Monday, June 8, 2015

Stroke prevention with the Mediterranean diet

Fad diets abound, but none appear to be as positively impactful to health as the Mediterranean diet. Even the likes of Jennifer Garner, Elizbath Hurley, and Catherine Zeta-Jones adhere it, and they are all very attractive. Although it won't help increase attractiveness, it may contribute to preventing strokes.

The diet consists of eating primarily plant-based foods such as fruits, vegetables, whole grains, legumes, and nuts. The health benefits of eating such foods were confirmed in an epidemiological and longitudinal study known as the as the Seven Countries Study, which began in 1956 and was finally published in 1970. Ancel Keys, a biologist and director of the study, publicized the diet in 1975, but it didn't gain recognition until the 1990's.

In a recent review paper by Lakkur and Judd (2015), published in the journal Stroke, the authors looked at the different components of the popular diet and examined which foods were found to be truly effective for preventing strokes. After reviewing the research literature, they saw that consuming fruits, vegetables, fish, olive oil, and white meat were proven to be effective while eating tree nuts/peanuts, legumes, dairy, red/processed meat, and wine were not. The diet studies referenced in the review paper were published between 2011 to 2014, so we can assume that the studies were conducted somewhat recently (although one may be surprised how long of a lapse can take place between study-end and publication).

However, there are a few limitations that Lakkur and Judd point out regarding their write-up. The first limitation is that they could not account for the possibility that subjects who "choose to adhere to healthier dietary patterns may also engage in other health-promoting behaviors such as physical activity and may be more likely to maintain a healthy weight". Secondly, the types of strokes (hemorrhagic or ischemic) were not described in many of these studies. Lastly,  "there was a lack of racial and ethnic diversity in many of the epidemiological studies and many racial and ethnic minorities were not well represented", much like the aforementioned case of my "attractive actors only" reference pool.

Nonetheless, this paper makes a compelling point that eating like the Greeks, Italians, and Spaniards will help stave off having a stroke. What's even better is that you don't have to be gassy or drunk while doing it.


Lakkur S, & Judd SE (2015). Diet and Stroke: Recent Evidence Supporting a Mediterranean-Style Diet and Food in the Primary Prevention of Stroke. Stroke; a journal of cerebral circulation PMID: 25967574

Original image taken from

Wednesday, June 3, 2015

Motion blindness found in some dyslexics

Several years ago, I worked as a clinician at a treatment program for adults with learning disabilities, many of whom were diagnosed with dyslexia; a disorder that negatively impacts a person's ability to read, perceive speech, remember language, and recognize/manipulate language-based sounds. Many of my patients had difficulties advancing in their jobs, struggled to pay the rent or perform daily financial tasks that required reading, and thus relied on others to get by. The countless stories I listened to were heart-breaking, especially when one highly motivated and bright young adult became tearful while relaying to me his strong desire to advance in his career and to make something of himself, but struggled because he couldn't find a way around having to read on the job, no matter what compensatory strategies he used.

Approximately 5 to 17% of the entire population are estimated to have dyslexia. Some famous individuals with dyslexia include Albert Einstein, Whoopi Goldberg, Orlando Bloom, Cher, and Scott F. Fitzgerald. As dyslexia can be inherited, a few of these individuals may have had alterations in a gene known as DCDC2, for which deletion of this gene has been found to be a risk factor for dyslexia. It turns out, they may have also had issues with motion detection. 

Cicchini and colleagues (2015), in a recent study published in The Journal of Neuroscience, found that dyslexic individuals who inherited this particular phenotype were found to have impairments for motion processing at high spatial frequencies compared to dyslexics who had the DCD2 gene. 

The authors recruited 10 young adult subjects for the experimental group (dyslexics without the DCD2 gene) and 11 for the control group (dyslexics with the DCD2 gene). They then had the subjects fixate on the center of a computer screen while reporting whether they saw patterned black and white lines move from left to right or top to bottom. 

Those who lacked the DCD2 gene virtually demonstrated motion blindness. The authors propose that these deficits may be due to anatomical deficits of the lateral geniculate nucleus magnocellular cells (important for vision) as a consequence of DCD2 deletion. 

It's a good thing Legolas didn't seem to share the same genetic fate as the experimental group. Otherwise, he'd really be screwed. Legolost? ::rimshot, crickets chirping::


Cicchini GM, Marino C, Mascheretti S, Perani D, & Morrone MC (2015). Strong Motion Deficits in Dyslexia Associated with DCDC2 Gene Alteration. The Journal of neuroscience : the official journal of the Society for Neuroscience, 35 (21), 8059-64 PMID: 26019324

Tuesday, June 2, 2015

Possible link between Alzheimer's disease and disrupted sleep-dependent memory consolidation?

It has been well established that certain kinds of sleep consolidate certain kinds of memory. Mander and colleagues (2015) discovered that in older adults, beta-amyloid (the main component of amyloid plagues found in Alzheimer's disease) appears to disrupt slow wave activity in the medial frontal cortex during NREM sleep, which then impairs hippocampus-based memory consolidation.

It would also be interesting to investigate possible disruptions in thalamic sleep spindle activity to see how this may further contribute to memory impairment in this population. I wrote about this possibility in my Sleep Medicine Review's paper a few years ago.

Here is Mander et al.'s abstract, which appears under the advanced online publication section of Nature Neuroscience:

Independent evidence associates β-amyloid pathology with both non-rapid eye movement (NREM) sleep disruption and memory impairment in older adults. However, whether the influence of β-amyloid pathology on hippocampus-dependent memory is, in part, driven by impairments of NREM slow wave activity (SWA) and associated overnight memory consolidation is unknown. Here we show that β-amyloid burden in medial prefrontal cortex (mPFC) correlates significantly with the severity of impairment in NREM SWA generation. Moreover, reduced NREM SWA generation was further associated with impaired overnight memory consolidation and impoverished hippocampal-neocortical memory transformation. Furthermore, structural equation models revealed that the association between mPFC β-amyloid pathology and impaired hippocampus-dependent memory consolidation was not direct, but instead statistically depended on the intermediary factor of diminished NREM SWA. By linking β-amyloid pathology with impaired NREM SWA, these data implicate sleep disruption as a mechanistic pathway through which β-amyloid pathology may contribute to hippocampus-dependent cognitive decline in the elderly.

Mander, B.,A., Marks, S.,M., Vogel, J.,W., Rao, ,Vikram, Lu, ,Brandon, Saletin, J.,M., . . . Walker, M.,P.Beta]-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation.

Lu, W., & Göder, R. (2012). Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Sleep Medicine Reviews, 16 (4), 389-394 DOI: 10.1016/j.smrv.2011.08.001