A Modest Proposal for Peer Review Research

With the advent of, and inexpensive nature of online sharing of information, I propose that all peer-review research should include (anonymous) raw data for each subject.  At the very least, there should be scatter plots presented for the individual data points for the main outcomes.

I frequently teach statistics, and one of the first things we discuss in that class is sort of the "first purpose" of it all.  Because before we can analyze data, first we must summarize and present the data in such a way that the "consumer" can readily glean information.  In one classic stats text -- Triola -- this part is given the acronym CVDOT.  C = Center, V = Variation, D = Distribution, O = Outliers and T = Time.  So we go through the various ways we can convey the center of a data set, it's variability, distribution, etc.  In most of the studies we discuss here, data is presented as a mean value +/- either the standard deviation or standard error (C +/- V in the acronym).  And further statistical analysis compares these means between groups for statistically significant differences.   If I have 20 subjects in a study, I can provide you with a table of all results sorted by subject number assigned randomly.  This tells you very little.  If all I do is sort the data ascending or descending, you can now readily pick out the range and "center" of the data.  Perhaps if data is of a more rounded nature, you might be able to pick out the most frequent or common values.  Outliers will jump off the page.  

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Fiber and CRP

Came across this so just putting it out there.  It's a meta study of 7 clinical trials in which fiber was studied or reported.  In 6 of 7 CRP was reduced.  One study involving just psyllium showed no effect.

The effects of dietary fibre on C-reactive protein, an inflammation marker predicting cardiovascular disease

Conclusions: In the presence of weight loss and modified saturated, monounsaturated and polyunsaturated fat intakes, significantly lower CRP concentrations (25–54%) are seen with increased fibre consumption 3.3 g/MJ). Mechanisms are inconclusive but may involve the effect of DF on weight loss, and/or changes in the secretion, turnover or metabolism of insulin, glucose, adiponectin, interleukin-6, free fatty acids and triglycerides. Clinical studies of high- and low-fibre diets are needed to explore the potential favourable effects as observed epidemiologically, and to understand individual susceptibility to its anti-inflammatory effect and long-term cardiovascular reduction.

Unfortunately for those interested, full text is not free.

C-Reactive Protein and Cardiovascular Disease Risk: Still an Unknown Quantity?

Just putting this one out there:

C-Reactive Protein and CVD Risk   (full text article available at link, abstract below)

The role of C-reactive protein (CRP) in cardiovascular disease risk remains controversial, and several interrelated questions are unresolved. Although it is clear that higher circulating CRP levels are associated with coronary heart disease (CHD) incidence and mortality rates in prospective studies, the magnitude of this association has been downgraded in recent years (1). It is also clear that CRP levels are strongly related to many potential confounding factors that influence CHD incidence and mortality rates. In predictive models that appropriately account for these confounders, the magnitude of the association between CRP levels and CHD outcomes is considerably attenuated toward the null (2). Whether CRP is a marker of cardiovascular disease risk or is causally related to cardiovascular disease is uncertain. Nonetheless, some authors have recently claimed that CRP itself is indeed a promoter of atherosclerosis and increased CHD risk (3, 4). If this is true, CRP would become a clear and explicit target for therapeutic intervention.

Low Carbohydrate, High Fat Diet Increases C-Reactive Protein during Weight Loss

Low Carbohydrate, High Fat Diet Increases C-Reactive Protein during Weight Loss
Janet W. Rankin, PhD and Abigail D. Turpyn 
Journal of the American College of Nutrition, Vol. 26, No. 2, 163-169 (2007)

Studied Variable: Dietary Carbohydrate

Variables Measured: Body weight, IL-6, CRP, urinary 8-epi-prostaglandin, FBG, FFA (fasting)
Variables controlled for: Caloric intake

Protocol Summary: Subjects were ed into two groups followed calorie restricted (~1360 kcal/d) diets varied in composition: LC = 58F/12C/30P ; HC = 24F/59C/18P. Weight, inflammatory markers (IL-6 and CRP) and oxidative stress (8-epi) were measured weekly.

Human Study
Gender:  Women
Age:  adult, premenopausal
Number of Participants: 29
Weight Status: Overweight BMI 32.1 ± 5.4 kg/m2
Health Status: weight stable for at least 6 months, nonsmokers, sedentary, otherwise healthy and unmedicated
Study Duration: 4 weeks

Summary of results:

* LC lost a bit more weight (3.8 ± 1.2 kg LC vs. 2.6 ± 1.7 HC, p=0.04)
* CRP increased an average of 25% in the LC group whereas it decreased 43% in the HC group (p=0.02)
* FBG decreased similarly for both groups
* IL-6 increased similarly for both groups
* 8-epi varied differently between groups but with no consistent pattern.
* Serum NEFA increased for both groups, the increase was greater for LC


Here is a screenshot of the results:  (click on image to enlarge)

Researchers' Conclusion: "Diet composition of the weight loss diet influenced a key marker of inflammation in that LC increased while HC reduced serum CRP but evidence did not support that this was related to oxidative stress."

My Comments: 

Although apparently not statistically significant, the LC group (~190 lbs) was a bit heavier than the HC group (~175 lbs) to begin with in this study.  This could be related to the LC group starting at a higher (although also not indicated as significant) average CRP level.

But look at the CRP graph showing the individual results vs. baseline -- the horizontal axis is the baseline CRP.  I find this disturbing.  The first thing that jumps out is that almost all of the LC group had increases while all of the HC group had decreases.  Also disconcerting is that this effect seems more pronounced for those who had a low level of CRP to begin with -- IOW, LC seems to induce an inflammatory state according to the CRP indicator.   This is not seen for HC where in most cases CRP declines.  If one looks at the right side of the graph, you have the subjects in the highest baseline "inflammatory state".  What happens?  Significant decreases in CRP for the HC group, negligible change either way for LC.

Whether or not to be stressed over CRP levels is a matter of continued confusion and controversy, but higher CRP levels are never, as far as I've seen, considered a good thing.

I came across this article while researching plasma free fatty acids (NEFA, FFA) and am concerned with the effect the LC diet had on fasting FFA's.  The highest fasting level for the LC group was almost 1.5X (50% higher) than the highest fasting level for the HC group.  The high level vs. baseline for LC was ~1.8X vs. ~1.5X for the HC group. 

I don't know enough about 8-epi at this time to comment on that aspect of this study.