A news story on Science a Gogo reports that obesity is linked to stupidity, according to a new study based on brain scans. Apparently the reporter can’t read. That’s not at all what the study showed.
What the Study Really Said
The study was entitled “Brain structure and obesity.”It was published in Human Brain Mapping. There were 10 authors listed, with the two interviewed for the news report being the lead author (CA Raji) and the last listed author (PM Thompson). The study evaluated MRI scans of 94 elderly subjects who were cognitively normal and remained cognitively normal for at least 5 years after their scan. It found that obese people had 8 percent less brain tissue than people with normal weight, while overweight people had 4 percent less tissue. The deficits were in areas of the brain that have been associated with Alzheimer’s disease. The story reports that this put the subjects at high risk for Alzheimer’s disease. But the subjects remained cognitively normal for at least 5 years after the scan. They were not rendered stupid. They did not develop Alzheimer’s. They remained cognitively normal. You might also interpret the study as showing that obese patients with those findings on brain scan could be predicted not to develop Alzheimer’s or develop any other cognitive deficits for at least five years.
To show that obesity is linked to stupidity you would have to show that more obese people were less intelligent. To show that it is linked to Alzheimer’s, you would have to show that obese people were more likely to have Alzheimer’s. To show an association between the deficits detected by MRI and stupidity or Alzheimer’s, you would have to show that subjects with those deficits were more stupid or more likely to be diagnosed with Alzheimer’s. This study did not even attempt to do any of those things.
If the concern is Alzheimer’s, the headline about “stupidity” is inaccurate. Alzheimer’s is a form of dementia, not of “stupidity.”
The Study Raises Questions
MRI scanning is a blunt instrument that can detect some abnormalities of structure but that can’t detect details about how areas of the brain are functioning and whether there are any cognitive deficits. It’s a bit like determining that there are fewer telephones in a community but not knowing what that means in terms of things like the total number of phone calls made, how efficiently calls are routed, the number of busy signals, or the sound quality of the transmissions. Fewer telephones might or might not have any impact on the ability of community residents to communicate by telephone.
The specific findings raise a number of questions.
An “obese” BMI of >30 was associated with atrophy in the frontal lobes, anterior cingulate gyrus, hippocampus, and thalamus. An “overweight” BMI of 25-30 was associated with atrophy in the basal ganglia and corona radiata of the white matter. The lists of affected areas are different. What could explain that?
While they found volume deficits of 4% and 8% in certain brain areas, the overall brain volume did not differ between overweight and obese persons. That seems to indicate that obese patients must have had some areas of hypertrophy to compensate for the areas of atrophy. What areas were they, and what does that mean?
The listed areas of atrophy did not correspond to the listed areas of atrophy in previous studies of younger obese patients. What does that mean?
There are a number of other published studies showing areas of brain atrophy in obese subjects, as well as studies showing areas of atrophy in Alzheimer’s patients, but the list of areas is different in every study with only some overlap. A Japanese study showed that BMI was correlated with cerebral volume loss in Japanese men but not in women. It is not yet possible to diagnose Alzheimer’s on MRI scans.
Many other factors have been associated with Alzheimer’s disease, including metabolic syndrome, HBP, diabetes, hyperlipidemia, and the APOE4 genotype. They attempted to control for some of these potential confounders but not all. A previous study found that Apolipoprotein E epsilon 4 genotype status appears to have a greater deleterious effect on gross hippocampal pathology and memory performance in women compared with men. Interestingly, in this study the APOE4 genotype was not related to any detectable alterations in brain structure.
With all these variable findings, is it possible that some or all of them are due to “noise?”
The Authors Speculated Beyond the Data
The reporter quotes two of the authors of the study. They confused the reporter even more by going beyond the data, offering unsupported speculations, and offering clinical advice for preventing Alzheimer’s.
“That’s a big loss of tissue and it depletes your cognitive reserves, putting you at much greater risk of Alzheimer’s and other diseases that attack the brain,” noted Thompson. “But you can greatly reduce your risk for Alzheimer’s, if you can eat healthily and keep your weight under control.”
“Along with increased risk for health problems such as type 2 diabetes and heart disease, obesity is bad for your brain: we have linked it to shrinkage of brain areas that are also targeted by Alzheimer’s,” added co-researcher Cyrus A. Raji. “But that could mean exercising, eating right and keeping weight under control can maintain brain health with aging.”
The news article quoted one researcher as saying
The brains of obese people looked 16 years older than the brains of those who were lean, and in overweight people looked eight years older.
This is an irresponsible and misleading statement. It is not possible to estimate someone’s age from a brain scan.
Is There Evidence Associating Obesity with Cognitive Impairment?
This study that did cognitive testing on Framingham subjects found adverse effects of obesity on cognitive performance for men only.
In this study “Midlife measures of central obesity (WHR in the uppermost quartile- Q4) and of hypertension (BP > or = 140 / > or = 90 or use of anti-hypertensive medication) were each significantly related to poorer performance on executive function & visuomotor skills. Neither HTN nor obesity was individually or synergistically related to verbal memory (immediate or delayed recall).” This does not fit the pattern of deficits in Alzheimer’s disease.
Another study found that obese adolescents had evidence of attention deficits and executive dysfunction. Again a different pattern, which might be either cause or result.
Another study found that abdominal fat in late life appears to confer an increased risk for dementia/CIND [cognitive impairment not demented], whereas overall obesity appears to be protective.
Another study found cognitive deficits in older but not younger obese subjects. It commented that these changes might be attributable to comorbid conditions such as congestive heart failure, obstructive sleep apnea, or metabolic lipid abnormalities.
This study found that elevated BMI is not associated with cognitive function in healthy children and adolescents.
Another study concluded:
A statistically significant link was found between subjects’ performances on all of the cognitive tests and their body mass index—in other words, body mass index was inversely related to performance on all cognitive tests. Yet, after taking age, gender, IQ, years of education, and other possibly confounding factors into consideration, only impaired executive function significantly differentiated overweight or obese subjects from those of normal weight.
It pointed out that if there is a causal link it could be in either direction:
it is also possible that persons with a defective executive function are more likely to become overweight or obese since many aspects of executive function—for instance, impulse control, self-monitoring, goal-directed behavior—seem to bear directly on the ability to maintain weight.
This study found a decreased whole brain volume in obese individuals compared to normal weight and overweight individuals, which is inconsistent with the results of the new study.
With the inconsistency between studies, it is hard to determine whether this study means anything or whether it amounts to another instance of “the new phrenology” where too much is read into brain scans. The study showed a correlation, and correlation is not causation. No clinical lessons can be drawn from this data. At any rate, we already recommend weight control to reduce the risk of a number of other diseases.
The reporter did a terrible job of reporting, and the researchers only muddied the waters. The way they reported the meaning of their findings was not exactly a model of scientific objectivity.
This report is an insult to overweight and obese people and perpetuates the “fat dumb and happy” stereotype.
This article was originally published in the Science-Based Medicine Blog.
