Research We’re Reading
NRI scientists are reading latest findings in the field of nutrigenomics to share new information with you.
Research We’re Reading: From the desk of Jing Xue, Ph.D
Vitamin D deficiency in pregnant moms is shown to negatively affect fetal growth and children’s health in the long run. Deficient gestational vitamin D status is surprisingly high both globally and in the US. One of the findings that draws attention is the role of vitamin D during pregnancy in children’s chances of developing Autism Spectrum Disorders (ASD). Vitamin D is acquired through sun exposure or food intake. The circulating form of vitamin D can travel through the fetal-placental barrier, thus, developing babies depend solely on their mothers for getting this beneficial nutrient.
A group of researchers from Australia and the Netherlands recently showed that mothers with vitamin D deficiency during mid-gestation are more than twice as likely to give birth to an autistic child. The study was carried out on a group of 4334 pregnant women from different ethnic backgrounds. In the group, 16.5% of the subjects were deficient in vitamin D during mid-gestation, while 25.9% had higher vitamin D levels although not reaching the optimum levels. Compared with mothers with optimum levels of vitamin D during pregnancy, those with deficient levels were 2.42 times as likely to have their children diagnosed with ASD later in life.
A Swedish group of researchers conducted a population-based study where they looked into the health records of more than half a million Swedish-born children and similarly found that maternal vitamin D deficiency status is a potential contributing factor for ASD, especially for children with intellectual disability. The approach taken by this group is less direct, as they extrapolated vitamin D status during pregnancy by using secondary care records from the mothers. However, a wide variety of confounding factors were taken into consideration so that their result still warranted further investigation of the causal relation between maternal vitamin D and ASD.
Taking a different approach, researchers looked into 58 pairs of siblings from various ethnic groups. One sibling in each pair was diagnosed with ASD and the other not. Vitamin D levels were measured from blood that had been collected immediately after birth. The results show that children with ASD have significantly lower vitamin D levels at birth than their paired siblings. Because fetal vitamin D status is directly determined by the mothers, these results indicate that vitamin D status among pregnant women is closely linked to ASD risks for babies as they grow.
IMPORTANT THINGS TO KEEP IN MIND ABOUT VITAMIN D
The current dietary recommendation for vitamin D is 600 international units (IU) per day according to the US Institute of Medicine. Unfortunately, the recommendation is sufficient only to maintain optimum bone health, while evidence for a proper level of vitamin D to maintain extra-skeleton functions is lacking. Thus, it is urgent that more efforts are made to further study the causality between vitamin D and many health outcomes, such as immune function, neurological development, birth outcomes, and reproduction.
Saraf R, et al. Global summary of maternal and newborn vitamin D status – a systematic review. Matern Child Nutr. 2016 Oct;12(4):647-68. doi: 10.1111/mcn.12210. Epub 2015 Sep 15. PMID: 26373311
Vinkhuyzen AAE, et al. Gestational vitamin D deficiency and autism spectrum disorder. BJPsych Open. 2017 Apr 10;3(2):85-90. doi: 10.1192/bjpo.bp.116.004077. eCollection 2017 Mar. PMID: 28446959 PMCID: PMC5385921
Magnusson C, et al. BJPsych Open. Maternal vitamin D deficiency and the risk of autism spectrum disorders: population-based study. 2016 Apr 7;2(2):170-172. eCollection 2016 Mar. PMID: 27703770 PMCID: PMC4998950
Fernell E, et al. Autism spectrum disorder and low vitamin D at birth: a sibling control study. Mol Autism. 2015 Jan 14;6:3. doi: 10.1186/2040-2392-6-3. eCollection 2015.
From the desk of: Saroja Voruganti, Ph.D.
While drinking at least eight glasses of water a day may not be necessary under normal conditions, maintaining adequate hydration, especially during physical exertion in warm weather, is essential for optimal health.
A recent article published in the American Journal of Kidney Disease suggests that exercise and dehydration contribute to development of chronic kidney disease, particularly the type that is related to heat stress. Heat stress-related kidney disease is increasingly observed in farmers, fishermen, miners, and transportation and construction workers. This type of kidney disease is also called Mesoamerican nephropathy since it was first observed in sugarcane workers in Latin America. Even though they drank a lot of water, these workers suffered high rates of chronic kidney disease.
The authors noted decreased sodium levels and increased uric acid levels after heavy exertion. Uric acid is a breakdown product of DNA and can become elevated with muscle damage. Thus, exercising or working under hot conditions results not only in water loss, but also sodium loss and low-grade muscle injury, which ultimately affect kidney function. Muscle injury and dehydration also cause uric acid to increase, which again results in kidney injury. Kidney injury intensifies with continuous exposure to heat, exercise and dehydration and finally develops into chronic kidney disease. Therefore, maintaining an adequate level of hydration by drinking water with electrolytes at frequent intervals seems to prevent the increase in uric acid levels that occur with heat and exercise.
TAKE HOME MESSAGE
Maintaining adequate hydration in conditions of heat and exercise is important to minimize risk of kidney injury, but chronic heat and physical exertion stress kidney function and can cause kidney damage even when water is consumed. Under these conditions, it is important to stay extra hydrated to avoid increased uric acid levels and muscle damage, which also contribute to the risk of long-term kidney damage.
Reference: American Journal of Kidney Diseases 2015; Oct 5. pii: S0272-6386(15)01156-7. doi: 10.1053/j.ajkd.2015.08.021
From the desk of: David Horita, Ph.D.
In a recently published paper1, NRI investigator Phil May and colleagues showed that the prevalence of fetal alcohol syndrome (FAS) and partial fetal alcohol syndrome (PFAS) is two to three times higher than previously estimated.
Dr. May’s study differs from most FAS prevalence studies in its use of active case ascertainment testing methods to estimate prevalence. This technique includes developmental testing of the child and detailed one-on-one interviews of the mother. The interview questions covered alcohol use during pregnancy, but also asked questions related to secondary factors, such as overall drinking history, marital status; socioeconomic status, and diet/nutrition. This approach is much more labor-intensive than the more common survey approach that relies on self-reported alcohol use information. However, it is also more accurate: self-reported alcohol usage surveys often underestimate FAS because of the stigma of drinking during pregnancy.
This study estimated prevalence of FAS as 3-8 per 1,000 and PFAS as 8-18 per 1000 children in the community. This suggests that up to 2.5 % of children in the US have some degree of FAS. These numbers are significantly higher than previous estimates2 of less than 1 %. In concordance with other studies, May and colleagues found correlations between maternal drinking and child physiology – children with FAS and PFAS were shorter, had lower weight and distinct facial characteristics. Additionally, FAS and PFAS children scored lower on IQ tests and in reading, spelling, and arithmetic ability, and they exhibited more communication, socialization, and behavior disorders than non-FAS children.
WHY IS THIS IMPORTANT?
Knowing the prevalence of FAS and PFAS guides prioritizing prevention and intervention efforts. Numerous studies have placed the economic cost of FAS and associated disorders at over $1 million per case per lifetime3. These costs include increased medical treatments, increased educational costs, decreased worker productivity, and increased societal costs (youths with FAS are estimated to be nineteen times more likely to be in prison than youths without FAS4). Across the US, the difference in prevalence of 1 vs 2.5 % translates to a difference of several billion dollars per year in real costs. Dr. May’s research clarifies the social and economic value of FAS prevention efforts.
There is no cure for FAS. The finding that 2-3 times more children in the US show FAS symptoms than previously estimated underscores the importance of FAS research that could lead to treatments. For instance, other ongoing NRI studies are investigating the potential of nutritional supplements to ameliorate symptoms in young children with FAS5.
David Horita joined the NRI in 2013 as a grant writer. He assists faculty by identifying funding opportunities and writing/editing research proposals. David developed research and writing experience in metabolism and cell signaling during his 13 years as a faculty member in Biochemistry at Wake Forest University School of Medicine. He did postdoctoral work at the NCI/NIH and obtained a Ph.D. in physical chemistry from the University of Wisconsin and a B.A. in chemistry from Carleton College.
1May PA, Keaster C, Bozeman R, Goodover J, Blankenship J, Kalberg WO, Buckley D, Brooks M, Hasken J, Gossage JP, Robinson LK, Manning M, Hoyme HE (2015). Prevalence and characteristics of fetal alcohol syndrome and partial fetal alcohol syndrome in a Rocky Mountain Region City. Drug Alcohol Depend 155:118-2
3Popova S, Stade B, Lange S, Bekmuradov D, Rehm J (2012). Economic impact of fetal alcohol syndrome (FAS) and fetal alcohol spectrum disorders (FASD). Public Health Agency of Canada. Ottawa, Ontario, CA
4Popova S, Stade B, Lange S, Rehm J (2012). A model for estimating the economic impact of fetal alcohol spectrum disorder. J Popul Ther Clin Pharmacol 191:e51-e65
5Wozniak JR, Fuglestad AJ, Eckerle JK, Fink BA, Hoecker HL, Boys CJ, Radke JP, Kroupina MG, Miller NC, Brearley AM, Zeisel SH, Georgieff MK (2015). Choline supplementation in children with fetal alcohol spectrum disorders: a randomized, double-blind, placebo-controlled trial. Am J Clin Nutr (in press)
From the desk of: Mirko Hennig, Ph.D.
“Wishing you a long, happy and healthy life” is what we repeatedly say as we get older. A recent, global study published in The Lancet (2015; 386, p.743-800) clearly emphasizes the importance of the latter referring to our quality of life. According to the Global Burden of Disease (GBD) study, worldwide life expectancy at birth rose by 6.2 years between 1990 and 2013. However, these additional years come at a price as healthy life expectancy at birth increased by only 5.4 years over the same 13 year time span. The massive, country-specific assessment utilized age-specific mortalities and data accumulated for 306 diseases in 188 countries between 1990 and 2013. While the study highlights the need for more and better data about disabilities to estimate healthy life expectancies in a more reliable manner, several consistent trends emerge:
Implications of this study
Living longer but suffering more? While life expectancy in 1990 in the US averaged 71.9 and 78.8 years for male and female population, respectively, it increased significantly reaching averages of 76.3 and 81.4 years in 2013. However, the years of life expectancy gained are not necessarily lived healthily. On average, 9.2 (8% of life expectancy) and 11.9 (15%) years of male and female lives born in 1990 are associated with disability. This burden of disease increases to 10.5 (14%) and 12.8 (16%) years for male and female population born in 2013. Thus, the data suggests a widening gap between longer and healthy lives.
Neglected, age-related diseases. The reason for an increased disease burden over our longer life spans can at least partially be attributed to a rising prevalence of age-related conditions. While the GBD team shows that health loss due to cardiovascular and circulatory diseases and cancer stagnated or even decreased over the period 1990-2013, the drivers of the difference between longer and healthy life expectancies are musculoskeletal disorders, mental and substance use disorders, neurological disorders, and diabetes, accompanied by vision and hearing loss.
While the leading cause of increased disease burden in the US in 2013 continues to be ischemic heart disease, it is now followed by back and neck pain. Chronic obstructive pulmonary disease ranks third. Tracheal, bronchus and lung cancer, depression, diabetes, Alzheimer’s, other musculoskeletal disorders, stroke and sense organ disorder round out the 2013 top ten in the US.
Research and development investments by the National Institutes of Health (NIH) and the pharmaceutical industries have traditionally focused on cardiovascular diseases, endocrine disorders and cancer. As a consequence, sustained gains have been made against the majority of the leading causes of death worldwide. On the other hand, few age-related diseases such as musculoskeletal disorders, neurological disorders, diabetes and hearing and vision loss receive the attention they deserve in public policy discussions and health research priorities. A balanced diet rich in antioxidants and anti-inflammatories plays an important role to forestall the onset of age-related disorders. Therefore, researchers at the Nutrition research Institute (NRI) in Kannapolis including Drs. Cheatham, Surzenko and Zeisel investigate the interplay of nutrition and cognitive function. However, more investment and research has to shift towards diseases that debilitate, rather than kill in order to maintain health progress in ageing populations.
From the desk of: Katie Meyer, Ph.D.
Everyday we learn more about how the gut microbiome may influence health. Our gut microbial community—a super-organism, with trillions of members—has been associated with obesity, diabetes, cancer, heart disease, and immune disorders, and even moods. These findings have generated enormous enthusiasm among researchers and the lay public, as they suggest a largely untapped area for health-promoting interventions. One mechanism through which the gut microbiome may affect health is through the metabolism of food and nutrients. We know that the production of some bioactive metabolites is dependent on the genetic machinery of gut microbes. We also know that individuals differ in the production of bioactive metabolites following nutrient ingestion. A critical next step is delineating the gut microbiome-specific pathways from food consumption to metabolite production to health status. This is an area of active research at the NRI, and the focus of a new scientific publication.
A group at the Fred Hutchinson Cancer Research Center recently characterized individuals with respect to their blood levels of plant food metabolites and their gut microbial community. The researchers focused on enterolignans, metabolites of polyphenolic compounds (micronutrients) called lignans, found in plants. The intake of lignans, such as through the consumption of seeds and whole grains, has been associated with decreased colon and breast cancer risk. Enterolignans are some of the bioactive metabolites that may directly contribute to the health benefits of plant food-rich diets.
The production of enterolignans has large individual variability, which may reflect individual differences in the gut microbiome. To test this, the researchers compared the gut microbial community in people with different levels of enterolignans, controlling for differences in diet and other lifestyle factors. Their results revealed significant differences between features of the gut microbiome—including in the diversity of microbiota and taxonomic composition—and blood levels of one enterolignan, enterolactone, showing that enterolignan production is defined, at least in part, by an individual’s gut microbiome. These results connect differences in the gut microbial community and the presence of beneficial metabolites, illustrating the potential for the gut microbiome to influence health through the production of health-related bioactive compounds.
WHY IS THIS IMPORTANT?
This study is an example of how we will move towards a detailed understanding of the gut microbiome’s role in health status through dietary metabolites and individual differences in the health effects of diet. Ultimately, we aim to identify the specific gut microbial features related to the production of beneficial metabolites so that we can design personalized diets to optimize health and intervene at the microbiome level.
Reference: Huller MAJ, Lancaster SM, Li F, et al. Enterolignan-producing phenotypes are associated with increased gut microbial diversity and altered composition in premenopausal women in the United States. Cancer Epidemiol Biomarkers Prev 2015;24:546-554.
From the desk of: Jessica Sisneros, M.S., R.D., L.D.N.
It’s spring! Farmers markets are opening and these are great places to find a variety of local, seasonal produce, which flourishes now. Making room for these powerhouses in your everyday food choices is important for your health. A 2012 peer-reviewed analysis in Food and Chemical Toxicology states that approximately 20,000 cancer cases could be prevented every year if one-half of Americans were to increase their serving of fruits and vegetables by one serving per day. The recommended serving size for one serving of vegetables is equal to 1 cup of raw leafy vegetables, ½ cup of other vegetables or 1/2 cup of vegetable juice. The recommended serving size for one serving of fruit is 1 medium fruit (medium is defined as the size of a baseball), ½ cup chopped, cooked or canned fruit or ½ cup juice.
There are several reasons to take advantage of the fruits and vegetables at your local farmers market. This produce is the freshest and tastiest available. Fruits are allowed to ripen in the field and are brought directly to you—no long-distance shipping, no gassing to interrupt the ripening process, no sitting in storage for weeks. This is as real as it gets—fresh food from the garden.
One of the first delicacies of spring is fresh asparagus. In the southeast asparagus is in season from February to June. Fresh asparagus is usually bright green, although some markets may also sell purple or white varieties. The tips should be firm and tight, not mushy. When choosing your asparagus the stalk size is not an indicator of tenderness.
Eating asparagus is an excellent way to protect yourself against heart disease, as it contains folate, as well vitamins E, A, and C. In addition to helping your heart, folate helps cells regenerate; vitamin E provides antioxidant protection; and vitamins A and C prevent cancer. Asparagus also contains potassium, which helps to lower blood pressure. Asparagus is an excellent low-calorie, high-fiber vegetable to add to your meals this spring. Other seasonal produce that can be found at the farmers market in May includes arugula, artichoke, beets, cabbage, garlic, green beans, peppers, onions, kale, lettuce, spinach and strawberries. Enjoy this bounty of fresh produce and stay well!
Roasted Asparagus from the Produce Lady
1 lb. asparagus
2 tbsp. olive oil
1 cup crumbled blue cheese, Parmesan or other cheese (optional)
Preheat oven to 350 degrees F. In a large bowl, toss the asparagus and olive oil. Pour asparagus and oil into a nonstick pan, top with cheese. Bake 15 to 20 minutes. Serves 4.
Nutrition Information Per Serving
75.1 Calories, Total Fat 6.9 g, Cholesterol 0.0 mg, Sodium 1.3 mg, Total Carbohydrates 3.0 g, Dietary Fiber 1.4 g, Protein 1.5 g
Farmers markets are found throughout the country depending on growing seasons. To find a farmer’s market close to you, click here.
Why “good” and “bad” are irrelevant when talking about genes and nutrition
From the desk of: Mihai Niculescu, M.D., Ph.D.
…“How to override your bad genes with food.” “Can Exercise Override Bad Genes?” “Good Nutrition Can Overcome Bad Genes”…
We are bombarded by media with these kinds of messages. The main theme, of course, is that many of us may have “bad” genes that would put us at risk of a certain poor health outcome unless we eat less of “this” and more of “that.” Knowing myself as a bearer of several such genetic variations, I almost feel, at times, guilty that I am harboring such “bad” genes, albeit without my consent.
Here is why such thinking is wrong, and why the paper I have read recently is a good example of how the public should understand what nutrigenomics is, and why there are no such things as “bad” or “good” genes when it comes to nutrition (except for very few documented cases). And here I am talking about those genetic variations (changes in our genetic code) that are quite frequent (being present in up to 50 percent of us).
First, let’s establish a couple of things. 1: Genetic variations that are at high frequency in a population are the result of Darwinian selection. If such genes are (still) frequent in the human population, all this means is that individuals who carry them had no troubles in reproducing and in disseminating their genes through their offspring. This only tells us that those individuals were okay in the environment (including nutrition) they used to live in. 2: Scientists discovered that, in many cases, genetic variations across one or more genes are not randomly combined, but rather they exist in only several combinations (called haplotypes). These combinations of genetic variations are inherited by descendants.
The study by Ameur and colleagues (see link below) looked at how these haplotypes, or combinations of genetic variations, evolved during human evolution for those genes responsible for processing omega-3 and -6 fatty acids acquired from vegetable oils. When comparing the present European populations with archaic hominins and distant primates, they concluded that a certain combination of such variations (called Haplotype D), appeared after the split from Neanderthals (around 500,000 years ago). Moreover, this means that the Haplotype D, being enriched in more recent populations (Africa, Middle East, Asia and Europe), while quite rare in the Americas, indicates that the Haplotype D shows positive selection (its frequency increases in more recent populations), meaning that it brought some type of survival advantage in the environment from Africa, Asia, and Europe, but not in the Americas.
WHY IS THIS IMPORTANT
Interestingly, the researchers also measured how Haplotype D influences the omega-3 and -6 metabolism, and they concluded that the Haplotype D accelerates the conversion of omega-3 and -6 fats from vegetable sources, into molecular species that are found mainly in fish oil (DHA and EPA), and also into arachidonic acid (main omega-6 component). Note: DHA and EPA have many health benefits, while arachidonic acid is a pro-inflammatory molecule. So, by all means, Haplotype D carriers were at an advantage during the development of the human race in the Afro-Eurasia continental mass. Is this, then, a “good” haplotype? “Definitely,” would answer the proponents of the “good” and “bad” genes concept.
But here is the catch! The same Haplotype D (so beneficial during our evolution) proved to be a problem when it comes to our modern lifestyle and nutrition habits. It turns out that the Haplotype D actually increases the risk of having coronary artery disease, but only because we eat more omega-6 oils than we should (and not enough omega-3 oils). Because Haplotype D carriers are so efficient in converting omega-6 precursors to arachidonic acid, they have an increased inflammation status, which contributes in turn to the coronary artery disease. This is “bad,” isn’t it?
WHAT THIS MEANS FOR YOU
So how should we interpret these findings, and how do we know what we should eat? This study is a good example of how we can tackle individualized nutrition. It suggests that those people who have the Haplotype D should increase their intake of omega-3, and decrease the omega-6 intake.
“Good” and “bad” genes? Hardly. Rather, we should focus on how fit our environment (nutrition included) is for our genes. This is a much more productive approach, allowing us to reshape our lifestyle to what each of us needs.
Reference: Genetic Adaptation of Fatty-Acid Metabolism: A Human-Specific Haplotype Increasing the Biosynthesis of Long-Chain Omega-3 and Omega-6 Fatty Acids (Am J Hum Genet. 2012 May 4; 90(5): 809-820)
From the desk of: Sergey A. Krupenko, Ph.D.
Life expectancy keeps growing in developed countries, approaching 90 years on average in some. There is a forecast that more than 50 percent of girls born in the U.S. after 2010 will live to become 100 years or even older, and that the first person to live up to 150 years has already been born. Perhaps most people are curious about which factors define that people live longer. Obviously, genetic background plays a significant role in a person’s natural longevity. What about diet? Can nutrients help to prolong our life? One of the principal dietary factors influencing our overall health status is calorie consumption. Intuitively, limiting calories to some extent would be expected to improve health conditions and, as such, seems promising for longer life. Indeed, there is a common belief in modern society that skinny people are healthier than obese people. But, does it mean they will live longer? Numerous research papers beginning in the late 1990s and early 2000s indicate that calorie restriction extends lifespan in a wide spectrum of organisms. However, a paper published last year indicates that the issue regarding the influence of calorie restriction on lifespan might not be so simple.
In this study, an international research team led by scientists from the University of Sydney used 25 diets differing in protein, carbohydrate, fat content and energy density to feed mice. The team aimed to correlate macronutrient intakes to longevity, in particular testing the extent to which lifespan in ad libitum-fed (unlimited food) mice is determined by calorie intake per se or by the balance of protein to carbohydrate. With no surprise, this study showed a very complex interplay between dietary protein, carbohydrates, total energy intake and lifespan. Using a very sophisticated mathematical approach, researchers were able to untangle these complex data. They found that lifespan was greatest for animals whose foods were low in protein and high in carbohydrate, and it was not influenced by total calorie intake. This study also identified the molecular target, which is likely responsible for translating the dietary ratio of proteins and carbohydrates to lifespan. A protein kinase mTOR (stands for mammalian target of rapamycin), which regulates several key cellular processes, was activated as dietary ratio between proteins and carbohydrates was shifted towards the former. Since the activation of mTOR is pro-aging, this would explain the life-extending effects of a low-protein, high-carbohydrate diet.
IMPLICATIONS OF THIS STUDY FINDINGS
While it still needs to be confirmed that findings of this study are applicable to humans, they are in line with epidemiological studies showing that low-protein, high-carbohydrate diets are associated with improved health in humans. Accordingly, high-protein diets, widely promoted for weight loss and health, should be taken with precautions. Overall though, rather than specific macronutrients themselves, it is their interactive effects (i.e., balanced diet) that are more important for health and aging.
Excitingly, because mTOR can be targeted by drugs, this also opens a window of opportunity to pharmacological life extension in the future. However, while such an opportunity might be on the horizon, it is still a good idea to limit calorie consumption and engage in regular physical exercises.
From the desk of: Carol L. Cheatham, Ph.D.
As a developmental cognitive neuroscientist, I’m always interested in learning about studies that will inform my work. Recently, I attended the International Conference on Infant Studies where I heard a scientist speak about his research with non-human primates (i.e., monkeys). The studies that he described weren’t just informative—his results stopped me in my tracks! Since I returned home, I have been reading all his papers and I’m excited to share his findings.
In Japan, a scientist by the name of Tetsuro Matsuzawa has been working for 30 years with Ai, a chimpanzee and her offspring. Ai learned at an early age to recognize symbols on a keyboard and to name objects and colors. She and her kids have also been taught numbers and number order. For one number task, these chimpanzees are trained on a touch screen. Numbers from 1 to 9 are presented on a screen in random order and in random places on the screen. The chimps touch the numbers in ascending order to receive a treat.
This is a truly impressive feat in and of itself, however, more amazingly, these chimps can still successfully complete the task when the numbers on the screen disappear behind white boxes the instant they touch the number 1! Let me say that again: the numbers from 1 through 9 come up on the screen in random order and in random places. The chimp’s job is to touch the numbers in order. The instant that the chimp touches the number 1 (see photo A), the other numbers disappear behind white boxes (see photo B), and the chimp must finish the task basically blind. The chimps in this “masked” task are still successful even though they only saw all nine numbers for a split second. To put this in perspective, humans who are tested on this masked task can only touch the first three or four numbers correctly. Mind you, this skill cannot be taught. The brain has to encode the numbers and their positions in a flash and be able to recall the position of numbers. Why don’t humans have such a flash memory? Dr. Matsuzawa hypothesizes that language gets in our way. Basically, our brains get bogged down by attaching words to the numbers—a problem that the chimps do not have!
You can watch the chimps perform both the numbers and masked numbers tasks here. There are also videos of human subjects attempting the same tasks, but with far less success.
Finding out about this research has had me devising ways to test it in humans as well as trying to explain it in chimps. Why would chimps need flash memory? Can the human brain work similarly? How would we test that question when our lives are so tied to language? As I continue my work in cognitive development and decline, I will ponder Dr. Matsuzawa’s work with these chimpanzees and their extraordinary recall ability.
From the desk of: Karen D. Corbin, Ph.D., R.D.
As a registered dietitian, I am often asked: “What do you think about artificial sweeteners?” My answer is always the same: “Since they are artificial and not enough research has been conducted to know for certain if they can be harmful, I suggest using them in moderation, learning to drink beverages that are naturally sugar-free, or using regular sugar instead but in moderation.” New research published in the journal Nature indicates a negative impact of artificial sweeteners on the helpful bacteria that live in our intestines. The findings were intriguing and provide one important piece of the puzzle to help better understand the role of these food additives on health.
Artificial sweeteners have been shown to have beneficial effects on weight and metabolism, while other studies have shown the opposite. Despite this controversy, the Food and Drug Administration has approved six different artificial sweeteners for use in the United States. Most artificial sweeteners pass through the intestinal tract without being digested, making them available for processing by the bacteria that reside normally in the gut. These bacteria are very important for processing nutrients and can affect our metabolism and health.
A group of scientists at the Weizmann Institute of Science in Israel wanted to find out if artificial sweeteners affect the types of bacteria in the gut and, if so, what the impact is on metabolism. In mice, the scientists found that artificial sweeteners lead to insulin resistance and an imbalance of bacteria in the gut (dysbiosis), compared to water alone or water with natural sugars like glucose or sucrose. When gut bacteria from mice fed artificial sweeteners were transferred to mice that had no bacteria in their gut, the same harmful metabolic effects occurred.
WHY IS THIS IMPORTANT?
This strongly suggested that the harmful metabolic effects of artificial sweeteners were due to their effects on the gut bacteria. In non-diabetic humans, the scientists also found that long-term consumers of artificial sweeteners had many traits characteristic of metabolic syndrome and fatty liver. Importantly, when they fed healthy volunteers who did not normally consume artificial sweeteners an acceptable daily amount of artificial sweeteners for six days, their metabolisms worsened and their gut bacteria changed.
The study was well done, but focused most of its efforts on one specific artificial sweetener, so the findings may not apply equally to all of them. The part of the study where people were asked to consume artificial sweeteners was very small, and some of the people did not have the same response as others.
WHAT THIS MEANS FOR YOU
Although this study does not provide conclusive evidence that all artificial sweeteners are harmful for all people, it does suggest one way that these food additives could have negative health consequences. Moderation still stands as a reasonable course of action.