Part I: Systematic Review of Weight Gain Correlates In Literature

Food Intake and Weight Gain

I am addressing the topic of weight gain and obesity in the scientific literature yet again.

This blog series has a great big WARNING attached to it. And that’s not because the data contradict anything that I have said to date regarding weight gain, obesity onset, obesity perseverance, or just fatness. It has a warning because child subjects were most certainly harmed both during and after the studies under review.

Boston Public Library: Flickr.com

Boston Public Library: Flickr.com

 

First of all I would like to address the strange contradiction that increased food intake and lowered activity levels do not correlate with weight gains when obviously in recovery from an eating disorder, a patient can only restore weight and health if she increases food intake levels and lowers activity levels.

 

The discrepancy lies in the fact that an energy-balanced individual has no need of any additional energy, whereas an energy-deficient individual has need of additional energy until such time as he or she is energy-balanced. The body handles excess energy very differently from how it handles needed energy. Primarily an energy-balanced body simply burns away excess energy and lowers subsequent energy demand to maintain homeostasis. Carefully note however that that is done unconsciously— managing your weight consciously will harm that energy balance.

We will now look at systematic review data in the research literature regarding food intake levels and food intake types searching for their correlation to either weight gain or obesity prevalence.

Systematic reviews are at the top of the hierarchy of data, as I explain in Orthorexia II: Doubt and Certainty. Wherever possible results gleaned from systematic reviews, or systematic reviews specifically provided by the Cochrane Collaboration, give us our best shot at having evidence that can shape the foundation of clinical practice. But, our best shot is not a sure thing especially when the data don’t match the conclusions offered in those systematic reviews.

Systematic Review: Intake Levels and Weight Gain

There are no systematic reviews in the search I conducted for any correlation to overall calorie intake and weight increase. How on earth is that even possible given the weight loss industry is positively fire-hosing monies and drenching the research community with the wherewithal to conduct such reviews? If any of you out there find one, let me at it. Until then, let’s look at what I did find.

There are several systematic reviews associated with calorie restriction and weight loss and, as you know, the weight loss is almost never maintained over a period of more than two years. 1,2 You will find more details on long term weight loss failure in the blog post: Basic Weight and Obesity Facts if you are interested, however in this post I am focusing my attention to calorie intake increase and weight gain.

Let’s look at the two systematic reviews associated with food type and weight gain: one looking at sugar-sweetened beverage (SSB) intake and the other at fast food intake. The concluding statement for SSBs confirm consumption of SSBs correlate with both weight gain and obesity:

The weight of epidemiologic and experimental evidence indicates that a greater consumption of SSBs is associated with weight gain and obesity.” 3

But, as usual we have to look at the details within the study to see if that conclusion is borne out in the actual review data. Of some 264 citations, the authors deemed 72 papers worthy of initial review. 47 of those 72 papers were disqualified “23 did not assess soft drink intake or report weight change data, 12 were editorials or commentaries, 11 were reviews, and one prospective cohort study was too short. Five extractions were added back after the original retraction (no reason was given for the return of these studies into the review). That left 15 cross-sectional studies, 10 prospective cohort studies, five clinical trials and two reports of both cross-sectional and prospective data.

Of the 15 cross-sectional studies, 13 looked at children and adolescents and two at adults.

Of the 13, six showed correlation between SSB consumption and overweight or obesity in children. Three showed non-significant association. Another three showed no association. The final study showed negative association with the high and low quartile consumption groups. So more than half the cross-sectional studies on children and adolescents do not support correlation of SSB consumption and the presence of overweight or obesity.

Of the two cross-sectional studies on adults, the probability that an individual who drank greater than one soda drink/week was overweight or obese was 70% vs. 47% for women and 77% vs. 58% for men. Translated that means that 70% of obese and overweight women were drinking greater than one soda/week and 47% of average-weighted women were drinking greater than one soda/week.

The other cross-sectional study found that women who consumed one soda/week were 0.21 kg (0.47lbs) heavier than the non-consumers and men who consumed one soda/week were 0.15 kg (0.33 lbs) heavier.

If soda drinking were a causative element of obesity onset, then we shouldn’t see half of all average-weighted women happily downing sodas each week with no commensurate increase in weight, should we?

So far we have no compelling evidence so we move onto the prospective cohort studies.

Six of the 10 studies were focused on children and adolescents. With breathless excitement, four of these studies confirm an actual correlation with soda intake increase year over year and weight gain: a 0.04 BMI increase per additional daily serving (over a three year period). Increasing by greater than two servings per day correlated with BMI increase of 0.14 in boys and 0.10 in girls. You might even gloss over the following statement the authors make regarding these strong correlations: “Adjustment for energy attenuated the magnitude of the estimated associations, possibly because of the contribution of sugar-sweetened beverages to total energy intake.” Stage whisper: correlations actually far weaker than what has just been presented, when adjusting for energy needs.

Two studies found non-significant correlations for BMI and SSBs. One of those two found no correlation between change in SSB consumption and BMI.

One of the four prospective cohort studies indicated that women who upped their intake of SSBs had an increase of weight that resulted in a BMI increase of 1.72 during the first period of study and an additional increase of 1.53 during the second period of study. Those who maintained their either high or low SSB consumption also had an increase in weight during the two study periods and it was less than those who had upped their SSB intake during the study. Those who dropped their SSB intake during the study period had BMI increases of 0.49 and 0.05. And the increase in weight for those who either maintained a high intake of SSB or a low intake of SSB didn’t statistically differ at all.

Another one of the prospective studies showed that those with a predisposition for gaining weight prior to the study period had a 60% greater odds of gaining weight if they were in the first quintile of SSB consumption. But those with no predisposition for gaining weight prior to the study period had no greater odds of gaining no matter SSB consumption.

The next prospective study found, over an eight period, slightly higher and non-significant odds of those consuming one soda/week being overweight or obese. The final study in this group showed a small non-significant increase in weight with greater than one soda/week.

Brief recap. Please remember that correlation (even when it is strong) does not show us that one experimental factor causes another. When you see the word non-significant it means they measured a correlation that was so weak that it should be classified as no correlation.

  1. Majority of cross-sectional studies show no correlation between sugar-sweetened beverage intake and overweight and obesity in children and adolescents. And none that SSB intake correlates to weight gain.
     
  2. Only two cross-sectional studies on adults were reviewed. We see that when SSBs are consumed at one soda/week, the individual doing the drinking is slightly more likely to be overweight or obese than average weighted.
     
  3. Four of the six prospective studies showed correlation between an increase in SSB consumption and an increase in BMI (weight gain). However when adjusted for energy, that correlation was weakened. One of the six found a statistically non-significant correlation between SSB and BMI. And the final one found no correlation between SSB and BMI.
     
  4. The prospective studies on adults suggest that everyone gains weight no matter their SSB consumption level. Those who up their consumption gain a bit more weight than those who don’t drink, or than those who drink a lot (but are stable in that consumption), or than those who reduce their intake of SSB consumption.
     
  5. Those who are predisposed to gaining weight have higher odds of gaining weight with high SSB consumption. But the odds were flat no matter SSB consumption level if the person was not predisposed to gain weight.
     
  6. And the remaining two studies showed a statistically irrelevant correlation between SSB consumption and the presence of overweight or obese status and between SSB consumption and weight gain, respectively.

So it turns out it’s the experimental studies that are being disproportionately weighted as relevant when it comes to the authors’ conclusions quoted above. Clearly the 25 cross-sectional and prospective studies provide no confirmation that SSB consumption is correlated with weight gain.

There are five experimental studies involved. The first used overweight men and women who were randomized to receive either sucrose or artificial sweetener supplements. The former group gained weight and the latter lost weight (in the 1 kg/2.2. lbs range and change) over ten weeks. In this study the experimenters used a daily supplement of either sucrose or artificial sweetener. They did this to create a double-blinding, where neither the individuals providing the supplements nor the subjects in the study would have known whether they were receiving a sugar or artificial sweetener supplement. But in generating a double-blind environment they also remove the natural way in which individuals consume SSBs.

The second study randomized subjects to consume soda sweetened with high-fructose corn syrup (HFCS) or aspartame. They applied a 3x3 crossover and that means that with intervening periods, each individual spent three weeks consuming HFCS sodas, three weeks consuming aspartame sweetened sodas, and three weeks consuming their habitual soda intake (which for some was as much as 1L a day and for others was zero – so not exactly a control washout period in fact). They were looking to determine if consuming SSBs created a compensatory increase in energy intake for the subjects.

Now of course this second study uses real beverages and not supplements, which means many subjects will identify a difference between the HFCS sodas and the aspartame sodas. The results were obtained from self-report diaries after the subjects underwent a training period with a dietician. During the soda part of the trial (both HFCS and aspartame) the subjects were required to drink 4 bottles of soda daily (basically 1L of soda a day). The experiment was run in two replications: once in the fall of 1987 and then again in the spring of 1988. The number of people in the trial was originally 13 women (one dropout) and 28 males (five dropouts). The subjects thought they were involved in a market research project and did not notice that when they were drinking either HFCS or aspartame sodas, their discretionary intake of sugar was reduced in their diet. The women gained weight drinking both HFCS and aspartame (slightly more with the former than the latter). Men gained non-significant weight drinking HFCS and lost weight drinking aspartame sodas.

Sounds ominous, but it’s a poorly designed trial on several levels. First of all, the number of subjects involved is very small, particularly the women. Strangely, there should have been 12 women according to the drop out information the authors provided, but the graphed results list only nine.  Secondly, the average intake per person of soda per day in the US is 0.5L/day. Now obviously some drink far more than that and many more drink far less. However, enforced drinking of 1L/day doubles that average intake. Thirdly, the subjects were variously drinking 1L/day to no sodas at all during the control period. As a result no effective control was placed in the washout period meaning that the weight change occurring during active HFCS or aspartame soda intake may have been due to holdover effects from the control period. The weight variation in question is 0.6 kg and the entire experiment relied on lying to the subjects that their intake could be confirmed through urinalysis (it could not) and that they needed to be particular and accurate in their self-report diaries of daily intake. 4 And we already know from Homeodynamic Recovery Method, Doubly-Labeled Water Method Trials and Temperament Based Treatment how accurate self-reports are for food intake.

The third trial involved 450 kcal-sodas and jellybeans. Yet again a tiny trial with eight women and seven men involved. Four weeks with soda load, four weeks washout and four weeks jellybeans. 24-hour dietary recalls were solicited by phone interview. Subjects were told that their weekly saliva tests would confirm adherence to eating the jellybeans and drinking the sodas (a lie to promote adherence). The actual data in the table show that the pre and post jellybean period involved a change of body mass index of + 0.1. The pre and post soda period involved a change of body mass index of + 0.1. As a result, this trial focuses more on the fact that there appears to have been compensation (lowering) of total calorie intake when the subjects were eating jellybeans and there was no compensation during the soda intake period of the trial, although clearly that difference was not realized in weight change. 5

A randomized clustered trial was conducted on school children that I really don’t even want to discuss as I find the ethics make me seriously squeamish. I feel about the same level of discomfort as I did when reading about a trial of feeding lily plant parts to cats to determine dose response where all the cats were euthanized when the onset of acute kidney failure occurred.

In this study, the children had a mean age of 8.7 years (ranging 7 to 10.9 years old). The intervention group was subjected to an educational program. The initial hour-long presentation was delivered to assigned classes by an investigator to discourage the consumption of “fizzy” drinks with a positive affirmation of a balanced healthy diet. The kids were also provided with a website for further information and a rap competition “Ditch the Fizz”. Teachers assisted in the program with further emphasis on drinking water, eating fruit to get a sense of natural sweetness and dunking teeth in carbonated drinks to assess its effect on dentition. The final session involved art presentations and a classroom competitive quiz based on a popular game show.

In the press the results were hailed as follows: Weight gain in children may be controllable by reducing their intake of fizzy drinks, according to the organisers of a year-long experiment involving more than 600 children at six primary schools.” [The Guardian]

These are children right on the cusp of major pubertal development that necessarily includes significant weight gain. I can only hope that the parents of the five boys and one girl who withdrew their initial consent recognized how incredibly damaging this intervention was going be to their children and that was the reason for their change of heart.

But what a success it was! There was a 7.5% increase in the mean percentage of overweight and obese children in the control group, and a 0.2% decrease in the mean percentage of that poor intervention group.

And the authors clearly had to provide relative percentage rates rather than actually list the hard data found in their tables. The mean body mass index change at the 12-month point for the control group was 0.8 and for the intervention clusters is was 0.7. 6

What obviously also isn’t assessed is the negative impact even such a small weight decrease as was realized in the intervention group, might actually have on overall health and development for those children.

That brings us to the final randomized controlled trial where 103 subjects ages 13-18 were randomly assigned to either receive a house delivery of non-carbonated beverages for 25 weeks or not. The net difference change of BMI -0.14 was not statistically significant. There was however a greater net difference for those at higher starting BMI levels of -0.63.  7

Sugar-Sweetened Beverages, Weight Gain & Conclusions

As of 2014 an entire consortium’s worth of Canadian and American researchers developed and published an open-access systematic review protocol that will be undertaken to definitively determine whether sugar-sweetened beverages cause adverse health outcomes in children. I note that an adverse health outcome includes “overweight” and “change in weight” in their classification and these are not adverse health outcomes, although they could be described as adverse social outcomes.

I get the distinct impression that obesity researchers are frustrated by the fact that, in their own wordsThe available systematic review evidence is conflicting and presents with several methodological issues, making firm conclusions difficult.” 8

And for that complete fail, researchers will continue to subject children to BMI measurements and educational fat-shaming sessions until we get the systematic review we want. I know who should be ashamed, and it’s not the children.

Fast-Food Consumption and Weight Gain

The systematic review on fast-food consumption and its correlation to weight gain included 16 cross-sectional studies, seven prospective cohort studies and three experimental studies. Given that the researcher was forced to admit defeat in the summary, I’ll leave it to readers should they want to actually look out the entire paper, but here’s the executive summary:

Whether an association exists between fast food consumption and weight gain is unclear.” 9

As a bonus systematic review, I’ll include a monstrously thorough review on the childhood predictors of adult obesity:

Studies investigating the role of diet or activity were generally small, and included diverse methods of risk factor measurement. There was almost no evidence for an influence of activity in infancy on later fatness, and inconsistent but suggestive evidence for a protective effect of activity in childhood on later fatness. No clear evidence for an effect of infant feeding on later fatness emerged, but follow-up to adulthood was rare, with only one study measuring fatness after 7 y. Studies investigating diet in childhood were limited and inconclusive. Again, confounding variables were seldom accounted for.” 10

Conclusion

In past blog posts where I mention that food intake and activity levels are not correlated with obesity development or onset, I will now update the references in those posts to reference these systematic reviews as they rather handily trump single studies and trials in any case.

It is upsetting to spend any real time in this entire line of research given that I spend my days immersed in trying to help people who are tortured by eating disorders. I wonder how many of those intervention subjects are now living with an activated eating disorder as a direct result of classroom-driven focus on BMI and “ditching the fizz”.

In the following posts in this series, I will unpack data associated with physical activity, weight gain and obesity, and then I will address the prevalence of metabolically healthy obese individuals.


1. MJ Franz, JJ VanWormer, AL Crain, JL Boucher, T Histon, W Caplan, JD Bowman, NP Pronk, Weight-loss outcomes: a systematic review and meta-analysis of weight-loss clinical trials with a minimum 1-year follow-up, Journal of the American Dietetic Association, Vol.107(10), pp.1755-1767, 2007.

2. AG Tsai, TA Wadden, Systematic review: an evaluation of major commercial weight loss programs in the United States, Annals of internal medicine, Vol.142(1), pp.56-66, 2005.

3. VS Malik, MB Schulze, FB Hu, Intake of sugar-sweetened beverages and weight gain: a systematic review, The American journal of clinical nutrition, Vol.84(2), pp.274-288, 2008.

4.  MG Tordoff, AM Alleva, Effect of drinking soda sweetened with aspartame or high-fructose corn syrup on food intake and body weight, The American journal of clinical nutrition, Vol.51(6), pp. 963-969, 1990.

5. DP DiMeglio, RD Mattes, Liquid versus solid carbohydrate: effects on food intake and body weight." International journal of obesity, Vol.24(6), pp.794-800, 2000.

6. J James, P Thomas, D Cavan, D Kerr, Preventing childhood obesity by reducing consumption of carbonated drinks: cluster randomised controlled trial, Bmj, Vol.328(7450), p.1237, 2004.

7. CB Ebbeling, HA Feldman, SK Osganian, VR Chomitz, SJ Ellenbogen, DS Ludwig, Effects of decreasing sugar-sweetened beverage consumption on body weight in adolescents: a randomized, controlled pilot study, Pediatrics, Vol.117(3), pp.673-680, 2006.

8. A Stevens, C Hamel, K Singh, MT Ansari, E Myers, P Ziegler, B Hutton, A Sharma LM Bjerre, S Fenton, R Gow, S Hadjiyannakis, K O’Hara, C Pound, E Salewski, I Shrier, N Willows, D Moher,  M Tremblay, Do sugar-sweetened beverages cause adverse health outcomes in children? A systematic review protocol, Systematic Reciews, Vol 3.(1), p.96, 2014.

9.  R Rosenheck, Fast food consumption and increased caloric intake: a systematic review of a trajectory towards weight gain and obesity risk, Obesity Reviews, Vol.9(6), pp. 535-547, 2008.

10.  TJ Parsons, C Power, S Logan, CD Summerbelt, Childhood predictors of adult obesity: a systematic review, International Journal of Obesity, Vol.23, 1999.