned parameters (HR, SBP, DBP) in healthy, exercise-trained subjects [3]. Contrary to their previous study, researchers found that neither Jack3d nor OxyElite Pro significantly increased SBP or DBP over the 2-week study period. This is good news for USPLabs. However, there are some differences in study protocols that can potentially explain the initial results seen in the first study and the null-effects seen in this one.

First off, the dosages of caffeine and DMAA contained within Jack3d and the dosage of DMAA contained within OxyElite Pro are unknown (both list DMAA as part of proprietary blend). Therefore, the levels of DMAA could have been below what was used in the previous study. Furthermore, the caffeine content in OxyElite Pro (100mg) is well below the dosage given in the previous study (250mg), again possibly explaining the differences seen between the two studies. Therefore, the unknown quantities of the compound in question (DMAA) and the lower dosage of caffeine in OxyElite Pro could potentially explain the null-effects seen on SBP and DBP.

Another difference seen between the two studies is that Jack3d contains extra ingredients, like that of arginine, a non-essential amino acid that has been shown to reduce blood pressure (SBP and DBP) [4], at least in subjects with pre-existing clinical manifestations like hypertension. Therefore, the arginine in Jack3d may have helped to counteract the hypertensive effects of DMAA. Although this may seem like a logical justification, it still doesn’t explain why OxyElite Pro had effects similar to Jack3d without the addition of arginine. This, however, could come down to the small n-size used (Jack3d = 7, OxyElite Pro = 6) and the fact that the results may be simply due to chance.

A major limitation of this follow-up study is that compliance of intake was measured via self-reporting and the collection of empty supplement bottles by the researchers at the end of week two. Because there was no strict control over intake, subjects could have potentially A) skipped some dosages (or all, aside from the two study conditions) and thrown out the rest, or B) taken even more than the recommended intake and run out of servings well before the follow-up test therefore eliminating any effects of the supplement by virtue of the “wash-out days” leading up to testing. Given these limitations, in conjunction with a small n-size, the study leaves us questioning the validity of the results.

Nevertheless, despite the various limitations, this study does lend some initial – albeit weak – credence to the argument that normal consumption patterns of either Jack3d or OxyElite Pro (which would be half of what was consumed in this study) are potentially safe when it comes to cardiovascular parameters. Obviously (many) more well-controlled studies are needed to confirm or deny these results.

But What about the Ergogenic Capacity!?!?

Unfortunately, this study tells us nothing about the ergogenic capacity of Jack3d. The researchers didn’t even try to measure it. I mean, sure, we can argue all day that it may be safe to consume, but if it doesn’t actually help with your workout then what the hell is there to argue about?! The simple answer to all of this is that there must be more well-controlled studies looking at realistic, chronic consumption of Jack3d by independent researchers with no financial ties to USPLabs. Unfortunately, these studies do not exist. To my knowledge there are only two other studies that evaluate the safety and efficacy of DMAA as a weight loss supplement [5, 6] and produce equivocal results. Moreover, both studies have limitations worthy of discounting their results altogether, aside from commercial backing; those being no control of dietary intake [5] and no actual measure of weight loss [6]. This essentially leaves us right back at square one.


So, to summarize today’s talking points:

  1. DMAA’s legal marketing and use as a dietary supplement hinges on one study that has (apparently) come into question, the facts of which I cannot comment upon
  2. Jack3d and OxyElite Pro have very few studies evaluating their safety and even fewer studies which effectively provide any insight into whether or not they’re even effective supplements
  3. All of the studies which do evaluate Jack3d and OxyElite Pro are from one group of researchers with direct funding from USPLabs

In the end, like most other hugely-hyped supplements, Jack3d appears to be nothing but another waste of money. You can argue all day that it might be safe, but for what? There’s nothing in Jack3d that can’t be purchased separately and for much less. Until there is compelling data that shows that Jack3d is superior to the individual, well-studied constituents contained within it (creatine monohydrate, beta-alanine, and caffeine) I will gladly sit back while others blindly buy-out what’s left of the, now banned, DMAA products.


1. Ping Z, Jun Q, Qing L. A study on the chemical constituents of geranium oil. J Guizhou Institut Technol. 1996;25(1):82–85.

2. Bloomer RJ, Harvey IC, Farney TM, Bell ZW, Canale RE. Effects of 1,3-dimethylamylamine and caffeine alone or in combination on heart rate and blood pressure in healthy men and women. Phys Sportsmed. 2011;39(3):111-20.

3. Farney TM, McCarthy CG, Canale RE, Alleman RJ, Bloomer RJ. Hemodynamic and hematologic profile of healthy adults ingesting dietary supplements containing 1,3-dimethylamylamine. Nutrition and Metabolic Insights 2012;5:1-12.

4. Dong JY, Qin LQ, Zhang Z, Zhao Y, Wang J, Arigoni F, Zhang W. Effect of oral L-arginine supplementation on blood pressure: a meta-analysis of randomized, double-blind, placebo-controlled trials. Am Heart J. 2011;162(6):959-65.

5. McCarthy CG, Canale RE, Alleman RJ, Reed JP, Bloomer RJ. Biochemical and anthropometric effects of a weight loss dietary supplement in healthy men and women. Nutrition and Metabolic Insights 2012;5:13-22.

6. McCarthy CG, Farney TM, Canale RE, Alleman RJ, Bloomer RJ. A finished dietary supplement stimulates lipolysis and metabolic rate in young men and women. Nutrition and Metabolic Insights 2012;5:23-31.

Posted in Supplements | 6 Comments

Growth Hormone and Nighttime Carbs: Much Ado About Nothing

Opening Comments

Today I want to talk about growth hormone. From what I’ve gathered over the past couple of weeks, there seems to be a prevailing notion that eating carbohydrates at night will somehow prevent natural growth hormone release from occurring and therefore hinder muscle protein synthesis. This is presumably due to carbohydrates causing insulin to be raised and therefore causing growth hormone to be inhibited. As some of you may already be aware, growth hormone secretion is at its maximum during sleep. It makes sense to want to maximize your natural hormonal milieus in order to promote anabolism.  However, what proponents of this misconstrued theory choose to forget – or just flat out don’t know – is that insulin, too, is anabolic. Nonetheless, for argument’s sake, I will solely focus on growth hormone and how a carbohydrate meal at night might – potentially (never?) – lead to less muscle protein synthesis.

For starters, it is true that when insulin is elevated (via ingested carbohydrate), growth hormone is inhibited and therefore low in concentration. However, this hardly deserves much attention given the numerous other factors that go into muscle hypertrophy. Nevertheless, some still translate this single piece of information into meaning that growth hormone will somehow be blunted to the point of no release and therefore inhibiting muscle protein synthesis altogether. This is just plain ridiculous and completely misleading, not to mention that there is not ONE study which even slightly suggests this. Nevertheless, in lieu of today’s topic, I’ll start by describing some of the physiology behind growth hormone and it’s functions and then follow it up with some research studies that will put everything into perspective (hopefully). However, before we begin, be warned, today’s article will be quite lengthy and somewhat sciency.

Growth Hormone Secretion  

Growth hormone (GH) is a peptide hormone secreted from the anterior pituitary of the brain. GH is secreted throughout life but is most important during childhood wherein peak concentrations are the highest they will ever be [1]. For the purposes of today’s article, we will just discuss GH as it pertains to muscle growth and hypertrophy.

In skeletal muscle, GH promotes a positive protein balance by increasing muscle protein uptake/synthesis and by potentially preventing muscle protein breakdown [2]. There are various stimuli which affect the release and inhibition of GH, namely nutrients (such as carbs, protein, and fats), age, stress (exercise), gender, circadian rhythm, and the presence of other, counter-regulatory hormones such as insulin [1, 3]. To say that the regulation of GH is simple is a complete understatement. In fact, the interplay between exercise, diet and GH regulation is not fully understood [3]. It is at this point that I want to discuss what controls GH secretion and inhibition and the relative impacts of the various macronutrients on GH regulation. After all, that’s what you came for, right?

Growth Hormone Regulation

GH is primarily acted on by growth hormone-releasing hormone (GHRH) – aptly named – which signals GH to be released into circulation. In opposition to GHRH is another hormone called somatostatin (SS) which inhibits GHRH and therefore prevents GH to be secreted. Throughout the day both GHRH and SS control the release and inhibition of GH and inevitably dictate the overall magnitude of GH release [3]. This manner of release and inhibition is often termed a pulsatile pattern wherein the largest release happens within the first two hours of sleep (see below). This is thought to be prime time for anabolism.

Like many biochemical and physiological mechanisms GH, too, has feedback inhibition. This simply means that the products of a pathway also turn that pathway off once sufficient levels of product are made. The inhibitory products for GH include, glucose, free fatty acids, IGF-1 and potentially GH itself [3].

IGF-1 (insulin-like growth factor-1) is stimulated when GH is released and acts on the liver and muscle tissue. This causes insulin-like growth factor-1 to be released into circulation where it can act of various tissues such as muscle. It is through IGF-1 that GH indirectly mediates some its anabolic effects. Therefore, it may not be GH per se that causes muscle protein synthesis, but rather IGF-1. However, to date, there is still some controversy as to which one is the primary stimulator of muscle protein synthesis. Nevertheless, as I already mentioned, IGF-1 causes GH to stop being secreted once sufficient levels of IGF-1 have been made. The same applies for glucose and free fatty acids which are also products of GH release. During exercise, GH optimizes the body’s fuel sources by decreasing tissue glucose uptake, stimulating lipolysis, and increasing gluconeogenesis [4]. This makes sure that blood glucose levels are preserved during exercise.

An important thing to keep in mind when talking about GH release and inhibition is that SS causes GH secretion to be inhibited BUT does not cause GH to stop being produced. Therefore, even though GH may not be released into circulation, the pituitary gland is still synthesizing more GH which will inevitably be released once the inhibition is removed. This concept is very important because there seems to be a ‘rebound’ effect for GH secretion after the inhibition is taken away [5].

Therefore the real question is whether or not the initial inhibition presented by a carbohydrate meal will actually reduce the amount of total GH secreted over the course of the day. If this ‘rebound’ effect holds true than GH will just be secreted in higher levels than it would have originally been and therefore reaching its daily quota, so to speak. To my knowledge, there are no studies which directly look at this theory in respect to a nighttime carbohydrate meal and subsequent levels of GH over the course of the night. Moreover, there also needs to be evidence that shows that muscle protein synthesis is somehow reduced because of this inhibition. Because a study like this does not exist, not only is the original argument completely speculative, but it is also founded on very little fact. Nevertheless, let us take a look at some effects of food on GH after a meal and see if we can’t postulate some conclusions about diet and GH.

Post-prandial GH Response to Feeding


It has been shown multiple times that an oral glucose tolerance test results in reduced levels of GH [6-9]. Furthermore, another study demonstrated that carbohydrate alone or in conjunction with protein also caused GH levels to be decreased [10]. However, this study was done in a group of sedentary diabetics who may not serve as the best example for what might occur in a non-sedentary, athletic population. Furthermore, it has also been shown that hypoglycemia is a potent stimulator of GH [7, 11].  Although interesting, this is virtually irrelevant given that hypoglycemia is not something likely to occur in most athletes/bodybuilders who consume anywhere from 4-6 meals a day. Nevertheless, as insulin levels tend to go down, GH levels tend to increase [12].


Next we will consider protein, and more specifically amino acids. Amino acids have come under scrutiny for their potential to increase levels of GH. Although certain amino acids (arginine, ornithine, lysine) taken orally and intravenously in gram doses have been shown to increase levels of GH in sedentary participants, this is not the case in bodybuilders and those who consume high protein diets [13]. Sorry guys.


In 1993, Cappon et al. wanted to test the effects of a high fat drink consumed 45 minutes before a 10 minute bout of intense exercise on subsequent GH levels [14]. Researchers found that, compared to a non-caloric placebo, GH was reduced by 54% and blood concentrations of SS were significantly elevated. The authors postulated a potential link between fat and somatostatin (SS). In fact, in a separate study done a few years earlier, a group of researchers found that both a mixed meal and a fat-rich meal had the greatest effects on elevating SS levels with carbohydrate having the least effects [15].


Obviously keeping SS low and GH high would be the best case scenario in terms of body composition; however, as is life, things are not that simple. The relative impact and relevance of the aforementioned studies on body composition are essentially worthless and at best speculative. They are acute studies which tell us nothing about long-term effects of diet on hormonal responses. Not to mention many of these studies were done with macronutrients in isolation; a situation not relevant to normal eating behaviors to begin with. Finally, there was no direct measurement of lean body mass in any of the studies. Therefore they really tell us little about the potential effects of food on GH in relation to body composition. So where do we go from here?

Well, it just so happens that there is one study which comes close to answering the question at hand, although not entirely. Nevertheless, it draws upon some of the themes I’ve already laid out so far, so let’s see if we can’t inch one step closer to a definitive answer and drive a nail into this coffin.

Effects of Heavy Weightlifting on GH Release at Night

A study done in 2001 looked the effects of heavy resistance exercise on the pulsatile released of GH in humans [16]. At that point, it was well established that exercise was a potent stimulator of GH; however, it was not fully understood on how resistance exercise affected GH throughout the rest of the day, specifically during the nighttime. What the researchers found, contrary to their original hypothesis, was that heavy resistance exercise – completed in the afternoon – actually decreased overnight maximum GH concentrations (see below).

In spite of this overall reduction in maximal GH concentration, they saw that total GH concentration by the end of the night was not significantly reduced when compared to the control. AHA! To put it another way, GH was lower during the first half of sleep (perhaps what might happen if one ate a carbohydrate meal) but remained elevated during the second half of sleep to maintain normal GH concentrations (think about the ‘rebound’ effect I mentioned earlier). As you can see, when faced with lower than normal secretion patterns, most likely due to SS inhibition, GH was released at higher concentrations during the rest of the night in order to meet its ‘quota.’ As I mentioned earlier SS does not affect GH synthesis, only release. In fact, the researchers postulated that the temporal changes in GH over the course of the night were possibly due to the ‘rebound effect’ of SS on GH secretion.

So, if you got nothing from what I just stated, remember this: it appears that GH release has some form of homeostatic mechanism which maintains a certain quota for GH concentrations over the course of the day. Therefore, when something like exercise interacts and alters the normal release pattern of GH, the brain is smart enough to save it and release it later when the inhibition is gone. This presumably keeps GH concentrations unchanged over a 24-hr period. My guess is that this is also true for something as trivial as a carbohydrate meal consumed at night wherein GH might be slightly inhibited by the time you fall asleep. This is probably not something to get worried about at all.

Unfortunately, this study provides very little insight into what would happen with chronic patterns of nightly carbohydrates. What it does do, however, is provide evidence for the ‘rebound’ effect postulated earlier, which seems to be a good model for maintaining normal levels of GH over a 24-hr period. Obviously more studies are needed, especially ones that pertain to nutrition. This also brings me to something I should have mentioned earlier. Had this topic of carbs and GH been such a revelation in the field nutritional science, don’t you think more studies would have been done on it? Usually scientific interest is a good indicator of the importance of a given nutritional topic. Just some food for thought.

Rapid Suppression of GH from Overeating

There is one more study which I would like to cover, and it has to deal with the possibility of GH being completely suppressed by food intake. Obviously this is what nighttime Carbophobics are worried about, so it makes sense to look at the closest study I could find that mimics this question. In a recent study done in 2011, researchers looked to see if GH secretion could be significantly suppressed by the act of overeating [17]. There were essentially three phases of the study; baseline, 3 days post-overeating, and 2 weeks post-overeating. During the entire study period following baseline, researchers had participants consume ~175% of their daily caloric needs while limiting their daily activity to 1500 steps per day (not very active). At baseline GH levels were essentially normal. By day 3, GH levels had significantly dropped by ~80% wherein they remained relatively unchanged during the remaining 2-week period (see below).

Obviously these conditions are not relevant to normal consumption patterns, even among those who are bulking. However, as you can see, GH can be suppressed, although this relates little to our argument because I doubt a single carbohydrate meal at night will reproduce anything like what was seen during this study, even under chronic conditions of nighttime carb meals.

Nevertheless, the question remains; will this negatively affect gains in lean body mass? Well, here’s the kicker! Even with GH being suppressed by up to 80%, participants actually increased their lean body mass (~2lb increase)! Let me repeat that; they actually increased their lean body mass. Now, I will admit that it wasn’t statistically significant, although it was bordering significant, and that the LBM gains could have been tissue other than skeletal muscle. Nonetheless, the fact still remains that protein synthesis wasn’t completely inhibited, even in the face of dramatically low GH levels and almost complete inactivity. Would greater gains in LBM have been seen if GH wasn’t reduced as much? Would activity have nullified the results and attenuated the drop in GH levels? Who knows? The key thing to keep in mind is that muscle protein synthesis is a complex system that involves multiple players. Singling out two factors amongst a host of others is flat out ridiculous.

Concluding Remarks

The fact of the matter is that those who fear carbs at night are basing their fear off of one piece of information that holds little scientific backing. Hopefully by now I’ve convinced you that GH regulation is a complex system with many factors that each plays a role. To say that carbs at night will reduce the capacity to build muscle is completely ludacris and unfounded – that is unless that meal is part of a diet which comprises 175% of your daily needs. So, in the end, there is no scientific evidence whatsoever to suggest that carbs consumed at night will reduce one’s goal of gaining muscle, and I doubt there ever will be. The main thing to keep in mind is that there is much more to building muscle than splitting-hairs. The people who care the most about this stuff are the ones who should care the least, and those who capitulate to stupid misinformation like that are worse off than they were when they knew nothing at all. If you learned nothing, remember this:

Lift heavy, eat right, rest up, and most importantly don’t concern yourself with trivial aspects of dieting that are at best speculative and at worst completely false. Dichotomous thinking never did anyone any good. Ever.


1. Silverthorn DU. Endocrine control of growth and metabolism. In: Human physiology: an integrated approach, 5th ed. Pearson Education, Inc.: San Francisco, CA, 2010.

2. Rooyackers OE, Nair KS. Hormonal regulation of human muscle protein metabolism. Annu Rev Nutr. 1997;17:457-85.

3. Kraemer WJ, Nindl BC, Gordon SE. Resistance exercise: acute and chronic changes in growth hormone concentrations. In: The endocrine system in sports and exercise. Blackwell Publishing: Malden, MA, 2005.

4. McArdle WD, Katch FI, Katch VL. The endocrine system: organization and acute and chronic responses to exercise. In: Exercise physiology: energy, nutrition, and human performance, 6th ed. Lippincott, Williams and Wilkins: Baltimore, MD, 2007.

5. Giustina A, Veldhuis JD. Pathophysiology and neuroregulation of growth hormone secretion in experimental animals and the human. Endocrine Reviews 1998;19(6):717-797.

6. Bernardi F, Petraglia F, Seppala M, et al. GH, IGFBP-1, and IGFBP-3 response to oral glucose tolerance test in perimenopausal women: no influence of body mass index. Maturitas 1999;33:163-179.

7. Frystyk J, Grofte T, Skjaerbaek C, Orskov H. The effect of oral glucose on serum free insulin-like growth factor-I and –II in healthy adults. J Clin Endocrinol Metab. 1997;82:3124-3127.

8. Hjalmarsen A, Aasebo U, Aakvaag A, Jorde R. Sex hormone responses in healthy men and male patients with chronic obstructive pulmonary disease during an oral glucose load. Scand J Clin Lab Invest. 1996;56:635-640.

9. Nakagawa E, Nagaya N, Okumura H, et al. Hyperglycaemia suppresses the secretion of ghrelin, a novel growth hormone-releasing peptide: responses to the intravenous and oral administration of glucose. Clin Science 2002;103:325-328.

10. van Loon LJ, Saris WH, Verhagen H, Wagenmakers AJ. Plasma insulin responses after ingestion of different amino acid or protein mixtures with carbohydrates. Am J Clin Nutr. 2000;72:96-105.

11. Roth et al. 1963.

12. Volek JS, Sharman MJ. Diet and hormonal responses: potential impact on body composition. In: The endocrine system in sports and exercise. Blackwell Publishing: Malden, MA, 2005.

13. Chromiak JA, Antonio J. Use of amino acids as growth hormone-releasing agents by athletes. Nutrition 2002;18:657-661.

14. Cappon JP, Ipp E, Brasel JA, Cooper DM. Acute effects of high-fat and high-glucose meals on the growth hormone response to exercise. J Clin Endocrinol Metab. 1993;76-1418-1422.

15. Ensinck JW, Vogel RE, Laschansky EC, Francis BH. Effect of ingested carbohydrate, fat, and protein on the release of somatostatin-28 in humans. Gastroenterology 1990;98(3):633-638.

16. Nindl BC, Hymer WC, Deaver DR, Kraemer WJ. Growth hormone pulsatility profile characteristics following acute heavy resistance exercise. J Appl Physiol. 2001;91:163-172.

17. Cornford AS, Barkan AL, Horowitz JF. Rapid suppression of growth hormone concentration by overeating: potential mediation by hyperinsulinemia. J Clin Endocrinol Metab. 2011;96(3):824-830.

Posted in Carbohydrate | 10 Comments

Anabolic Arachidonic Acid: Mass-builder or Massive Waste of Money? – ARTICLE REVIEW

Effects of arachidonic acid supplementation on training adaptations in resistance-trained males

Roberts MD, Iosia M, Kerksick CM, Taylor LW, Campbell B, Wilborn CD, Harvey T, Cooke M, Rasmussen C, Greenwood M, Wilson R, Jitomir J, Willoughby D, Kreider RB.

J Int Soc Sports Nutr. 2007;4:21.

PubMed: http://www.ncbi.nlm.nih.gov/pubmed_arachidonic_acid


To determine the impact of AA supplementation during resistance training on body composition, training adaptations, and markers of muscle hypertrophy in resistance-trained males.


In a randomized and double blind manner, 31 resistance-trained male subjects (22.1 +/- 5.0 years, 180 +/- 0.1 cm, 86.1 +/- 13.0 kg, 18.1 +/- 6.4% body fat) ingested either a placebo (PLA: 1 g.day-1 corn oil, n = 16) or AA (AA: 1 g.day-1 AA, n = 15) while participating in a standardized 4 day.week-1 resistance training regimen. Fasting blood samples, body composition, bench press one-repetition maximum (1RM), leg press 1RM and Wingate anaerobic capacity sprint tests were completed after 0, 25, and 50 days of supplementation. Percutaneous muscle biopsies were taken from the vastus lateralis on days 0 and 50.


Wingate relative peak power was significantly greater after 50 days of supplementation while the inflammatory cytokine IL-6 was significantly lower after 25 days of supplementation in the AA group. PGE2 levels tended to be greater in the AA group. However, no statistically significant differences were observed between groups in body composition, strength, anabolic and catabolic hormones, or markers of muscle hypertrophy (i.e. total protein content or MHC type I, IIa, and IIx protein content) and other intramuscular markers (i.e. FP and EP3 receptor density or MHC type I, IIa, and IIx mRNA expression).


AA supplementation during resistance-training may enhance anaerobic capacity and lessen the inflammatory response to training. However, AA supplementation did not promote statistically greater gains in strength, muscle mass, or influence markers of muscle hypertrophy.

Opening Comments

The other day I got a request to do an article on arachidonic acid (AA) supplementation. Now, to be completely honest, I haven’t heard much about arachidonic acid in terms of supplementation for muscle and strength gains, although I am familiar with the lipid and its role within the inflammatory response. So, I figured why not, could be interesting. As it turns out, arachidonic acid research, in terms of supplementing for muscle hypertrophy, strength, etc. in humans, is quite scarce. To my knowledge this is the only study to look at arachidonic acid supplementation on muscle protein synthesis – contrary to what some supplement companies may have you think.  Furthermore, this study attempts to look AA’s effects on body composition and strength, two factors I’m sure many of you are interested in improving. I will first start with a short history of the literature surrounding AA – as it pertains to weightlifting – and then jump right into the above study wherein I will touch upon the strengths and weaknesses of the study and my views on/potential implications for AA supplementation.

Arachidonic Acid: A Quick Review of the Literature

Arachidonic acid (AA) is an omega-6 polyunsaturated fatty acid (PUFA) – denoted 20:4 ω-6 – found naturally in foods and in membrane phospholipids of humans. Contrary to what some people think, AA is not an essential fatty acid. The human body can effectively make enough AA through various enzymatic pathways which I will not get into. AA is converted into a group of eicosanoids known as prostaglandins (PGs). PGs play an important role in regulating the inflammatory response as well as other immune responses in the human body. It is estimated that the average 70kg man (~154lbs) contains about 50-100g AA spread throughout various tissues and membranes [1], although it is thought that the AA status of the body is dependent upon dietary intake [1] as well as activity level [2-3]. An interesting study from 2000 saw that the fatty acid profile of skeletal muscle differed between endurance-trained and sedentary individuals – with less AA and in the trained group – even though the fatty acid composition of the diet was similar [3]. This implies that physical activity may play a more important role than diet in terms of the fatty acid composition of cell membranes.

Early in vitro and animals studies demonstrated that PGs (and therefore AA) are implicated in the inflammatory response of muscles after mechanical stimulation (comparable to that of resistance exercise) as well as the rates of protein synthesis and degradation in both skeletal and cardiac muscle [4-7]. Because AA is converted to prostaglandins (PGs) via the COX-2 pathway – the same pathway inhibited by non-steroidal anti-inflammatory drugs (i.e. Ibuprofen, acetaminophen) – it is thought that commonly used pain killers (Advil, Tylenol, etc.) could potentially inhibit the necessary myogenic inflammatory response needed for muscle protein synthesis. Reaffirming this notion, a study done by Trappe et al. showed that subjects supplemented with normal doses of NSAIDs prior to resistance training completely eliminated PG synthesis of the inflammatory response as well as muscle protein synthesis following the exercise protocol [8]. Paired to together with research showing that 1.5g of AA/day for a month and half significantly increased PG synthesis [9], AA has now been implicated as a mass-building supplement for weightlifters and gym-rats alike. Today’s study gets at the crux of this argument, so without much further ado, let’s dissect this paper!

The Study

Study Strengths

Because you have the abstract above (and have the ability to read), I’ll start off by listing the study’s strengths, which to my surprise were a whole bunch. First off, big points to any study which uses healthy, resistance-trained subjects. This eliminates any effects that could be confounded by what are called, “beginner gains.” This study was also a randomized, double-blind, placebo-controlled study, which ensures that both groups are identical (aside from the experimental protocol) and that any biases from both researchers and subjects which might affect the results are eliminated. Body composition was measured using dual-energy x-ray absorptiometry (DXA), otherwise known as the “Gold Standard” for body comp measures. Another awesome feature of this study was the use of muscle biopsies. Not too often do people agree to donate a chunk of their own muscle tissue (nor is it permitted often). Biopsies were taken before strength testing to eliminate any effects that might occur due to exercise. You can’t get more accurate than actually looking at someone’s muscle tissue!

Nutritionally speaking, recommended calorie and protein intakes were well-above adequate (+500kcals/day above baseline needs and 2g/kg BW, respectively), although this was merely recommended and not tightly controlled. Nevertheless, a dietary supplement was given out (290kcals, 24g CHO/45g PRO/1g Fat) in order to reach the additional calorie and protein requirements needed to promote muscle gains. Subjects were also told to avoid foods high in omega-3 fatty acids as well as commonly used NSAIDS which might interfere with the inflammatory response of exercise.

Study Weaknesses

The fact that dietary intake was self-reported this potentially confounds the results, even though 4-day dietary records were used to validate intakes. Another potential weakness of the study was that the placebo group was given a corn-oil supplement which can be converted to AA (from linoleic acid) using various enzymatic pathways in the body. Dietary analysis, however, revealed similar levels of linoleic acid in the diets. This, however, is only as valid as the diet records. All in all, this was a well carried-out study with very few weaknesses.


The researchers found that there were no significant differences between the two groups in terms of body mass, fat free mass, fat mass, percent body fat, 1RM bench press, or 1RM leg press. Pity. However, anaerobic peak power was significantly different between the two groups, with the higher peak power coming from the AA group on days 25 and 50. This comes on the heels of previous research which showed that, 10 days of a soybean derivative – that naturally contains AA – increased time to fatigue in active males during a cycling test at 85% VO2 max [10] as well as in soccer players performing exhaustive, intermittent sprints [11]. Nevertheless, the major finding of this study was that AA supplementation did not lead to greater gains in strength, muscle hypertrophy or body composition when compared to a placebo, which, let’s be honest, is the main goal of most of the readers of this Blog.

Summary & Finals Comments

In the end, it appears that AA supplementation may be more of a waste of money rather than a muscle-building fatty acid (especially when AA supplements range from $50-60 a pop!). However, this is only one study. Obviously more studies need to be done in order to confirm or refute the findings presented here. Given that it’s been 5 years since this study was done, without any corresponding follow-up whatsoever, this tells me that AA supplementation doesn’t appear to be the “next big thing;” at least not now. There may be some potential benefits if you’re an endurance athlete, but right now, it’s still speculative and the results are more relevant to phosphatidylserine (the soybean derivative I mentioned earlier). So next time you hear outrageous claims about arachidonic acid providing awesome muscle and strength gains, just remember that it’s probably based off of speculation rather than sound scientific research.


1. Zhou L, Nilsson Å. Sources of eicosanoid precursor fatty acid pools in tissue. J Lipid Res. 2001;42(10):1521-42.

2. Helge JW, Wu BJ, Willer M, Daugaard JR, Storlien LH, Kiens B. Training affects muscle phospholipid fatty acid composition in humans. J Appl Pysiol. 2001;90(2):670-7.

3. Andersson A, Sjödin A, Hedman A, Olsson R, Vessby B. Fatty acid profile of skeletal muscle phospholipids in trained and untrained young men. Am J Physiol Endocrinol Metab. 2000;279(4):E744-51.

4. Vandenburgh HH, Shansky J, Karlisch P, Solerssi RL. Mechanical stimulation of skeletal muscle generates lipid-related second messengers by phospholipase activation. J Cell Physiol. 1993;155(1):63-71.

5. Vandenburgh HH, Shansky J, Solerssi RL, Chromiak J. Mechanical stimulation of skeletal muscle increases prostaglandin F2 alpha production, cyclooxygenase activity, and cell growth by a pertussis toxin sensitive mechanism. J Cell Physiol. 1995;163(2):285-94.

6. Rodemann HP, Goldberg AL. Arachidonic acid, prostaglandin E2, and F2 alpha influence rates of protein turnover in skeletal and cardiac muscle. J Biol Chem. 1982;257(4):1632-8.

7. Palmer RM. Prostaglandins and the control of muscle protein synthesis and degradation. Prostaglandins Leukot Essent Fatty Acids 1990;39(2):95-104.

8. Trappe TA, White F, Lambert CP, Cesar D, Hellerstein M, Evans WJ. Effect of ibuprofen and acetaminophen on postexercise muscle protein synthesis. Am J Physiol Endocrinol Metab. 2002;282:E551-556.  

9. Kelley DS, Taylor PC, Nelson GJ, Mackey BE. Arachidonic acid supplementation enhances synthesis of eicosanoids without suppressing immune functions in young healthy men. Lipids 1998;33:125-130.

10. Kingsley MI, Miller M, Kilduff LP, McEneny J, Benton D. Effects of phosphatidylserine on exercise capacity during cycling in active males. Med Sci Sports Exerc. 2006;38:64-71.

11. Kingsley MI, Wadsworth D, Kilduff LP, McEneny J, Benton D. Effects of phosphatidylserine on oxidative stress following intermittent running. Med Sci Sports Exerc. 2005;37(8):1300-6.

Posted in Fats, Reviews | 8 Comments

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

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.


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.


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

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 20th 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.


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!


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

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.


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.


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.


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.


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).


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.
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.  
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

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.
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.  
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.

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