What causes some people to be left-handed, and why are fewer people left-handed than right-handed?

What causes some people to be left-handed, and why are fewer people left-handed than right-handed?

Researchers who study human hand preference agree that the side of the preferred hand (right versus left) is produced by biological and, most likely, genetic causes. The two most widely published genetic theories of human hand preference argue that evolutionary natural selection produced a majority of individuals with speech and language control in the left hemisphere of the brain. Because the left hemisphere also controls the movements of the right hand–and notably the movements needed to produce written language–millennia of evolutionary development resulted in a population of humans that is biased genetically toward individuals with left hemisphere speech/language and right-hand preference. Approximately 85 percent of people are right-handed. These theories also try to explain the persistent and continuing presence of a left-handed minority (about 15 percent of humans).

The genetic proposal to explain hand preference states that there are two alleles, or two manifestations of a gene at the same genetic location, that are associated with handedness. One of these alleles is a D gene (for dextral, meaning ¿right¿) and the other allele is a C gene (for ¿chance¿). The D gene is more frequent in the population and is more likely to occur as part of the genetic heritage of an individual. It is the D gene that promotes right-hand preference in the majority of humans. The C gene is less likely to occur within the gene pool, but when it is present, the hand preference of the individual with the C gene is determined randomly. Individuals with the C gene will have a 50 percent chance of being right-handed and a 50 percent chance of being left-handed.

These theories of hand preference causation are intriguing because they can account for the fact that the side of hand preference of individuals with the C gene (most left-handers and some right-handers) can be influenced by external cultural and societal pressures, a phenomenon that researchers have documented. These theories can also explain the presence of right-handed children in families with left-handed parents and the presence of left-handed children in families with right-handed parents. If the familial genetic pool contains C genes, then hand preference becomes amenable to chance influences, including the pressures of familial training and other environmental interventions that favor the use of one hand over the other. The proposed genetic locus that determines hand preference contains an allele from each parent, and the various possible genetic combinations are DD individuals who are strongly right-handed, DC individuals who are also mostly right-handed, and CC individuals who are either right-handed or left-handed. These genetic combinations leave us with an overwhelming majority of human right-handers and a small, but persistently occurring, minority of left-handers.



This article was originally published in Scientific American. Read the original article.

For a Better Brain, Learn Another Language

For a Better Brain, Learn Another Language
There’s a certain sinking feeling one gets when thinking of the perfect thing to say just a moment too late. Perhaps a witty parting word could have made all the difference. There is no English word to express this feeling, but the French have the term l’esprit de l’escalier—translated, “stairwell wit”—for this very phenomenon.

Nor is there an English word to describe the binge eating that follows an emotional blow, but the Germans have kummerspeck—“grief-bacon”—to do just that. If we had the Swedish word lagom—which means something is just right—the English explanation of Goldilocks’ perfectly temperate soup could have been a lot more succinct. Or the term koi no yokan, a poetic Japanese turn of phrase that expresses the feeling of knowing that you will soon fall in love with the person you have just met. It’s not love at first sight so much as an understanding that love is inevitable. Keats and Byron could have really used a word like that.

There are many words that English speakers don’t have. Sometimes Anglophones take from other languages, but often, we have to explain our way around a specific feeling or emotion that doesn’t have its own word, never quite touching on it exactly.

“The reason why we borrow words like savoir faire from French is because it’s not part of the culture [in the United States] and therefore that word did not evolve as part of our language,” says George Lakoff, a professor of cognitive science and linguistics at the University of California at Berkeley.

“Speaking different languages means you get different frames, different metaphors, and also you’re learning the culture of the language so you get not only different words, but different types of words,” Lakoff told me.

But the benefits of speaking multiple languages extend past just having access to different words, concepts, metaphors, and frames.

Multilingualism has a whole slew of incredible side effects: Multi-linguals tend to score better on standardized tests, especially in math, reading, and vocabulary; they are better at remembering lists or sequences, likely from learning grammatical rules and vocabulary; they are more perceptive to their surroundingsand therefore better at focusing in on important information while weeding out misleading information (it’s no surprise Sherlock Holmes and Hercule Poirot are skilled polyglots). And there’s certainly something to be said for the cultural pleasure of reading The Odyssey in ancient Greek or Proust’s In Search of Lost Timein French.

“Cognitive traps,” or simple mistakes in spelling or comprehension that our brains tend to make when taking linguistic shortcuts (such as how you can easily read “tihs senetcne taht is trerilby msispleld”), are better avoided when one speaks multiple languages. Multi-linguals might also be better decision-makers. According to a new study, they are more resistant to conditioning and framing techniques, making them less likely to be swayed by such language in advertisements or political campaign speeches. Those who speak multiple languages have also been shown to be more self-aware spenders, viewing “hypothetical” and “real” money (the perceived difference between money on a credit card and money in cold, hard cash) more similarly than monolinguals.

One theory on why this might be is that there’s increased psychological distance when speaking a language that isn’t your mother tongue. Researchers in the spending study posited that subjects had less of an emotional reaction to things heard in their second (or third, or fourth) language, perhaps allowing for a more levelheaded decision.

More recently and perhaps most importantly, it’s been found that people who learn a second language, even in adulthood, can better avoid cognitive decline in old age. In fact, when everything else is controlled for, bilinguals who come down with dementia and Alzheimer’s do so about four-and-a-half years later than monolinguals.

Dr. Thomas Bak, a lecturer in the philosophy, psychology, and language sciences department at the University of Edinburgh, conducted the study and found that level of education and intelligence mattered less than learning a second language when it came to delaying cognitive decline.

“It’s not the good memory that bilinguals have that is delaying cognitive decline,” Bak told me. “It’s their attention mechanism. Their ability to focus in on the details of language.”

Polyglots tend to be good at paying attention in a wide variety of ways, especially when performing visual tasks (like searching a scene or a list for a specific name or object) and when multitasking, which, according to Bak’s theory, is likely improved thanks to the practice of mentally switching between one’s native and foreign language while learning the foreign language.

This is great news for anyone who is multi-lingual, but, really, it is positive news for everyone. The dementia-delaying effects of learning a second language are not contingent on becoming fluent; it just matters that a person tries to learn it. Even if you’re still confounding your ’s and oui’s, as Bak says, “Just having the basics of those linguistic connections can delay dementia.”

Plus, speaking more than one language means you’ll have access to all sorts of new words. So the next time you need to, let’s say, express your burning desire to squeeze a fat baby’s legs, you’ll know what to say. That’s gigil in Filipino.


This article was originally published in The Atlantic. Read the original article.

How Exercise Might “Clean” the Alzheimer’s Brain

How Exercise Might “Clean” the Alzheimer’s Brain

For the 50 million individuals worldwide ailing from Alzheimer’s disease, the announcements by pharmaceutical giants earlier this year that they will end research on therapeutics were devastating. The news is even more devastating considering projections that 100 million more people will be diagnosed with Alzheimer’s disease across the globe by 2050, all potentially without a medical means to better their quality of life.

As it happens, though, the pursuit of a therapeutic has been given a lifeline. New research shows that physical exercise can “clean up” the hostile environments in the brains of Alzheimer’s mice, allowing new nerve cells in the hippocampus, the brain structure involved in memory and learning, to enable cognitive improvements, such as learning and memory. These findings imply that pharmacological agents that enrich the hippocampal environment to boost cell growth and survival might be effective to recuperate brain health and function in human Alzheimer’s disease patients.

The brain of an individual with Alzheimer’s disease is a harsh place filled with buildups of harmful nerve cell junk—amyloid plaques and neurofibrillary tangles—and dramatic loss of nerve cells and connections that occur with severe cognitive decline, such as memory loss. Targeting and disrupting this harmful junk, specifically amyloid plaques, to restore brain function has been the basis of many failed clinical trials. This futility has led to a re-evaluation of the amyloid hypothesis—the central dogma for Alzheimer’s disease pathology based on the toxic accumulation of amyloid plaques.

At the same time, there have been traces of evidence for exercise playing a preventative role in Alzheimer’s disease, but exactly how this occurs and how to take advantage of it therapeutically has remained elusive. Exercise has been shown to create biochemical changes that fertilize the brain’s environment to mend nerve cell health. Additionally, exercise induces restorative changes relevant to Alzheimer’s disease pathology with improved nerve cell growth and connectivity in the hippocampus, a process called adult hippocampal neurogenesis. For these reasons, the authors Choi et al. explored whether exercise-induced effects and hippocampal nerve cell growth could be utilized for therapeutic purposes in Alzheimer’s disease to restore brain function.

The researchers found that exercised animals from a mouse model of Alzheimer’s had greatly enhanced memory compared to sedentary ones due to improved adult hippocampal neurogenesis and a rise in amounts of a specific molecule that promotes brain cell growth called BDNF.  Importantly, they could recover brain function, specifically memory, in mice with Alzheimer’s disease but without exercise by increasing hippocampal cell growth and BDNF levels using a combination of genetic—injecting a virus—and pharmacological means. On the other hand, blocking hippocampal neurogenesis early in Alzheimer’s worsened nerve cell health later in stages, leading to degeneration of the hippocampus and, subsequently, memory function. This provides preclinical proof of concept that a combination of drugs that increase adult hippocampal neurogenesis and BDNF levels could be disease-modifying or prevent Alzheimer’s disease altogether.

With this work, things don’t look promising for the amyloid hypothesis—that Alzheimer’s disease is caused by the deposition of amyloid plaques. In this study, it was shown that eliminating amyloid plaques were not to necessary to ameliorate memory defects, which is consistent with evidence that plaques can also be found in the brains of healthy individuals. On the contrary, we may be looking at a new and improved fundamental theory for Alzheimer’s disease based on promoting a healthier brain environment and adult hippocampal neurogenesis.

However, this inspiring news should be taken with an important caution—mouse models of Alzheimer’s are notorious for failing to translate into humans such that treatments that have worked to remedy mice have failed for humans. Besides, even if these findings translate into humans, it may apply to a fraction of Alzheimer’s individuals with relevant genetic components to the mouse model utilized. Future studies will need to replicate these results in mouse models emulating the range of known Alzheimer’s disease genetic milieus and, more importantly, prove its medical relevance to human disease.

Before translating these findings into human patients, there remains significant research to establish that a medication or drug could mimic the effects of exercise—exercise mimetics—by “cleaning up” the brain with BDNF and stimulating neurogenesis to combat Alzheimer’s disease. Currently, the method for administering BDNF to animals in the lab—by direct injection into the brain—is not ideal for use in people, and a hippocampal neurogenesis stimulating compound remains elusive.

Future attempts to generate pharmacological means to imitate and heighten the benefits of exercise—exercise mimetics—to increase adult hippocampal neurogenesis in addition to BDNF may someday provide an effective means of improving cognition in people with Alzheimer’s disease. Moreover, increasing neurogenesis in the earliest stages of the disease may protect against neuronal cell death later in the disease, providing a potentially powerful disease-modifying treatment strategy.



This article was originally published in Scientific American. Read the original article.