Human Study Links High Meal Frequency to Higher Weight Gain and Accumulation of Liver Fat: Are Our Sugary + Fatty Snacks the Reason We Are Sick & Obese?

The "average Westerner" is fat. That's for sure, but is it actually possible that it is the often recommended increase in meal frequency which is to blame for that?

A soon-to-be-published published study from the Academic Medical Centre Amsterdam sheds a whole new light on the role chocolate bars, potato ships, coke and even "healthy" *rofl* fruit juices may play in the etiology of the obesity epidemic (Thanks to reductions in life expectancy and fertility the US prevalence of overweight, obesity, and extreme obesity will plateau at about 28%, 32%, and 9% in 2030; cf. Thomas. 2013)

In a one of a kind human study, the researchers assigned 36 lean, initially healthy men to a 40% hypercaloric diet that was meant to emulate the contemporary food intake of US kids who get ~ 27% of their daily energy intake from high fat and high fat + high sugar snacks.

You can learn more about meal frequency at the SuppVersity

Grazin' Bad For the Obese!

Breakfast Keeps You Lean?!

Frequent Protein Consumption

Myth: Few Meals More Bodyfat

8 Meals = Stable, But High Insulin

Int. Fasting & Exercise

Instead of randomly adding a bunch of Snickers bars, Twinkies and DingDongs to the subjects diets, the researchers from the Department of Endocrinology & Metabolism had their subjects consume their "snacks" either with their three main meals, or as a true snack, 2h thereafter:

• Nutridrink Compact ® liquid meal with nutritive value of 240 kcal/100 ml (16% protein, 49% carbohydrates (mainly maltose and poly- saccharides), 35% fat (mainly unsaturated)).
  

  The high-sugar liquids were commercial soft drinks sweetened w/ 50% glucose and 50% fructose and had 43.3 kcal/100 ml.
  HFHS-size group: high-fat-high-sugar (HFHS) diet using Nutridrink Compact ®three times a day, consumed together with the three daily main meals. 
• HFHS-frequency group: high-fat-high-sugar (HFHS) diet using Nutridrink Compact ® three times a day, consumed two to three hours after each meal.
• HS-size group: high-sugar (HS) diet using commercially available sucrose-sweetened beverages three times a day, consumed together with the three daily main meals. 
• HS-frequency group: high-sugar (HS) diet using commercially available sucrose
  sweetened beverages three times a day, consumed two to three hours after each meal.

As you can see in Figure 1, this methodological twist produced quite astonishing results. Results of which the headline of today's SuppVersity article already revealed that they clearly suggest that " that snacking, a common feature in the Western diet, independently contributes to hepatic steatosis and obesity" (Koopmann. 2014).

Figure 1: Changes in body composition and resting energy expenditure on hypercaloric diets with different snacks & meal frequencies (Koopmann. 2014)

What I personally find pretty intriguing is are the intra-group differences in the "sweet beverage group" (high sugar, three meal) which appear to correspond with a phenomenon I hear you, my dear readers complain about pretty often. The complaints about that anonymous extremely lean friend of yours who drinks coke all day and appears to live on bonbons, popcorn and Gatorade and how unfair it is that you can't do just that... but I am digressing.

Eating too much and eating too frequently

In the end, the real news is obviously not that there are purported genetic outliers, but rather that these people are often not at a genetic advantage. In 99% of the cases I know in person, I had to realize that these guys and gals have a funny way of "intermittent fasting". Contrary to the average obese person complaining about his or her "genetic disadvantage", these folks still know the meaning of satiety and mix days with exorbitant energy over-consumption with days on which they skip breakfast, have a snickers for lunch and a regular dinner. That's certainly not healthy, but it keeps them lean and misleads bystanders and even close friends to assume that they were at a "genetic disadvantage", when the latter is in fact rather the result of eating too much and eating too frequently.

Figure 2: The increases in intra-abdominal fat, visceral fat, subcutaneous fat and intrahepatic fat were significant only in the "Snackers", i.e. those subjects who consumed their high fat + high sugar or high sugar "snacks" in-between meals, but not  in those who simply added them on top of one of their three regular meals (Koopmann. 2014)

I guess before you've have had a look at Figure 2 you may (rightfully) have been asking yourself what all that has go to do with the study at hand. Afterwards, however, you should realize that my previous ramblings were actually not so far off the intriguing insight that " snacking, a common feature in the Western diet, independently contributes to hepatic steatosis and obesity" (Koopmann. 2014) - or, to put it differently: If you combine eating much with eating frequently you blow up like a balloon (or the average Westerner - you decide which image you prefer).

Question: Is this true for protein snacks, as well? In the context of a hypercaloric diet with 40% more energy than you need, the answer is YES! We do in fact have the evidence from human studies: Protein is obesogenic! It may be "less effective" than the nasty combination of sugars and fats used in the study at hand, but if you simply add three 50g whey protein shakes on top of your regular 2,000kcal diet, this will provide a 25% increase in energy in- take and corresponding weight gain. Some of the latter will be muscle - but the chances that you won't accumulate some body fat as well are lower than the allegedly over- estimated increase in cancer risk from chronic mTOR (over-) activation (Zoncu. 2011).

Bottom line: In conjunction with a chronically hypercaloric diet as in the obese, yet not with an "intermittent fasting" + satiety guided snacking regimen as in the purported "genetic outliers" high fat and high sugar snacking does in fact promote the accumulation of unhealthy body and liver fat.

If, on the other hand, the overall energy intake does not exceed the energy demands, chronically. It's a mere question of thermodynamics that the amount of stored energy will not increase. And that's true regardless of the macronutrient composition (the latter will have direct and indirect consequences on the energy expenditure and intake, respectively, though).

Practically speaking the results of the study at hand do thus support the often-cited contribution of chronic anabolism aka diet-induced increases in insulin, IGF-1 and mTOR and put a huge questionmark behind the still often-heard recommendation to consume many small instead of three larger meals, if your goal is to maintain a healthy body fat level. Unlike you belong to the lucky few whose energy thermostat is still intact - the previously referenced "purported genetic outliers" - it's easier, safer and healthier not to snack in the hours between your main meals.

References:

• Koopmann, et al. "Hypercaloric diets with increased meal frequency, but not meal size, increase intrahepatic triglycerides: A randomized controlled trial." Hepatology (2014). Accepted Article.
• Thomas, Diana M., et al. "Dynamic model predicting overweight, obesity, and extreme obesity prevalence trends." Obesity (2013).
• Zoncu, Roberto, Alejo Efeyan, and David M. Sabatini. "mTOR: from growth signal integration to cancer, diabetes and ageing." Nature reviews Molecular cell biology 12.1 (2011): 21-35.