‘Tis The Season of Food Follies, Fa-la-la-la-la…


By Lori Bystrom, PhD


“Sleigh bells ring, are you listening?” It is hard not to hear the lyrics of these and other seasonal songs during the holidays, just as it is difficult to ignore the colorful array of decorations, and the aroma of pine trees, cinnamon, ginger, and cloves. Engulfed by the sensory overload of the holidays, many of us cannot help but become overzealous consumers of holiday foods. As one might imagine, however, this is not good for our health.


In fact, there is evidence that the dietary choices we make during the holidays or the days leading up to big festivities, such as Christmas and New Year’s, can take a toll on our health. Holiday overconsumption can especially pose a problem in developed countries, where obesity is on the rise and is linked to numerous health problems. A recent study in PLOS ONE, for example, has shown that during the 2010-2011 American holiday period (Thanksgiving to New Year’s) food expenditures increased 15% compared to the pre-holiday period (July to Thanksgiving). Moreover, 75% of this increase was due to expenses on less-healthy food.


Interestingly, the study also found that the sales of healthy foods increased by 29.4% during the post-holiday periods (New Year’s to March), while the sales of less-healthy food remained the same as the holiday period. As a result, the calories purchased/week increased by 9.3% compared to the holiday period, and by 20.2% compared to the pre-holiday (baseline) period. Such behavior does not bode well, given that there is an ongoing obesity epidemic in many developed countries.


Although it would appear we have little control over our behavior during the holiday season –many of us acting like zombie consumers enticed by the smells, sights, and sounds of the holidays— there must be a way we can control these festive compulsions. Perhaps one way to tackle the obesity epidemic would be to reduce the cumulative increase of calories/unhealthy food that result from the holidays. But how do we resist the many temptations of the holidays? And, if we cannot resist, how can we undo the effects of our holiday choices afterwards?


In a recent report by PBS NEWSHOUR, Sendhil Mullainathan, an economics professor at Harvard University and cofounder of the behavioral economics consultancy ideas42, discusses several holiday gifts that might improve our unhealthy behaviors during the holidays and beyond.


He suggests buying smaller plates (similar to the standard plate size of the 1960s) to reduce the amount of food we consume at one sitting. In addition, he recommends a product made by Meal Measure that is used to control the amount of starches, vegetables, fruits, and protein put on your plate. Furthermore, could a candy/cookie jar that locks you out for a few minutes after opening stop you from eating more candy or cookies? The makers of The Kitchen Safe think so.


Other gadgets that may help prevent or reduce holiday weight gain include the Fitbit  or the Jawbone UP, which help you keep track of your exercise, sleep, and food intake patterns. And, if you find yourself too sluggish after the holidays, then perhaps Clocky or Tocky  the runaway alarm clock will get your day started sooner and keep you more active.


It remains to be seen whether or not any of these products actually help us control our holiday food intake or weight gain. Regardless, understanding our dietary patterns before, during, and after the holidays is likely to help researchers/ product innovators develop new strategies that may improve our unhealthy holiday/everyday dietary habits.


For now, as we fa-la-la-la our way through the holidays, it might be best to be mindful of our food intake or at least to make more effective New Year’s resolutions so we can fa-la-la away our holiday food follies.

health benefits of fasting

Fasting Can Make You Healthier


By Jesica Levingston Mac leod, PhD

Believe it or not, breakthrough new research has shown that fasting could be good for you. The article was indeed featured in the Nature journal and the impact of this study relies on the conclusion that fasting promotes haematopoietic stem cell (HSC) function. Stem cells are good for you because they can differentiate into specialized cells and can divide to produce more stem cells.

I personally challenged myself by fasting during Ramadan. .Ramadan is one of the pillars of the Muslim religion. It consists of fasting during a month from sunrise to sunset in order to reflect the essence of piety and to be aware of the plight of the underprivileged. Other cultures include fasting in their practices. In the Jewish religion the fasting day is named Yom Kippur, the Day of Atonement. It is described as a Jewish festival without food, but full of praying, introspection and self-judgment.

During my fasting period, my friends noticed an off character onset of passive aggressiveness in me, and indeed I was pretty cranky… and super hungry. One of my favorite comedians, Luis CK, once said that we incorrectly overuse the “I am starving” phrase, while people in Africa are really dying for starvation… so I won’t say I was starving, but certainly I was in a glucose deprived state of mind, which was affecting my behavior.

The most challenging part for me was being dehydrated, as you should also fast liquids during Ramadan. Contrary to the great health guru; the actress Cameron Diaz, who taught in her book that drinking plenty of water is the basis for a healthy body, fasting liquids seemed counterproductive in my experience.

Fasting is often indicated in general medical practice particularly prior to surgery or other procedures that require general anesthetics, because of the risk of pulmonary aspiration of gastric contents after induction of anesthesia (i.e., vomiting and inhaling the vomit, causing life-threatening aspiration pneumonia). One should also fast if undergoing a cholesterol or glucose test, as these measurements require a 12 hour fasting period so that a baseline can be established. These acute/short fasting periods are generally safe.

What more, a study in mice published in 2008 showed that short-term fasting (less than 48 hours) is effective in protecting normal cells but not cancer cells against high dose chemotherapy. The following year another study published in Science proved that caloric restriction delays disease onset and mortality in rhesus monkeys. In a human study, including 10 cancer patients under chemotherapy, Sadfie and collaborators  did not report significant side effects caused by fasting alone other than hunger and lightheadedness. In this study all patients voluntarily fasted for a total of 48 to 140 hours prior to and/or 5 to 56 hours following chemotherapy administered by their treating oncologists. In those patients whose cancer progression could be assessed, fasting did not prevent the chemotherapy-induced reduction of tumor volume or tumor markers. Fasting was well-tolerated and was associated with a self-reported reduction in multiple chemotherapy-induced side effects, suggesting that fasting in combination with chemotherapy is feasible, safe, and has the potential to ameliorate side effects caused by chemotherapies.


In the significant article that I mentioned before, Chen and collaborators showed that prolonged fasting (PF), exceeding 48 hours, activates a metabolic switch to lipid- and ketone-based catabolism and decreases circulating insulin-like growth factor-1 (IGF-1), which has been shown to reduce chemotoxicity (1) How? They couldn’t find an answer yet. However they clearly demonstrated that the decrease of circulating IGF-1 in the blood was accompanied by a reduction in protein kinase A (PKA) pathway activity in a variety of cell types. PKA has several functions in the cell, I.e. regulation of glycogen, sugar, and lipid metabolism and it regulates other proteins with a valuable role in stem cell stress resistance, self-renewal and pluripotency maintenance.

Interestingly, when Chen and collaborators exposed mice to cycles of prolonged fasting followed by challenges with cyclophosphamide (a drug used in chemotherapy), they noticed the reduction in the mortality and apoptosis (programmed cell death) of long- and short-term HSCs as well as multipotent progenitors in the bone marrow. In addition, multi-lineage differentiation was improved in these animals compared with fed mice, in vitro and in transplantation experiments. These positive effects of prolonged fasting were independent of the chemotherapy treatment, as they were also present in aged animals, which naturally exhibit a reduction in HSC function and multi-lineage potential. The effects of prolonged fasting could be reproduced in mice lacking the growth hormone receptor, which also have low levels of IGF-1. Transplantation experiments showed that low levels of IFG-1 in animals led to a reduction in IGF-1-mediated PKA signaling, both in haematopoietic cells and in associated stromal cells. Strikingly, the researchers could restore haematopoietic function by reducing the levels of either IGF-R1 or the PKA catalytic subunit. Conversely, the benefits were abolished if exogenous IGF-1 was added.

The scientific community is excited about these findings, and we hope understanding the positive effects of fasting can have implications in improving the quality of life of cancer patients... and all the humanity in general. On the other hand, I must cite one of the best Americans: “He that lives upon hope will die fasting", Benjamin Franklin.

Let Us Eat Real Food


By Kelly Jamieson Thomas, PhD

Sugar, which is undeniably highly addictive, is the number one additive in our food. Food manufacturers are hiding added sugar in almost every food including pizza, juice, bread, ketchup, and even baby formula. Added sugar consumption causes several diseases, including obesity, cardiovascular disease, diabetes, gout, fatty liver disease, some cancers, and tooth decay. What are added sugars? Those not found naturally in foods. When you eat an apple, it’s sweet, but the sugar in an apple isn’t added. But, when you drink a soda or eat an energy bar, the sugar in both of those is added. Prior to 1950, there were no added sugars in food. Since then, with the onset of added sugar in our food, Americans consume 39% more sugar. On average, we are eating 152 pounds of sugar per year, which is 2/3 of a cup per day! With such an astounding increase in our sugar intake, it’s certainly not surprising we are seeing a hefty increase in diseases related to sugar consumption, specifically obesity.


Is there a true link between increased sugar intake and increased body weight, specifically, body fat content? In an attempt to answer this highly debated question, the World Health Organization (WHO) analyzed thousands of studies and selected the most reliable. They focused on identifying an overall indication of how population changes in added sugar consumption affects our health. The resounding results—yes, increased sugar intake leads to increased body fat (adiposity). In children, this was especially relevant to consumption of sugary beverages, such as soda. Just as Bloomberg faced backlash for attempting to rid New York of large soda bottles, WHO has also received similar resistance for encouraging us to consume 5% of our calories from added sugar. The guideline has been officially set at 10%, which is equivalent to approximately one 12-ounce soda per day.


With clear evidence linking excess added sugar intake to the rapidly growing obesity epidemic, it’s in our best interest to seriously consider how sugar may ruin our long-term health. If we don’t change our habit and instead continue to gorge on added sugar, we will continue to see a rise in obesity. Currently, in the US, about 78 million adults (more than 37%) and 12.5 million (17%) youths are obese. Obesity incidence has risen from 14.5% to 30.9%, more than doubling, between 1971 and 2000. Obesity, the leading cause of preventable death, poses a significant risk for decreased life expectancy, type 2-diabetes, heart disease, osteoarthritis and some cancers. Not only are we making ourselves fat, but we are also creating an enormous burden in healthcare costs. 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.


What are we doing to make a change? Recently, the FDA has set new standards for food labeling. Information about added sugars will be required and serving size portions will be adjusted to reflect our larger portion size. Unfortunately, to our dismay, food manufacturers will not be forced to limit added sugars, nor will 20-ounce sodas and other sugary drinks be banned from the markets. With such strong evidence supporting the link between our increased consumption of added sugars and obesity, it’s time we wean off added sugars. Clearly, we can’t rely on processed foods to help us do this. The bottom line: let’s eat real food! Have some strawberries instead of strawberry ice cream. Ditch that soda for sparkling water with fresh lemon in it. If we consider that our food is our fuel, would you want to run on processed junk or naturally nourishing fuel?

What We Can Learn About The Flu From Elderberries


By Lori Bystrom

Flu season is still upon us and many of us will fall under influenza's nasty spell, if we have not already. Folklore suggests that elderberries can ward off evil spirits and many illnesses, and although they may not be the first remedy that comes to mind when you have the flu, these fruits may be worth a second look. Recent research suggests that these dark purple berries have antiviral properties and the mechanisms that contribute to their effects may provide additional clues on how to fight off this winter virus.


Currently, there are relatively few antivirals on the market, and their widespread use has led to increasing resistance and declining efficacy.  As a result, scientists are trying to better understand influenza and what confers resistance. Moreover, the specter of a deadly influenza pandemic is leading many researchers to explore diverse and novel treatment options.


Elderberries have a long history of medicinal and dietary use. As well as being used to make pies, jellies, wine and liqueurs, they have also been used to make various medicinal concoctions. These berries have also shown activity against both bacterial and viral pathogens, including several strains of influenza.There are also many commercial preparations of elderberry that are available (e.g., syrups and lozenges), some of which have alleviated flu symptoms in clinical trials.1,2

Despite mounting evidence that elderberries might be valuable for treating the flu, their mechanistic effects are not well understood, especially at the molecular level. Swaminathan et al., demonstrated that an anthocyanin pigment (cyanidin-3-sambubiocide), found in European elderberries (Sambucus nigra), have unique antiviral effects. As with several commercial antivirals, the anthocyanin inhibits viral neuraminidases — enzymes that allow progeny viruses to be released from the host cell. Specifically, viral neuraminidases cleave sialic acid groups, which enable the virus to detach from the host and spread the virus. In a video that demonstrates these effects, the neuraminidases are portrayed as blue monster-like enzymes with teeth that cleave sialic acid groups. This study shows for the first time that cyanidin-3-sambubiocide binds to an active site of influenza neuraminidase and potentially blocks the enzyme's effects (similar to the yellow objects in the video).


The authors used mass spectrometry to measure the mass fragments released from unbound and anthocyanin-bound neuraminidases. Based on these results, the researchers were able to predict which residues of the influenza neuraminidase bound to the anthocyanin. The precise location was further elucidated by computational studies that evaluated the interaction between the anthocyanin component  (excluding sugar groups) and the N1 neuraminidase from the 2009 H1N1 pandemic strain.  The antiviral effects of the compound were also confirmed to be effective by a neuraminidase inhibition assay. These experiments indicated that the anthocyanin favored binding to a so-called "430-cavity", which is different from the region where standard antiviral drugs bind.  Furthermore, the results showed that the bound anthocyanin was located away from two residues that that are known to regulate neuraminidase resistance.


Although the results are promising, more research is warranted to confirm that cyanidin-3-sambubiocide has antiviral effects in clinical studies, and whether or not other compounds in elderberries enhance, synergize or alter the activity of this compound. Nevertheless, elderberries may help scientists find more effective and less resistant-prone treatments that may prevent influenza from casting a dark shadow on our health.


Sexy Science: How Aphrodisiacs Work


By Chris Spencer

This Valentine’s Day, you may find a stunningly beautiful person staring at you with the piercing gaze that only comes from a feeling of pure, unadulterated lust. You then may notice that person’s look of longing slowly morph into a visage of confusion and dismay. The reason they look so dejected is that you clearly aren’t mentally undressing them. You’re lost in thought, trying to work out exactly what it is about oysters that seems to get everyone going. If I were you, I’d satiate my scientific curiosity now, and focus on a different form of satisfaction on Valentine’s Day.


Using studies in rats, nutmeg has been proven to enhance sexual desire. In fact, reading the study lead me to one of my favourite scientific phrases; “feeding nutmeg increased mountings onto females.” It is as clear cut as that ladies and gents. The probable mechanism nutmeg more than likely stems from its nerve stimulating properties, so grate some onto your risotto on the big night.

Spanish Fly (Lytta vesicatoria)

If like me, you’re a fan of the 1987 Beastie Boys classic “Brass Monkey,” then you’ll be aware of the aphrodisiac potency of the Spanish fly. The beetle secretes cantharidin when threatened – a toxin which is toxic to humans in high enough doses. Despite this, people have been grinding Spanish fly up and putting it in peoples’ drinks for at least 2000 years. The toxin inhibits phosphodiesterase and protein phosphatase activity and stimulates a mild urethral irritation that can lead to priapism (a sustained erection of the penis or clitoris). This one seems to be a difficult one to administer safely, so maybe give it a wide berth. I certainly don’t condone spiking anybody’s drink with it.

Red Wine

That leads me neatly onto alcoholic beverages, specifically red wine. Red wine is a double whammy in terms of getting you in the mood. The high concentration of phenolic compounds such as resveratrol and tannins are present in numerous traditional aphrodisiacs, and they have been shown to increase blood flow to your danger zone. This is another compound which has been shown to make rats mount other rats under experimental conditions. The other side of the coin with red wine is alcohol. Of course alcohol relaxes you, and if you’re with someone new (or trying something a bit new) – that feeling of relaxation may well be vital. Don’t get carried away though, or you gentlemen might find that priapism won’t feature on your list of problems.

Chilli Peppers

The erotic component of hot chillies is capsaicin, a molecule which fools our thermoreceptors into thinking it’s hot. Capsaicin works in two ways: not only does it release endorphins to stimulate a mild euphoria, but it increases circulation and speeds up metabolism, which are similar responses to those experienced during sex.

This one comes with a caveat. If you’re preparing any spicy dishes yourself, take it from me, you’ll probably want to wear gloves while you’re chopping the chillies. There are a couple of rather intimate mucosa that you probably don’t want to get capsaicin anywhere near. “Burning loins” are just a figure of speech, you should endeavour to keep it that way.


That is right, chocolate has done it again. The pharmacologically active substances in chocolate are phenylethylamine, which reportedly enhances pleasurable sensations in the brain and affects serotonin and endorphin levels, and N-acylethanolamines, which may activate cannabinoid receptors to increase tactile sensitivity. Pass the dessert.

Symbolic Aphrodisiacs

A fair number of reported aphrodisiacs don’t actually have a proven mechanism of action. Examples such as the avocado (avocado comes from the Aztec word for testicle tree) and the banana are pretty much just phallic symbols. Oysters are used primarily because of their association with the Aphrodite herself.

That’s not to say that these foods won’t get you going of course. If you and your partner sit down to a candlelit dinner of oysters, then I’d imagine you’ll both know it’s on.

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.


Can Black Soybeans Improve Blood Disorders?


By Lori Bystrom

Studies have suggested that eating a rainbow of colorful fruits and vegetables provides a diverse array of vitamins, as well as phytonutrients and other goodies for the body. So what benefits should we expect from black-colored foods?  In traditional Chinese medicine several "black foods" are believed to be a good source of nutrients and beneficial for blood production. A recent paper in the British Journal of Nutrition have evaluated several "black foods" and have found that black soybeans (Glycine max) affect a key regulator in iron metabolism and may be beneficial for certain types of blood disorders.

Hemoglobin is an iron-dependent oxygen transporter found in red blood cells. Low hemoglobin is indicative of anemia, as well as iron-poor and pale red blood cells. Anemia can result from dysregulation of iron metabolism or lack of dietary iron.

One of the master regulators for iron metabolism is hepcidin, a liver-derived peptide hormone that is encoded by the gene HAMP. Normally when excess iron is available, hepcidin levels increase and bind to the iron exporter ferroportin. This results in degradation of ferroportin and prevention of iron from being absorbed into the body, mobilized, and recycled for red blood cell production. However, some diseases, such as anemia of chronic disease (also known as anemia of inflammation) and iron-deficiency anemia, overexpress hepcidin regardless of the body's iron requirements. Therefore, reducing hepcidin expression may have therapeutic implications.

Mu and colleagues tested extracts from several "black foods", including black soybean, black fungus (Auricularia auricula-judae), black sesame seeds (Sesamum indicum), and date-plum (Diospyros lotus) for their effects on hepcidin expression in human liver cells. Only the black soybean seed coat extract (BSSCE) reduced hepcidin expression significantly. Interestingly, the iron content for this food was low and consisted of about 30% of anthocyanins, a pigment that most likely contributes to the blackish color of black soybeans. BSSCE also reduced the effects of a set of transcription factors (SMAD1/5/8) that activate HAMP gene expression. Moreover, induction of hepcidin gene expression by bone morphogenetic protein 6 (BMP6) and interleukin-6 induction (IL-6) was significantly reduced by BSSCE.

Animal studies also showed promising results. Mice were fed a diet consisting of 2% BSSCE for up to 30 days. At day 7, the mice had a 50% reduction in liver hepcidin expression and a 35% decrease in spleen iron concentrations, as well as a 135% increase in serum iron concentration. In other words, iron absorption and mobilization were increased in the mice. Moreover, by day 30 there was an increase in red blood cell counts (by 111%) and hemoglobin values (by 109%), as well as several other hematological parameters.

Similar to the vitro studies, there was a reduced effect on transcription factors (SMAD1/5/8) that activate hepcidin expression by day 7, but these effects returned to nearly control levels by day 30. In addition, the gene expression of 2 inducers of hepcidin expression (hepatic inhibitor of DNA binding 1 and BMP6), were also significantly reduced by day 7 and were slightly less affected by day 30. Other contributors of hepcidin expression were not affected. The researchers suggest that BSSCE may inhibit hepcidin expression by specifically inhibiting the signaling pathway that involves BMP/SMAD, but not the signal transducer and activator of transcription (STAT) pathway that also is associated with hepcidin expression.

This study suggests that BSSCE may be a potential dietary treatment for people with anemia of chronic disease or iron-deficiency anemia. Future studies will need to assess animal models with diseases that cause hepcidin overexpression to confirm the therapeutic benefits of BSSCE. Although it has not been confirmed, the authors suggest that the active component of BSSCE may be due to the anthocyanins in black soybeans. If these compounds and their effects are validated, then perhaps certain black pigments may shed more light on how blood can become a deeper shade of red.