Can Chocolate be Good for You? The Dark and Light Side of the Force

By Jesica Levingston Mac leod, PhD

It is this time of the year again: San Valentin (aka Valentine’s Day) –  the best excuse to give and more importantly to EAT a lot of chocolate. But, maybe a better gift that receiving chocolate,  is to know that eating chocolate might be good for your health.

In the beginning chocolate was “created” as a medicine –  a healthy beverage –  around 1900 BC by Mesoamerican people. The Aztecs and Mayas gave it the name of “xocolatl”, it means bitter water, as the early preparations of the cacao seeds had an intense bitter taste. Almost one year ago, a longitudinal study, done in the US East Coast, connected eating chocolate with better cognitive function. Yay! Great news, right? The scientists gathered information over a period of 30 years (starting in 1976) from 968 subjects (aged 23-98 years) in the Syracuse-Maine area. The results showed that more frequent chocolate consumption was meaningfully associated with better performance on the global composite score, visual-spatial memory and organization, working memory, scanning and tracking, abstract reasoning, and the mini-mental state examination. Importantly, they pointed out that with the exception of working memory, these relations were not attenuated with statistical control for cardiovascular, lifestyle and dietary factors across the participants.

More good news arrived last summer: an Italian research team announced that flavanol-rich chocolate improves arterial function and working memory performance counteracting the effects of sleep deprivation. The researchers investigated the effect of flavanol-rich chocolate consumption on cognitive skills and cardiovascular parameters after sleep deprivation in 32 healthy participants, who underwent two baseline sessions after one night of undisturbed sleep and two experimental sessions after one night of total sleep deprivation. Two hours before each testing session, participants were assigned to consume high or poor flavanol chocolate bars. During the tests the participants were evaluated by the psychomotor vigilance task and a working memory task, systolic blood pressure (SBP) and diastolic blood pressure (DBP), flow-mediated dilation and pulse-wave velocity. As you might know, sleep deprivation increased SBP/DBP. The result was that SBP/DBP and pulse pressure were lower after flavanol-rich treatment respect to flavanol-poor treatment sleep deprivation impaired flow-mediated dilation, flavanol-rich, but not flavanol-poor chocolate counteracted this alteration. Flavanol-rich chocolate mitigated the pulse-wave velocity increase. Also, flavanol-rich chocolate preserved working memory accuracy in women after sleep deprivation. Flow-mediated dilation correlated with working memory performance accuracy in the sleep condition.

The European Food Safety Authority accepted the following statement for cocoa products containing 200 mg of flavanols: “cocoa flavanols help maintain the elasticity of blood vessels, which contributes to normal blood flow”. This statement means that flavanol-rich chocolate counteracted vascular impairment after sleep deprivation and restored working memory performance. In another study led by Columbia University Medical Center scientists,  dietary cocoa flavanols—naturally occurring bioactives found in cocoa—reversed age-related memory decline in healthy older adults. One possibility is that the improvement in cognitive performance could be due to the effects of cocoa flavonoids on blood pressure and peripheral and central blood flow. Following on this other chocolate attribute, it was shown than weekly chocolate intake may be beneficial to arterial stiffness.

But, there are some bad news!  A review of 13 scientific articles on this topic, provided evidence that dark chocolate did not reduce blood pressure. However, the reviewers claimed that there was an association with increased flow-mediated vasodilatation (FMD) and moderate for an improvement in blood glucose and lipid metabolism. Specifically, their analysis showed that chocolates containing around 100 mg epicatechin can reliably increase FMD, and that cocoa flavanol doses of around 900 mg or above may decrease blood pressure if consumed over longer periods: “Out of 32 cocoa product samples analyzed, the two food supplements delivered 900 mg of total flavanols and 100 mg epicatechin in doses of 7 g and 20 g and 3 and 8 g, respectively. To achieve these doses with chocolate, you will need to consume  100 to 500 g (for 900 mg flavanols) and 50 to 200 g (for 100 mg epicatechin). Chocolate products marketed for their purported health benefits should therefore declare the amounts of total flavanols and epicatechin”.  The method of manufacturing dark chocolate retains epicatechin, whereas milk chocolate does not contain substantial amounts of epicatechin.

The first epidemiological “indication” for beneficial health effects of chocolate were found in Kuna natives in Panama with low prevalence of atherosclerosis, type 2 diabetes, and hypertension. This fact correlated with their daily intake of a homemade cocoa. These traits disappear after migration to urban and changes in diet.

 

There are many  claims about the potential health benefits of chocolate, including anti-oxidative effect by polyphenols, anti-depressant effect by high serotonin levels, inhibition of platelet aggregation and prevention of obesity-dependent insulin resistance. Chocolate contains quercetin, a powerful antioxidant that protects cells against damage from free-radicals. Chocolate also contains theobromine and caffeine, which are central nervous system stimulants, diuretics and smooth muscle relaxants, and valeric acid, which is a stress reducer. However, chocolate also contains sugar and other additives in some chocolate products that might not be so good for your health.

 

Oh well, maybe the love of chocolate is like any other romantic affair: blind and passionate. Apparently, the beneficial dosage is 10 g of dark chocolate per day (>70% cocoa), so enjoy it as long as the serotonin boost for rewarding yourself with a new treat last.

 

Happy Valentine’s Day!

 

 

Cancer Prevention: Affecting Epigenetic Changes with Diet

 

By Kelly Jamieson Thomas

Ending cancer needs to become a global health priority. Cancer, the leading cause of death worldwide, caused 8.2 million deaths in 2012. With 575,000 deaths attributable to cancer in 2010 in the United States, cancer-related deaths in the US are second only to those caused by heart disease, which caused 594,000. Bringing worldwide support behind ending cancer is one of the goals of World Cancer Day this February 4th. How can we end cancer? First and foremost, focus on prevention—the most viable option as a cure.

Historically, cancer has been perceived as a disease in which our genetic makeup dictates our likelihood of developing cancer. Presently, it has become broadly recognized that the initiation and progression of cancer is an intricate web of both genetic makeup and epigenetic events that alter our gene expression. Many studies have proven that epigenetic alterations are key components of the initiation and progression of cancer. These epigenetic processes—including DNA methylation, histone modification, and microRNA expression—are potentially reversible.

Global hypomethylation is a hallmark of almost all human cancers. CpG island hypermethylation and down-regulation is common for many genes involved in a broad range of functions that are deregulated in cancer. As a result, a breadth of research is now dedicated exclusively to understanding how epigenetic alterations are involved in the earliest stages of tumor progression in order to develop epigenetic-based cancer prevention strategies. NIH funding for epigenetic research has dramatically increased from approximately $500,000 to more than $13 million dollars. Support for pinpointing the relationship between diet, exercise, and cancer prevention is clearly on the rise.

Is it possible to affect epigenetic changes through our diet? Dietary compounds have been shown to elicit epigenetic changes in cancer cells. To fully understand how we can modulate cancer prevention through lifestyle, research must focus on how diet and bioactive food components specifically impact epigenetic processes. Antioxidants such as carotenoids and fiber found in many vegetables and fruit offer a variety of anti-cancer benefits. Increased dietary folate, a soluble form of B6 vitamin, consumption has been linked to a decrease in colorectal cancer through its affect on DNA methylation. Dietary phytochemicals, that act as anti-cancer agents (including polyphenols, genistein, sulforaphane, resveratrol, and curcumin) have been shown to act through epigenetic mechanisms.

Population studies are also instrumental in linking diet and cancer prevention. Through the American Cancer Society’s Cancer Prevention Study-3, more than 300,000 men and women ranging from 30-65 years old with no personal history of cancer are participating in an epidemiological cohort study to examine the interplay between genetics, lifestyle, behavior, environment, blood factors, and waist circumference in relation to cancer risk. Large epidemiological studies in combination with rigorous scientific studies help unravel the mechanisms of cancer initiation and progression.

Cancer prevention is the best way to ultimately cure the disease. To work towards cancer prevention, we must further explore how dietary modifications may achieve epigenetic reprogramming, resulting in the maintenance of normal gene expression and reversal of tumor progression.

 

Obesity: Prevention is the Cure

 

Kelly Jamieson Thomas

 

Over the past thirty years, we have witnessed an astronomical increase in worldwide obesity, which has reached epidemic proportions. Worldwide, more than 1.1 billion adults are overweight, of those 312 million are obese, with the remaining on the path to becoming obese. In the US, obesity rates rose from 14.5% to 30.9%, more than doubling, between 1971 and 2000. Currently, in the US, more than 37% of adults, about 78 million, and 17% of youths are obese. If the obesity rate continues to grow at current rates, healthcare costs attributable to obesity, which were $147 billion in 2008, are predicted to increase to $957 billion dollars by 2030, a startling 18% of total US health expenses.

 

As the leading cause of preventable death, obesity, characterized by a Body Mass Index (BMI) greater than 30, poses an enormous burden in healthcare costs and a significant risk for decreased life expectancy, type 2 diabetes, heart disease, osteoarthritis and some cancers. We need to take responsibility for our long-term health by developing public strategies to combat weight gain. How can we accomplish this goal? By making small and consistent changes that include increasing physical activity and modifying our food choices.

 

Energy in, Energy Out

One contributing factor to the rise in obesity has been a substantial decrease in daily physical activity. This has led to changes in energy balance tipping the scale in favor of a gradual weight gain of 1.1-2.2 lb per year. In “The Importance of Energy Balance”, the authors explain how the delicate seesaw of energy balance has been disturbed by our decrease in physical activity, resulting in a state where any excess food consumption results in weight gain. To prevent weight gain, and ultimately obesity, energy in (food) must balance energy out (exercise).

 

Several studies that show that increasing our physical activity, combined with controlling our food choices, is the best way to combat obesity. In a 20-year long study, men with high levels of physical activity gained 5.7 lb less than those with low physical activity and women who exercised more in this study gained 13.4 lb fewer than those who didn’t. BMI, which is used to measure obesity, was also inversely associated with physical activity in 5 different long-term studies. Another study showed that either walking or high-intensity exercise one time per week led to a decrease in body weight of 1.76 lb for men and 1.39 lb for women over a two year period.

 

Unfortunately, most weight loss programs solely focus on restricting diet, not increasing exercise and curbing food intake. Studies have shown that calorie-restricting diets lead to 33-66% of dieters regaining more weight than they lost on the diet. Long-term, this does not help fight obesity. Weight gain prevention is key. Making small changes in our diet and exercise now, as little as 100 kcal/day, prevents weight gain and obesity over time. In the morning, go for a run or power walk outside. After work or on the weekends, meet with friends for a game of Frisbee. If it’s too cold outside, follow an exercise program on TV.

 

How to fight obesity: Community-based prevention

The most effective way to prevent obesity is to do so as a community, with partnership programs that provide education on how to exercise and eat properly and community aid in following prevention guidelines. While public strategies focused on obesity prevention have had varying degrees of success, one strategy, EPODE (Ensemble, Prévenons l’Obésité des Enfants), has been developed around a successful prevention program tested in France, the FLVS study, which decreased childhood obesity 9% in 4 years. EPODE, according to a recent article in US Endocrinology, aims to reduce childhood obesity by encouraging and monitoring healthy eating and exercise both at school and at home, as intervention solely targeting schools was unsuccessful. The EPODE model stresses the critical role of awareness, willingness, and involvement of initiatives that combine efforts from NGOs, private partners, and government to fight obesity. As of 2012, 17 countries have implemented EPODE-inspired programs, including VIASANO in Belgium, JOGG in the Netherlands, and OPAL in South Australia. Implementation of such programs requires comprehensive community effort, but the long-term results may significantly alleviate our obesity problem.

 

Prevention is the Cure

There are no safe and efficient drugs to cure the obesity epidemic, but we can prevent it by making small and consistent changes in our lives, starting at a young age. It is time to take responsibility for our long-term health and prevent obesity by exercising daily and eating healthier. In doing so, we not only prevent obesity, one of the largest public health problems we face as a population, but also lower our risk for type 2 diabetes, heart disease, osteoarthritis, decreased longevity and cancer.

Leafing through the Literature

Thalyana Smith-Vikos

Highlighting recently published articles in molecular biology, genetics, and other hot topics

Can I get some of your gut bacteria?

While there have been many reports popping up in the literature that demonstrate a connection between gut microbiome and diet, Ridaura et al. have elegantly showed how the mammalian microbiome affects diet in a specific yet alterable manner that can be transmitted across individuals. The researchers transplanted fecal microbiota from adult murine female twins (one obsess, one lean) into mice fed diets of varying levels of saturated fats, fruits and vegetables. Body and fat mass did depend on fecal bacterial composition. Strikingly, mice that had been given the obese twin’s microbiota did not develop an increase in body mass or obesity-related phenotypes when situated next to mice that had been given the lean twin’s microbiota. The researchers saw that, for certain diets, there was a transmission of specific bacteria from the lean mouse to the obese mouse’s microbiota.

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In vivo reprogramming

Abad et al. have performed reprogramming of adult cells into induced pluripotent stem cells (iPSCs) in vivo. By activating the transcription factor cocktail of Oct4, Sox2, Klf4 and c-Myc in mice, the researchers observed teratomas forming in multiple organs, and the pluripotency marker NANOG was expressed in the stomach, intestine, pancreas and kidney. Hematopoietic cells were also de-differentiated via bone marrow transplantation. Additionally, the iPSCs generated in vivo were more similar to embryonic stem cells than in vitro iPSCs by comparing transcriptomes. The authors also report that in vivo iPSCs display totipotency features.

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Connection between pluripotency and embryonic development

Lee and colleagues have discovered that some of the same pluripotency factors (Nanog, Oct4/Pou5f1 and SoxB1) are also required for the transition from maternal to zygotic gene activation in early development. Using zebrafish as a model, the authors identified several hundred genes that are activated during this transition period, which is required for gastrulation and removal of maternal mRNAs in the zebrafish embryo. In fact, nanogsox19b and pou5f1 were the top translated transcription factors prior to this transition, and a triple knockdown prevented embryonic development, as well as the activation of many zygotic genes. One of the genes that failed to activate was miR-430, which the authors have previously shown is required for the maternal to zygotic transition. Thus, Nanog, Oct4 and SoxB1 induce the maternal to zygotic transition by activating miR-430.

 

A microRNA promotes sugar stability

Pederson and colleagues report that a C. elegans microRNA, miR-79, targets two factors critical for proteoglycan biosynthesis, namely a chondroitin synthesis and a uridine 5′-diphosphate-sugar transporter. Loss-of-function mir-79 mutants display neurodevelopmental abnormalities due to altered expression of these biosynthesis factors. The researchers discovered that this dysregulation of the two miR-79 targets leads to a disruption of neuronal migration through the glypican pathway, identifying the crucial impact of this conserved microRNA on proteoglycan homeostasis.

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Establishing heterochromatin in Drosophila

It is known that RNAi and heterochromatin factor HP1 are required for organizing heterochromatin structures and silencing transposons in S. pombe. Gu and Elgin built on this information by studying loss of function mutants and shRNA lines of genes of interest in an animal model, Drosophila, during early and late development. The Piwi protein (involved in piRNA function) appeared to only be required in early embryonic stages for silencing chromatin in somatic cells.  Loss of Piwi leads to decreased HP1a, and the authors concluded that Piwi targets HP1a when heterochromatin structures are first established, but this targeting does not continue in later cell divisions. However, HP1a was required for primary assembly of heterochromatin structures and maintenance during subsequent cell divisions.

 

The glutamate receptor has a role in Alzheimer’s

Um and colleagues conducted a screen of transmembrane postsynaptic density proteins that might be able to couple amyloid-β oligomers (Aβo) bound by cellular prion protein (PrPC) with Fyn kinase, which disrupts synapses and triggers Alzheimer’s when activated by Aβo-PrPC . The researchers found that only the metabotropic glutamate receptor, mGluR5, allowed Aβo-PrPC  to activate intracellular Fyn. They further showed a physical interaction between PrPC and mGluR5, and that Fyn is found in complex with mGluR5. In Xenopus oocytes and neurons, Aβo-PrPC caused an increase in intracellular calcium dependent on mGluR5. Further, the Aβo-PrPC-mGluR5 complex resulted in dendritic spine loss. As a possible therapeutic, an mGluR5 antagonist given to a mouse model of inherited Alzheimer’s reversed the loss in synapse density and recovered learning and memory loss.

 

Keep playing those video games!

Anguera et al. investigated whether multitasking abilities can be improved in aging individuals, as these skills have become increasingly necessary in today’s world. The scientists developed a video game called NeuroRacer to test multitasking performance on individuals aged 20 to 79, and they observed that there is an initial decline in this ability with age. However, by playing a version of NeuroRacer in a multitasking training mode, individuals aged 60-85 achieved levels higher than that of 20-year-olds who had not used the training mode, and these successes persisted over the course of 6 months. This training in older adults improved cognitive control, attention and memory, and the enhancement in multitasking was still apparent 6 months later. The results from playing this video game indicate that the cognitive control system in the brains of aging individuals can be improved with simple training.

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