Review of Intervention Studies Shows: Weight Loss Success Independent of Meal Frequency

"Eat 3 large meals à day!", "Eat smaller meals every 2 hours!", "Eat a single meal and fast the rest of the day!" If you have been trying to find information on how to lose weight effectively, you probably heard all these "expert" advises. What if I told you that a recent review of 25 weight loss interventions shows that it simply does not matter!

In an extensive review of the literature, Palmer et al. (Palmer. 2011) conclude:

Manipulating the EF [eating frequency] of a client seeking weight management is unlikely to provide any additional benefits to weight, body composition or health. The theoretical benefits of manipulating EF may not be sustained in the real life clinical setting as a change to EF may be difficult to maintain over the longer term. Current evidence does not support many of the theories that encourage manipulating EF for weight management. Focus needs to be placed on dietary weight management strategies that are achievable and sustainable over the longer term.

Better body composition? Only inconclusive evidence. Better glucose tolerance in non-diabetics? Definitely not. Decreased risk of heart disease? Unlikely. Less hunger? At least not with three vs. six meals. Bottom line: Another myth debunked!

Want to Burn More Fat During Your Cardio Training? Eat Low Carb Before Workout!

Modulation of substrate utilization is the key to effective weight loss. For years we have been told that "training in the zone" (referring to a specific heart rate) would do the trick - recent research does yet suggest otherwise: High Intensity Interval Training (HIIT) has been shown to be at least as effective in burning off unwanted body fat, as the longstanding "gold standard", Low Intensity Steady State (LISS) in the "fat burning zone".

Researchers from the Department of Exercise Science and Sports Studies at Springfield College, Springfield, MA, USA, have now found that apart from the type of exercise you chose to perform, the nutrition, especially in the hours before working out, determines whether you will predominantly burn fat or carbs to sustain the workout.

In their study (Gregory. 2011), Gregory et al. compared the metabolic responses of a group of 8 "active, pre-menopausal" women to a 30 minute exercise regimen performed after either a low carbohydrate (LC: 392 kcal @ 15% carbohydrate, 68% fat, and 18% protein) or a low fat (LF: 396 kcal @ 78% carbohydrate, 7% fat, and 15% protein) meal. Respiratory gas exchange (RER), blood glucose (G), insulin (IN), triglycerides (TG), and free fatty acids (FFA) were measured. While "no significant differences existed between test meals for fasting blood measurements", the post-exercise results showed significant differences:

Postexercise (PE) FFA (mEq·L-1) levels were significantly greater following LC [1.1 (0.3) vs. 0.5 (0.3)]. PE TG (mg·dL-1) levels were significantly greater following LC [152.0 (53.1) vs. 114.4 (40.9)]. RER was significantly lower at all time points following LC compared to LF.

With the respiratory gas exchange being a measure of the relative contribution of fatty acids to fulfill the exercise-induced energy demand (Chessex. 1995), the researchers rightly conclude "ingestion of a single LC meal resulted in greater lipid oxidation at rest and during exercise as compared to a single LF meal." But, let's be honest - did you expect anything else?

More Conflicting Evidence on Leucine Metabolite: HMB Makes Volleyballers Stronger.

The leucine metabolite HMB, i.e. β-Hydroxy-β-Methylbutyric acid, is unquestionable the comeback kid of the supplement industry. "It works!", "It's useless!", ... every now and then a new study supports one side of the debate. A group of international scientists does now present a study, which would support the use of the expensive, yet readily available amino acid.

Portal et al. (Portal. 2011) investigated the effect of 3g HMB/day "on body composition, muscle strength, anaerobic and aerobic capacity, anabolic/catabolic hormones and inflammatory mediators in elite, national team level adolescent volleyball players (13.5–18 years, 14 males, 14 females, Tanner stage 4–5) during the first 7 weeks of the training season". The results were unequivocal, yet not overtly impressive:

HMB led to a significant greater increase in FFM by skinfold thickness (56.4 ± 10.2 to 56.3 ± 8.6 vs. 59.3 ±  11.3 to 61.6 ± 11.3 kg in the control and HMB group, respectively, p < 0.001). HMB led to a significant greater increase in both dominant and non-dominant knee flexion isokinetic force/FFM, measured at fast (180°/sec) and slow (60°/sec) angle speeds, but had no significant effect on knee extension and elbow flexion and extension. HMB led to a significant greater increase in peak and mean anaerobic power determined by the Wingate anaerobic test (peak power: 15.5 ± 1.6 to 16.2 ± 1.2 vs. 15.4 ± 1.6 to 17.2 ± 1.2 watts/FFM, mean power: 10.6 ± 0.9 to 10.8 ± 1.1 vs. 10.7 ± 0.8 to 11.8 ± 1.0 watts/FFM in control and HMB group, respectively, p < 0.01), with no effect on fatigue index.

With no measurable effect on aerobic fitness, anabolic hormone levels or inflammatory mediators, the use of HMB appears to be advisable only in power and strength athletes.

If you are a bodybuilder on a high protein diet, I would however doubt that you would see any benefits from additional HMB. A diet rich in quality protein (high BCAA and particularly leucine content) should provide you with adequate amounts of leucine to keep endogenous HMB levels elevated.

Low Dose Caffeine Ameliorates Catabolic Effects and Increases AMPK and PPAR Expression During Reduced Food Intake in Mice

Caffeine, "the mother of all stimulants", has lately developed a bad reputation. Stress, Cortisol, Adrenal Fatique, Insulin Resistance etc. are only the most recognized buzzwords occurring within the context of caffeine consumption. A very recent paper (Shermann. 2011) coming from scientists from the University of Jerusalem draws a wholly different picture.

Shermann et al. investigated the effect of caffeine consumption (3.5 mg/kg/day or 7 mg/kg/day) on circadian rhythms and expression of disease and metabolic markers in mice under two distinct dietary conditions over a period of sixteen weeks. When the rats were fed an ad libitum diet (meaning they could consume as much food as they wanted), ...

caffeine reduced the average daily mRNA levels of certain disease and inflammatory markers, such as liver alpha fetoprotein (Afp), C-reactive protein (Crp), jejunum alanine aminotransferase (Alt), growth arrest and DNA damage 45β (Gadd45β), Interleukin 1α (Il-1α), Il-1β mRNA and serum plasminogen activator inhibitor 1 (PAI-1).

For those of you who still want to shed some pounds of fat, it may yet be even more interesting to read that "caffeine supplementation led to decreased expression of catabolic factors under RF". With the RF = restricted feeding condition being comparable to what is known as "intermittent fasting" in the fitness community, this finding is highly significant.

Figure 1: Metabolic markers PPAR-Gamma (above) and PPAR-Alpha (below) in mice fed an ad libitum (AL) or a restricted diet (RF) (Shermann. 2011)

This is particularly valid given the fact that there was a highly significant increase in PPAR-Gamma, PPAR-Alpha (cf. figure 1) and AMPK (not shown) activities in the group receiving "high dose" (7mg/kg; for humans this would equal a pretty low dose of about 0.6mg/kg) caffeine. Both, peroxisome proliferator activated receptor (PPAR), as well as AMPK are regarded as master metabolic regulators that have been implicated in the physiology of fat loss. A moderate caffeine consumption, i.e. about one cup of coffee, in the course of an intermittent fast, may thus well spare muscle protein and burn body fat, at the same time.

Omega 3 Attenuates Exercise Induced Rise in Inflammatory Markers, BUT is This Necessarily a Good Thing?

I want to take the results of a recent study (Bakhtyar. 2011) published in the Clinical Journal of Sport Medicine as an opportunity to readdress the question of whether or not the Omega 3 induced suppression of inflammation must be considered a good or a bad thing, both in view of athletic performance, as well from a health and longevity perspective.

Those of you, who listened to my interview on Carl Lenore's Super Human Radio show, will know that my understanding of "inflammation" is somewhat different from the mass market "explanation" of "a fire that causes damage". To be precise inflammation, or what scientists generally measure, is the release of signals (inflammatory markers) that tell immune cells to do their jobs. So, saying that inflammation is the root of all disease would be like saying that someone who calls the firefighters is to blame for the fire - but I am digressing from the topic at hand...

After administering 1.5g/day of an omega 3 supplement (experimental group) to every third of 45 previously untrained volunteers, Bakhtyar et al. found the subjects' "inflammatory" response to eccentric exercise to be modified:

The experimental group showed less elevation in TNF-α and PGE₂ immediately, 24, and 48 hours after exercise, when compared with the other groups. Significantly less elevation was shown in the concentration of IL-6, CK, and Mb for the experimental group at 24 and 48 hours after exercise. The experimental group also demonstrated a significant trend toward reduction in the plasma concentration of LDH immediately, 24, and 48 hours after the exercise program.

Now, what does this tell us about the training effect and health outcomes of the exercise regimen?

• With inflammation being a not yet fully understood prerequisite for muscular repair and hypertrophy, it would warrant further investigations like muscle biopsies and consistent training regimens with continuously monitored strength and muscle gains to conclude that omega 3 supplementation is beneficial in terms of physical performance.
• In view of the conclusions Pedersen draws in a recent review (Pedersen. 2011) of the role of exercise induced myokines, i.e. inflammatory markers released by muscles (myo- = muscle-), in chronic disease, blunting of muscular IL-6 release, which has been linked to muscular AMPK activation, increased glucose uptake and fat oxidation, omega 3 supplementation is probably counter-indicated in a health oriented exercise regimen, anyway.

I hope more scientists such as Pedersen will begin to question the current "anti-inflammatory" paradigm, so that major players in the medial landscape will be forced to take on their findings and stop portraying long chain polyunsaturated fatty acids in general and fish oil in particular as the savior of the fat and diabetic. Instead they should encourage people to finally get their asses off their sofas to induce exactly that amount of healthy, exercise-induced inflammation omega 3 supplementation appeared to suppress in the aforementioned study.

Flavanol-Rich Lychee Fruit Extract Displays Potent Antioxidant Activity in Trained Long-Distance Runners

If I told you about each and every "new" antioxidant that produced some marvelous effects in the petri-dishes of some scientists somewhere on a random university campus, there would hardly be any space left for interesting information on this blog. In the case of the particular lychee fruit extract (FRLFE), Nishizawa et al. (Nishizawa. 2011) selected for their study, we do not only have a human study, but also direct information on how supplementation with 50mg of Oligonol (brand name of the extract) influenced inflammatory markers and performance of 20 university level marathon runners over the course of 2 months:

Some parameters, including the white blood cell count, were significantly modified by FRLFE supplementation [46.3 FRLFE vs. 57.6 control]. Compared with the placebo group, the change in the serum interleukin-6 level between pre- and mid-training were significantly lower in the FRLFE group, while the change in the transforming growth factor-β level between pre- and post-training was significantly greater in the FRLFE group.

This increase in TGF-Beta is significant, because...

...TGF-β controls cell growth and proliferation (Massagué, 1998), and may be secreted in response to strenuous physical training and cell damage during training.

TGF-beta is thus another case, where an "inflammatory marker" indicates repair and (possibly) hypertrophy rather than damage and catabolism. Consequently, it is unlikely that the consumption of a highly anti-oxidant flavanol-rich lychee fruit extract hampers muscle growth. Who knows, maybe we are going to see respective supplements in the near future - meanwhile, I suggest you get yourself some of these Chinese soapberries at your local fruit store ;-)

Heart Protective Effect of Red Wine not Exclusively Due to Resveratrol. Melatonin Potentially the Major Player!

Resveratrol, the red wine polephynol still is in everyone's mouth (literally, as well as metaphorically), yet a recent (Lamont. 2011) study published in the Journal of Pineal Research indicates that another hitherto overlooked constituent of the fermented grape juice factors into its protective value: Melatonin.

Lamont et al. found that, at the doses which can be found in red wine, naturally, individually, as well as in combination resveratrol and/or melatonin ...

... significantly reduced infarct size compared with control hearts in wild-type mouse hearts (25 ± 3% and 25 ± 3% respectively versus control 69 ± 3%, P < 0.001) [...] Furthermore, perfusion with either melatonin or resveratrol increased STAT3 phosphorylation prior to ischemia by 79% and 50%, respectively (P < 0.001 versus control).

Both, melatonin, as well as resveratrol, appear to work via the "survivor activating factor enhancement" [SAFE]. What I consider more important, yet is the scientists' finding that

 [...] melatonin confers a comparable protective effect to resveratrol but at a concentration 30,000 times lower.

And their conclusion that "melatonin may be considered as a primary antioxidant in red wine". So what else could be healthier than a glas of good wine right before a good night's sleep?