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SKEPTOID BLOG:

Does Bullying Cause Chronic Health Problems, Or is It Just Bull?

by Stephen Propatier

May 14, 2014

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Donate Science reporting of health research is terrible. I have noticed an ever-growing component of researcher promotion that is making the problem worse, not better. This week the Los Angeles Times, the New York Times, Time magazine, and multiple smaller news outlets are reporting on a study recently published online by the PNAS. The title of this study "Childhood bullying involvement predicts low-grade systemic inflammation into adulthood," has been turned into a media circus of supposition and conjecture. Generally the news outlets, and the primary investigator William E. Copeland, suggest that bullying produces a long-term biological response resulting in long-term health changes.

The science has been split into two equally wrong narratives. Both of the narratives are conjecture. The storylines promote the idea that being a bully is protective for future health, or conversely that being bullied is predictive of poor health. Frankly that is beyond the scope or rigor of this research. That has not stopped anyone including the primary investigator from promoting the presumptive conclusions credulously.

I have reviewed the research and although it has some interesting findings it does not infer a causal relationship. Conclusions proposing a causative link between bullying and prediction of future health risks are complete bull.

Findings from the study:
Bullying is a common childhood experience that involves repeated mistreatment to improve or maintain one's status. Victims display long-term social, psychological, and health consequences, whereas bullies display minimal ill effects. The aim of this study is to test how this adverse social experience is biologically embedded to affect short- or long-term levels of C-reactive protein (CRP), a marker of low-grade systemic inflammation. The prospective population-based Great Smoky Mountains Study (n = 1,420), with up to nine waves of data per subject, was used, covering childhood/adolescence (ages 9—16) and young adulthood (ages 19 and 21). Structured interviews were used to assess bullying involvement and relevant covariates at all childhood/adolescent observations. Blood spots were collected at each observation and assayed for CRP levels. During childhood and adolescence, the number of waves at which the child was bullied predicted increasing levels of CRP. Although CRP levels rose for all participants from childhood into adulthood, being bullied predicted greater increases in CRP levels, whereas bullying others predicted lower increases in CRP compared with those uninvolved in bullying. This pattern was robust, controlling for body mass index, substance use, physical and mental health status, and exposures to other childhood psychosocial adversities. A child's role in bullying may serve as either a risk or a protective factor for adult low-grade inflammation, independent of other factors. Inflammation is a physiological response that mediates the effects of both social adversity and dominance on decreases in health.
This study has a lot of inferential flaws that the researchers failed to address. I also think that they make several assumptions about CRP levels significance. There is no doubt they are making a (previously) unsupported and implausible conclusion about inflammation. Namely that transient mental/physical stress results in a lifelong physiologic inflammation. The researchers are proposing that bullying somehow provides a lasting health benefit. This is trying to draw a causation inference: that there is an evolutionary benefit to bullying, and that it has a life long health benefit or detriment depending on their victimization status—a poor conclusion by the researchers. There is no way to draw a causal relationship from this study, even if it is 100% accurate, and it isn't.

The authors lack a fundamental understanding of what the elevated CRP means, they have failed to address major structural issues in the evaluations and make post hoc conclusions that are implausible and tenuous at best.

I think the researchers said it best in their own study: "Little is known about how this social adversity becomes biologically embedded to influence health status."

Exactly my point.

There is no known direct mechanism for prolonged immune manipulation by episodic childhood social adversity, especially years after the time frame of the experience. There can be lifelong maladaptive psycho-social behaviors developing due to the event. Long-lasting biologic immune changes are not plausible and would be a whole new understanding about the immune response to episodic emotional stress.

The authors are making three critical assumptions that have no scientific support:
  1. There is a single biological factor that is a dependable measure of systemic inflammation.

  2. There is a known/plausible mechanism from a social interaction that would produce a permanent biological immune response, positive or negative.

  3. Pre-pubescent children are biochemically identical to adults, and that measuring pre-pubescent CRP values provide a baseline to measure against adult levels.

Even if you dismiss the methodological problems (heterogeneous population, poor racial distribution, no interviewer blinding, exceptionally small statistical variation, small blood sample frequency, limited controls, and self reporting by subjects), you will find that you have a low plausibility biological effect that has no mechanism. The findings are supported only by a researcher assumption that physiologic response to stress equals lasting immune inflammation.

If you let all those questions go and start from the argument that the study is structurally sound and plausible, what does elevated CRP mean?

CRP is C-reactive protein. Experimental and clinical evidence accumulated since 1990 have established inflammatory processes as important contributors to atherogenesis, as well as to the vulnerability of an atherosclerotic lesion to rupture or erosion.

Based upon this evidence, protein markers of inflammation have been studied as noninvasive indicators of underlying atherosclerosis in apparently healthy individuals and of the risk of recurrent events in patients with established atherosclerotic vascular disease. The most extensively studied biomarker of inflammation in cardiovascular diseases is C-reactive protein (CRP), for which standardized high-sensitivity assays (hs-CRP) are widely available. [1,2]

CRP is an acute-phase protein that is produced predominantly by hepatocytes under the influence of cytokines such as interleukin (IL-6) and tumor necrosis factor-alpha. [3]

Layman's terms: high-sensitivity CRP may be a predictive factor in determining your risk for cardiovascular disease. I am stressing that it MAY BE predictive. The jury is still out on the benefit of measuring CRP or treating based solely on CRP levels.

For those interested in the technical details of this methodology, I have included problems using CRP as a test to predict cardiovascular health:

?What is the appropriate range of "normal" concentrations for serum hs-CRP if one were to target therapy?

?How often should hs-CRP be measured for screening? Most studies that have evaluated the prognostic value of serum CRP in patients with cardiovascular disease (CVD) have relied upon a single measurement. However, systemic inflammatory status can fluctuate over time.

?How does the lack of specificity of hs-CRP for cardiovascular disease influence the interpretation of hs-CRP?

?Should patient management be altered based upon the results of CRP testing? Until the publication of the JUPITER trial, there was no direct evidence that lowering CRP alone would result in a reduction of cardiovascular risk. Because the trial did not include a group with low hs-CRP, it is not possible to know whether the demonstrated benefit of rosuvastatin in the trial was specifically related to underlying vascular inflammation manifest by hs-CRP. However, the primary results of the JUPITER trial suggest a benefit to statin therapy among individuals with an LDL-cholesterol level below 130 mg/dL and a CRP level of at least 2.0 mg/L. [2]

Again in Layman's terms: CRP does not define cardiovascular risk, it is a factor that may help stratify risk for cardiovascular disease. It is not a marker that identifies chronic systemic inflammation level. It is controversial for CV disease and its benefit as a predictive tool is minor compared to major risk factors, e.g. BMI, smoking, exercise, and family history.

Although a poorly structured correlational study can lead to new discoveries, this research fails to be up-to-snuff enough to provide even a starting point. There are several mutually detrimental layers to this onion. CRP says nothing about general health or longevity. CRP is not helpful by itself for stratifying cardiovascular risk factor. The author is drawing implausible and unsupported conclusions about human biology. The study has several inherent structural flaws. The researcher is publicly drawing prospective conclusions about the significance of the data.

Here is the kicker in my opinion, the reason why the research is pretty much worthless. The researchers failed to define the single most important key element to this study.

What does bullying mean?

When you do this kind of research it is critical to define parameters for bullying. I have no idea what "waves of bullying" means (the researchers' term for the events).

Bullying, whatever that means, is a complex social behavior. It involves a myriad of individual and environmental factors that are involved in that experience. How individuals react to these events physiologically and psychologically has even more variability. It is like trying to nail Jell-O to the wall. It is impossible to isolate out these individual factors by longitudinally following an individual. You cannot simply exclude co-variants through an un-blinded interview.

Worse this research has been reported as "bullies live longer." It is almost criminally negligent to promote bullying by giving the parents the false excuse that their child will be superior socially or medically. Also it adds another layer of concern to the bullied.

I suspect that this study got published and submitted just because of the controversial conclusions. I am betting that the principal researcher thinks that his conclusions (even if wrong) will help support the suppression of bullying, failing to realize that it can have the unintended opposite effect.

This story is a trifecta of bad science reporting: a controversial public issue; a complicated, multifaceted correlational study; and a scary narrative.

Bottom line I call BS on this conclusion. CRP levels are not a test you should be checking, there is no one factor to predict health, and bullying is a social issue. Bullying needs to be addressed but trying to add an implausible biological component to the mix is confusing and problematic.

I personally feel that America has a fascination with trying to ascribe biologic causes to psycho-social issues, due to a cultural bias towards psychiatric issues. It's a cultural bias that psychiatric disease is a self-controllable human weakness, the quintessential blame the victim mentality. This cultural bias consistently makes us try to put a square peg in a round hole. That makes people seek out bogus useless treatments instead of dealing with the problem, a problem that can be just as real and just as deadly as the plague.

Being bullied may not give you a heart attack and being a bully isn't a license to smoke, but it can be deadly.

References:
  1. Roberts WL, Moulton L, Law TC, et al. Evaluation of nine automated high-sensitivity C-reactive protein methods: implications for clinical and epidemiological applications. Part 2. Clin Chem 2001; 47:418.

  2. Ridker PM. Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation 2003; 107:363.

  3. Kushner I. The phenomenon of the acute phase response. Ann N Y Acad Sci 1982; 389:39.

Bully CRP Study

Tables

by Stephen Propatier

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