Introducing: Science Says!

The former SPCG is now “Science Says”!! According to news headlines, science says a lot of things, but what do we really learn from scientific studies, and how do these findings impact our daily lives?

Wading through science-related news can be difficult, but science isn’t an elite league of geniuses or a collection of hard facts. Science is a process of gathering evidence from carefully controlled tests to gain understanding of the natural world. Our goal is to empower everyone to investigate how scientific findings impact their daily lives. We’re cultivating a community of science communicators to demystify the scientific process and challenge misconceptions. So what does science really say?

Think Responsibly: Your Vodka-Red Bull Isn’t Exactly Like Cocaine.

Media outlets recently reported that mixing caffeine and alcohol has the “same effect” as cocaine. These articles, which refer to a study from Purdue University, have headlines that make you think twice about downing that vodka Red Bull. However, before treating UPROXX like the new WebMD, we should step back and unpack the central claim being asserted. What exactly does it mean to say that caffeine-mixed alcohol has the same effect as cocaine?

Caffeinated energy drinks are a relatively recent phenomenon, steadily increasing in popularity over the past few decades, particularly among adolescents and young adults. While many energy drinks contain additional ingredients such as “energy vitamins” (a pseudoscience of its own not to be addressed here), the core active ingredient is caffeine, which varies widely in its concentration among brands. Even without alcohol, the consumption of energy drinks, particularly by teens, has been considered risky by scientists and physicians for quite some time. The same can, obviously, be said about alcohol in the absence of caffeine.

But what happens when the two are mixed? One concern is the “wide awake drunk” effect: people inebriated from caffeine-mixed alcohol inaccurately gauge their level of intoxication and drink more, increasing the risk of alcohol poisoning. After a few high profile cases of caffeine-related alcohol poisonings in 2010, the FDA introduced a de facto ban on the sale of caffeinated alcoholic beverages. Still, people can-and do-mix energy drinks with alcohol on their own.

In addition to the “wide awake drunk” effect, there may be long-term consequences. But testing the effects of caffeine-mixed alcohol on humans is tough, because researchers can’t ethically ask people to consume copious amounts of alcohol and caffeine in the name of science. Instead, animal models which have significant biological similarities to people must be used.

This leads us to our first caveat on the interpretation of this research. While animal models are incredibly informative, we cannot easily extrapolate experiments done on mice to humans. Animal research can be used as an approximation, a way to test otherwise impossible-to-test hypotheses that can provide direction for future research. A great deal of care must be taken when interpreting animal data, and journalists are not historically the best caretakers. When you see articles reporting conclusions from animal studies in popular media, don’t dismiss the results out of hand, but be more cautious in your interpretation.

So what did the Purdue researchers actually do? They repeatedly exposed adolescent mice to caffeine, alcohol, caffeine-mixed alcohol, or plain water. Caffeine made the mice more active, but the caffeine-mixed alcohol really got them going. Each treatment of caffeine-mixed alcohol had a greater effect on movement than the last. You know what else has the same effect? Cocaine. Aha! There we have the basis for our claim that caffeine-mixed alcohol has the same effect as cocaine. Case closed, science done, headlines written. Good night, everybody!

Well, no. Drugs have multiple, complex effects, and a single overlap in these effects does not make them equivalent. The researchers also measured another hallmark of cocaine dependency that comes with increased movement: the accumulation in certain regions of the brain of the protein ΔFosB which has been classified as somewhat of a “molecular switch” for addiction. When they measured ΔFosB in mice exposed to the same treatments listed above, they found that in one of two brain regions tested, ΔFosB accumulated only in mice exposed to caffeine-mixed alcohol. Ah, the comparison grows stronger.

Next, the researchers tested if repeated caffeine-mixed alcohol consumption increased sensitivity to cocaine as a reward. Importantly, caffeine on its own was previously shown to have this effect. Caffeine-mixed alcohol surprisingly had the opposite effect: a reduced cocaine preference compared to caffeine alone. The interpretation? Repeated caffeine-mixed alcohol use actually desensitizes the mice to cocaine reward responses, so higher dosages of cocaine are required to be satisfied. Thus, desensitization could potentially lead to the abuse of rewarding substances. The researchers tested this by providing access to a natural reward which the mice could self-administer. Consistent with their hypothesis, they found that mice treated with caffeine-mixed alcohol voluntarily gobbled up a lot more of this reward compared to controls.

How has the popular press treated these results? The headlines were prone to overgeneralization and sensationalization. Take this example from UPROXX: “Science Says Your Vodka-Red Bull Is Just As Bad For You As Cocaine.” As I said, we should not treat caffeine-mixed alcohol and cocaine as complete equals in terms of their effects, even if there are notable and important similarities between the two. Equating their harms, in particular, is naïve and misleading.

The worst headline came courtesy of The Inquisitr: “Mixing Alcohol and Energy Drinks Can Make You A Cocaine Addict Later In Life.” We got in touch with one of the lead researchers on the article, Meridith Robins, who addressed this particular example:

“[We did not] conclude that mixing alcohol and energy drinks can make you a cocaine addict later in life…. To properly [reach this conclusion] we would have had to conduct more experiments, such as cocaine self-administration after repeated caffeine-mixed alcohol exposure… Even then, drawing such a direct correlation between adolescent caffeine-mixed alcohol exposure and cocaine consumption later in life would require follow-up studies accounting for social factors, environmental factors, genetic factors, sex differences…”

Unlike the headlines, the body of the articles stuck mainly to the Purdue press release and did not generally present any outlandish claims. The main issue across the board is the loss of important details. Lead researcher, Dr. Richard van Rijn, commented:

“The biggest nuance that may not have come through is that we exposed our mice to the caffeinated alcohol solutions for nearly their entire adolescent period. Thus the effects we observe, in mice, are on the very extreme end of people consuming these mixed drinks. On the other hand… it is apparent that we actually mixed relatively low amounts of caffeine with the alcohol and already noticed signficant[sic] changes. Thus who knows what happens to an 18yr old binge drinking 3-4 ‘vodka-redbull or equivalent’ every weekend for a whole year.”

That last sentence is key: who knows how this really translates to humans? The research is important and informative, but at this point, there are still many unknowns. We should not hang our hats on the results of a single study—although that is how science is commonly reported, that is not how it actually works. This study does not exist in a vacuum, but instead in a larger body of literature. Other studies similarly suggest that caffeine and cocaine can have comparable effects, but the added factor of alcohol has not been as thoroughly studied Research like this will not answer all the important questions, but will hopefully lead to a synthesized, comprehensive understanding of the relevant issues in the future. For now, I think we have enough information independent of this research (re: the “wide awake drunk” effect) to be careful with how we consume caffeine-mixed alcohol while the scientists hash out the long-term effects on neurochemistry and propensity for drug addiction.

About the Authors

Christian Silva, Jenna E Gallegos, and Destiny J Davis are PhD students at the University of California in Davis. This post was written as part of a project called “Science REALLY says” which seeks to ensure scientific data is accurately represented by the media. For more content from the UC Davis science communcation group “Science Says“, follow us on twitter @SciSays

Acknowledgements

We thank Dr. Richard Van Rijn (Assistant Professor of Medicinal Chemistry and Molecular Pharmacology at Purdue University) and Meredith Robins (graduate student at Purdue university and first author of the referenced study) for helpful comments.

References

Arria AM, et al. (2010) Energy Drink Consumption and Increased Risk for Alcohol Dependence. Alcoholism: Clinical and Experimental Research 35(2):365–375.

Garrett BE, Griffiths RR (1997) The Role of Dopamine in the Behavioral Effects of Caffeine in Animals and Humans. Pharmacology Biochemistry and Behavior 57(3):533–541.

Miyake ER, Marmorstein NR (2015) Energy drink consumption and later alcohol use among early adolescents.. Addict Behav 43:60–5.

Nestler EJ, Barrot M, Self DW (2001) FosB: A sustained molecular switch for addiction. Proceedings of the National Academy of Sciences 98(20):11042–11046.

O’Neill CE, et al. (2014) Effects of Adolescent Caffeine Consumption on Cocaine Sensitivity. Neuropsychopharmacology 40(4):813–821.

Peacock A, Pennay A, Droste N, Bruno R, Lubman DI (2014) ‘High’ risk? A systematic review of the acute outcomes of mixing alcohol with energy drinks. Addiction 109(10):1612–1633.

 Reissig CJ, Strain EC, Griffiths RR (2009) Caffeinated energy drinks–a growing problem.. Drug Alcohol Depend 99:1–10.

Robins MT, Lu J, Rijn RM van (2016) Unique Behavioral and Neurochemical Effects Induced by Repeated Adolescent Consumption of Caffeine-Mixed Alcohol in C57BL/6 Mice. PLOS ONE 11(7):e0158189.

 

“What does science REALLY say about vegetable oils and cancer?”

The Woman’s lifestyle magazine M2Woman recently ran the headline “Science reveals that this commonly used kitchen staple is carcinogenic”****

The accused kitchen staple is vegetable oil: canola, sunflower, and olive specifically. M2Woman claims these common cooking emollients are “proven to be carcinogenic”. But what does the science really say about vegetable oils and cancer?

Following heating, refining, or storage, all oils can break down into different chemical compounds. Some of these compounds are considered carcinogenic, but they are not unique to oils. These compounds can also be produced when vegetables or meats undergo certain processing steps like grilling, smoking, roasting, or frying. Studies showing these compounds to be carcinogenic have mainly focused on the risk of inhaling cooking oil fumes. While this is certainly a risk to industrial kitchen workers, it’s not such a big deal for your nightly meal prep.

The study cited by M2Woman focused on a particular type of oil breakdown product caused by oxidation. Oxidation is a normal process that occurs in the breakdown of all fats. Some oxidation products are even essential to the flavor of our favorite foods. But food goes “rancid” when too much oxidation has occurred.  Vegetable oils, especially extra virgin oils, are actually particularly stable because they contain an abundance of antioxidants. Compounds like vitamin E and carotenoids in vegetables oils help suck up the negative products formed during fatty acid oxidation.

In the study cited, researchers monitored oils for oxidation products over 6 hours at 320 degrees fahrenheit (the high range for deep frying).  They found that all tested oils broke down, but sunflower oils did so more quickly than canola or olive oil. But according to Dr. Selina Wang of the University of California Davis Olive Center, the technique used to measure oxidation products in this study is “not considered to be a standard method for testing oil quality” and “cannot quantify or identify the exact compounds that are potentially toxic”. The main goal of the study was just to detect changes in oils during cooking. They did not actually examine the level at which those changes become hazardous, and not all oxidation products are toxic. Dr. Ameer Taha who studies oxidation of dietary fats says it is “premature to conclude that some ‘unidentified’ oxidation products are carcinogenic.”

So the conclusion printed by M2Woman–“find alternative ways of cooking…If you are in dire need of cooking oil, opt for canola or olive oil and just drop the sunflower oil in the bin”– is a bit overstated. Generally, vegetable oils are a good choice for cooking. Registered Dietitian and Nutritionist Leah McGrath commented “I would not normally recommend frying foods but see nothing wrong with using oils, especially ones with higher amounts of monounsaturated fats like canola and olive to cook, bake and prepare foods . Oils  can contribute not only taste but health benefits. Different oils have different properties like smoke point and taste and may provide different health benefits”. Specific studies examining the oxidized fatty acids in the body in response to diets of different vegetable oils would be necessary to truly assess the relative risks.

****After this was published, M2Woman changed the headline of their article to “Science reveals that this particular vegetable oil is carcinogenic

About the Authors

Jenna E Gallegos and Taylor Reiter are PhD students at the University of California in Davis. This post was written as part of a project called “Science REALLY says” which seeks to ensure scientific data is accurately represented by the media. For more content from the UC Davis science communcation group “Science Says“, follow us on twitter @SciSays

Acknowledgements

We thank Dr. Selina Wang (Assistant Adjunct Professor in Food Science and Technology at the University of California in Davis), Dr. Ameer Taha (Assistant Professor in Food Science & Technology at UC Davis), and Leah McGrath, RDN for helpful comments, and Zane Moore for assistance identifying relevant experts in the field of oil chemistry.

References

 Abdel-Shafy, Hussein I., and Mona S.m. Mansour. “A Review on Polycyclic Aromatic Hydrocarbons: Source, Environmental Impact, Effect on Human Health and Remediation.” Egyptian Journal of Petroleum 25.1 (2016): 107-23. Web.Chang, Louis W., Lo Wai-Sze, and Lin

Chiang, Tai-An, Pei-Fen Wu, and Ying-Chin Ko. “Identification of Carcinogens in Cooking Oil Fumes.” Environmental Research 81.1 (1999): 18-22. Web.

Kamal-Eldin, Afaf. “Effect of Fatty Acids and Tocopherols on the Oxidative Stability of Vegetable Oils.” European Journal of Lipid Science and Technology 108.12 (2006): 1051-061. Web.

Pinpin. “Trans, Trans-2,4-Decadienal, a Product Found in Cooking Oil Fumes, Induces Cell Proliferation and Cytokine Production Due to Reactive Oxygen Species in Human Bronchial Epithelial Cells.” Toxicology Science 87.2 (2005): 337-343. Web.

Vaskova, Hana, and Buckova, Martina. “Thermal Degradation of Vegetable Oils: Spectroscopic Measurement and Analysis.” Procedia Engineering 100 (2015): 630-635. Web.

“Does intelligence REALLY come from our mothers?”

You’ve probably seen the headlines:

New research confirms that kids get their intelligence from mom -GH Sep 12, 2016

Science says you can thank (or blame) your mum for your intelligence-Yahoo Sep 14, 2016

Children inherit their intelligence from their mother not their father, science says-UK Independent. Oct 7, 2016

But what is this “new research” and what does science really say about the source of our smarts?

It turns out the mother of all these headlines isn’t actually new research at all. These articles refer to a blog post that references studies ranging from 1972 to 2012. We reviewed these studies, contacted the scientists, and dug into the literature on IQ inheritance to figure out what the science really says.

First, intelligence is tough to define. IQ tests clearly don’t reveal a natural ability, because scores improve with practice. And genes linked to high IQ’s only account for about 1-2% of intelligence. With so little data on smart genes, how could anyone claim intelligence is inherited from our mothers?

The whole crux of the argument is that “most of a child’s intelligence depends on the X chromosome.”

In one study cited, more genes known to be associated with mental disabilities were found on the X chromosome than on non-sex chromosomes. But the authors note:

“cognitive ability is a complex trait… a healthy lifestyle of the mother during pregnancy, well-balanced nutrition, and intensive and responsible care by the parents are far more important factors”

Another study identified 7 genes linked to mental disorders on the X-chromosome, but X-chromosome mutations are inherently easier to study. Women have two X-chromosomes while men have an X and a Y, so we only actually need one functional X-chromosome. That’s why men are more likely to develop certain disorders such as Autism or color-blindness which are associated with mutations on the X-chromosome. The X chromosome is clearly important for brain development, but there are also mental disorders linked to other chromosomes. For example, Down Syndrome is caused by an extra copy of chromosome 21. The authors speculate:

“to keep a complex organ such as the human brain functioning normally requires not one, not two, but hundreds or thousands of genes”

Even if there are a host of genes important for brain function on the X-chromosome, females also inherit an X chromosome from their dad. Here’s how the blog accounts for this: “One of the first studies in this area was conducted in 1984…there are conditioned genes which are activated only when inherited from the mother…maybe they could even result in some brain functions”

The problem is, brain tissue isn’t actually mentioned in any of the studies referenced from 1984. These studies monitored the development of mouse embryos created by fusing either two female or two male genomes. There were differences which could be explained by imprinting: when one copy of a gene (either the maternal or the paternal) is turned off. These are the “conditioned genes” mentioned in the blog, but they were not linked to brain development in these studies.

Two additional studies (from 1995 and 1996) also created mouse embryos in which some cells contained only maternal or only paternal genes. In these, brain tissue was discussed, and the blog concludes: “cells that had paternal genes accumulate in some of the emotional centers of the brain…researchers have not found any paternal cells in the cerebral cortex, which is where are developed the most advanced cognitive functions”

Cells in the cerebral cortex were more likely to contain strictly maternal genes, but this was not universally true. A similar correlation was also found in primates (in 1996). We asked Dr. James Curley if this difference related to intelligence:

“I wouldn’t conflate expression of genes in the cortex being a proxy for intelligence.  The expression of these genes obviously contribute to the development of brain regions and neural circuits involved in the control of behaviors related to intelligence such as learning and memory – but each gene would need to be studied for its role to gain further understanding.”

On the other hand, another study (not cited in the blog post) showed that females with turner syndrome have a thicker cortex if their X chromosome is inherited from their father. Clearly, brain development is complicated.

The remaining studies cited by the blog all considered the effect nurturing has on intelligence, but did not measure differences between maternal and paternal care. The first study found that attachment with mom influenced how toddlers problem solve. This was described as enthusiasm, persistence, and cooperation. This could be described as intelligence, depending on your definition.

From a study investigating the link between breastfeeding and a child’s intelligence, the blog concluded that “the best predictor of intelligence was the IQ of the mother”

But this study mainly showed that intelligent mothers were more likely to breastfeed, and that breastfeeding had little to no effect on the child’s intelligence. The father’s IQ wasn’t even considered.

Of the most recent study cited (2012), the blog claims, “when the mothers were emotionally supportive…the hippocampus of the kids at age 13 was 10% greater.” But, the author of this study, Dr. Joan Luby, said this was not an accurate explanation:

“Our interpretation here was that this was a psychosocial phenomenon—not a genetic one and was caregiver specific not gender specific.”

The one study that did discuss a genetic component found that mutations in a certain paternally expressed gene in mice lead to poor nurturing habits in mothers, but intelligence wasn’t considered at all.

While it makes for a good headline, inheritance of complex traits can’t be boiled down to a simple statement like “intelligence is inherited from mothers”

 

About the Authors

Jenna E Gallegos, K Nichole Holmes, and Christian Silva are PhD students at the University of California in Davis. This post was written as part of a project called “Science REALLY says” which seeks to ensure scientific data is accurately represented by the media. For more content from the UC Davis science communcation group “Science Says“, follow us on twitter @SciSays

Acknowledgements

We thank Dr. Barry Keverne (Professor of Neuroscience, University of Cambridge), Dr. James Curley (Professor of Neuroscience and Development Columbia University),  and Dr. Joan Luby (Professor of Child Psychiatry, Washington University) for helpful comments.

References

Matas L, et al. (1978) Continuity of adaptation in the second year The relationship between quality of attachment and later competence. Child Development 49:547-556

Barton SC, et al. (1984) Role of paternal and maternal genomes in mouse development. Nature 311:374-376

McGrath J & Solter D. (1984) Completion of mouse embryogenesis requires both the maternal and paternal genomes. Cell 37(1):179-183

Surani MA, et al. (1984) Development of reconstituted mouse eggs suggests imprinting of the genome during gametogenesis. Nature 308(5959):548-550

Allen ND, et al. (1995) Distribution of parthenogenetic cells in the mouse brain and their influence on brain development and behavior. PNAS 92(23)10782-10786

Keverne EB, et al. (1996) Genomic imprinting and the differential roles of parental genomes in brain development. Dev Brain Res 92(1):91-100

Keverne EB, et al. (1996) Primate brain evolution: genetic and functional considerations. Proc Biol Sci 263(1371):689-696

Gecz J & Mulley J (2001) Genes for Cognitive Function: Developments on the X. Genome Res 10(2):157-63

Zechner U, et al. (2001) A high density of X-linked genes for general cognitive ability: a run-away process shaping human evolution? Trends Genet 17(12):697-701

Curley J, et al. (2004) Coadaptation in mother and infant regulated by a paternally expressed imprinted gene. Proc Biol Sci 271(1545):1303-1309

Der G, et al. (2006) Effect of breastfeeding on intelligence in children: prospective study, sibling pairs analysis, and meta-analysis. BMJ 333(7575):945

Chabris CF, et al. (2011) Most Reported Genetic Associations With General Intelligence Are Probably False Positives. Psych Sci 23(11):1314-1323

Davies G (2011) Genome-wide association studies establish that human intelligence is highly heritable and polygenic. Molecular Psychiatry 16(10):996-1005

Luby JL, et al. (2012) Maternal support in early childhood predicts larger hippocampal volumes at school age. PNAS 109(8):2854-2859

Hayden EC (2013) Ethics: Taboo genetics. Nature 502(7469):26-28

Lepage J-F (2013) Genomic Imprinting Effects of the X Chromosome on Brain Morphology. J of Neurosci 33(19):8567-8574

Rietveld CA (2013) GWAS of 126,559 Individuals Identifies Genetic Variants Associated with Educational Attainment. Science 340(6139):1467-1471

 

 

 

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Content on this page has been created with full academic freedom of expression by early career scientists at the University of California. Through our projects, Science Says early career scientists are refining effective scientific communication practices under the guidance of UC faculty. We strive to present fact-based information grounded in the primary scientific literature. If you notice any facts that conflict with the primary literature on a topic in food and ag, please send us the publication and we will review our project content to make sure we are representing the current scientific consensus. Questions, comments or suggestions should be directed tosnalbers(at)ucdavis(dot)edu. Thanks!

Welcome!

Welcome to the Science Says Website!  We are a group of early career scientists at UC Davis interested in sharing our research with diverse audiences. Science Says is supported by the UC Davis Institute for Food and Agricultural Literacy (IFAL), a unit of the Innovation Institute for Food and Health, and the Communication, Literacy, and Education for Agricultural Research (CLEAR) project (PI, Pamela Ronald). We collaborate and interact closely with our CLEAR colleagues at UC Berkeley and UC San Diego.

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