If you leave your job for three months without explanation, you’ll probably get fired. If you leave school for three months without a really detailed doctor’s note, you’ll probably get kicked out. If you leave your children unattended for three months, even with a good excuse, they’ll probably hate you, and CPS might take them away.

So, if you used to read my blog, but no longer feel that you can trust me as a webmaster, that’s well within your rights. I could go on and on about my hiatus with all the lab meetings and the presentations and the hours spent slaving away over tubes of clear liquids — but that’s not actually so interesting. You know what is?

What’s interesting is that I’m alive and relatively healthy despite my abominable (to some) diet and lack of exercise choices. Please read on for a heartbreakingly honest confession of my wicked health ways, with photographic examples of the devastation I’ve wreaked on myself, and sometimes on loved ones.

Disclaimer #1: The pictures herein may or may not induce diet fail.

Disclaimer #2: I may or may not use tons of hardcore scientific fact to back up my feeble excuses for my health choices.

Disclaimer #3: I may or may not be an advocate of unhealthiness per se, but I strongly defend people’s rights to make whatever unhealthful choices they wish…so long as they can live to tell about it, as I am.

First off, I can’t decide what my goal is with this post. Is it to absolve myself of the guilt I feel for what I’ve done? Is it to brag about the fact that I can do what I’ve done and get away with it? Or do I just want a platform to rage back against the hordes of people who provoke me time and time again by asking “Oh my gosh, you’re going to eat that?!”? Because the answer to this question is almost always “Yes. With seconds.”

So let’s say you make a cupcake. A cinnamon-y cupcake. You’re feeling indulgent, so you top it with streusel, which is basically butter and cinnamon and sugar. This adds a nice crunchy layer of devil-may-care deliciousness to your dessert.

This would be a fine place to stop and enjoy your creation. Would be, if it weren’t for maple buttercream. This is essentially maple syrup, butter (the real stuff), and powdered sugar.

Wow, you’re really throwing caution to the wind now! And since you’ve gone this far, you can’t think of any great argument against garnishing this confection with crumbled bacon, can you?

Paula Deen has nothing on you, obviously, but why are you doing this? Are you hosting a party? (No.) Do you have an amazing food blog, in addition to having an awesome science blog? (No.) Oh, so you just have a thing for unhealthy food! Lots of unhealthy food.

You don’t even really share these with people, you just eat them. The only reason you’ve taken pictures is to make your friends jealous on Facebook. But maybe you justify this as a rare treat! …What’s that? It’s not a rare treat? You mean you make unhealthy stuff, like, all the time? Surely you jest.

Alright, so I’m talking about myself here. I’m constantly making stuff like this, and not sharing it either. High sugar, high fat — and not just for dessert. My meals are technically not much better: cheap Chinese food, half of a large pizza, Ramen noodles. Even when I cook for myself, which is at least half the time, the meal is almost always along these lines:

Lots of frying, lots of butter. I’m not even going to talk about all of this stuff that I have on the side:

Alright, so you’re getting the picture. I’m not necessarily counting calories. Or fat, sugar, salt, cholesterol…. Maybe at this point you’re saying to yourself “Okay, this is disturbing, but what does it have to do with science?”

I’m not so sure, exactly. I guess I’m only just now becoming fully aware of the fact that I have eaten like this for my entire life, while making no attempt at formal exercise whatsoever, and yet I’m alive. Alive with an unremarkably normal BMI of around 20, normal cholesterol levels, no sign of diabetes, and blood pressure on the lower side. This probably sounds a lot like some sort of Humblebrag. And maybe it is. But I like to think of it as an anomaly of nature, an anomaly that should be questioned, challenged, and weakly explained in list form.

And so I present you with reasons why I’m not dead:

1. “I’m on a ketogenic diet!” A ketogenic diet is one that’s high in fats. I’ve got that covered. However, a ketogenic diet it also low in carbohydrates, so I can’t actually claim to be on a ketogenic diet. But it’s interesting to know that such a diet exists and is used as a form of treatment for epilepsy, brain cancer, and some genetic metabolic disorders. When the body has a relatively high amount of fat and low amount of sugar, the liver will burn fat instead of carbohydrates, which generates a byproduct called ketones. In people who can’t metabolize sugars because of enzymes deficiencies, a ketogenic diet is the way to go; in people who have seizures, it’s not well understood why a ketogenic diet helps, but it does.

"Tonight, we dine in hell! ...Because we hardly ate all day."

2. “I’m on the Warrior Diet!” The Warrior Diet is fairly straightforward: “under-eat” during the day and “overeat” at night. Now, I don’t technically follow the Warrior Diet or any diet at all, but I do find that my breakfast is small, my lunch is small, and my dinner is HUGE. For breakfast, I might grab some Greek yogurt (<200 calories). For lunch, I’ll have something like pita chips
and a cereal bar (<300 calories). And dinner is as much food as I can fit into my body. I’m talking 1200+ calories of pepperoni pizza, 1000+ calories of pasta, or 1400+ calories of fried chicken and biscuits. Followed by whatever my most recent baked good happens to be. So maybe I intake a normal number of calories (or so I’ll tell myself), but most of that happens after 6pm…where no one can see me.

3. “I’ve got good genes!” Ah, yes, those all-powerful “genes.” Those things that we use to excuse ourselves for not being runway models, Olympic swimmers, or (insert enviable profession here). And of course genes have a lot to do with everything we are…but, which genes are we talking about specifically? Very few people actually have a gene in mind when they praise “good genes” or lament “bad genes.” In fact, there aren’t many genes that can be solely blamed for why people are fat, athletic, smart, etc. Truth be told, there’s an enzyme known to break down fat in food and in the body and convert it to energy, and I know one of my two copies of this enzyme is mutated. So I don’t think I can say I have superior genes that let me eat tons of fat and sugar without consequence. If you still think it’s my genes, my dad developed Type 2 diabetes in his 50s, and my mom was diagnosed with high cholesterol in her 50s… neither of them were ever supermodels, either, so my genes probably aren’t terribly special.

4. “Just you wait!” And, after all this, it’s certainly possible that I’ve got some rough days in store for me. Everyone’s heard about how eating lots of fats and sugars predisposes to heart disease, diabetes, cancer, and just about every other negative biological outcome. It’s possible that my love of all things fatty is dooming me to a future with scarring in my brain, specifically in my hippocampus. I’m definitely not advocating for anyone to do as I do, but sometimes people break all the health “rules” and turn out just fine, and sometimes people follow every rule and are still struck with health misfortunes.

Honestly, I am in awe of people with well-balanced diets, those of you out there running marathons for fun, and the like. But…I’m just not like that. I’m sure as I get older, I will be forced to make concessions to nature and clean up my act a bit. But, until then, I’d love it if people would give me less grief about what I choose to eat, unless those people are doctors holding the results of my blood work.

And in the meantime, yes, I’m going to eat that.

Stay nerdy.

P.S. I really do apologize for so much time away from blogging. I’m going to shoot for updates every week or every other week, and hope for the best. Thanks as always for your continued support!

P.P.S. Check out this shiny new comedic science blog written by my buddy Tyler: http://www.biLOLogy.net

Lambrechts DA, Wielders LH, Aldenkamp AP, Kessels FG, de Kinderen RJ, & Majoie MJ (2012). The ketogenic diet as a treatment option in adults with chronic refractory epilepsy: Efficacy and tolerability in clinical practice. Epilepsy & behavior : E&B PMID: 22366051

Seyfried TN, Marsh J, Shelton LM, Huysentruyt LC, & Mukherjee P (2011). Is the restricted ketogenic diet a viable alternative to the standard of care for managing malignant brain cancer? Epilepsy research PMID: 21885251

Veggiotti P, Teutonico F, Alfei E, Nardocci N, Zorzi G, Tagliabue A, De Giorgis V, & Balottin U (2010). Glucose transporter type 1 deficiency: ketogenic diet in three patients with atypical phenotype. Brain & development, 32 (5), 404-8 PMID: 19515520

Thaler JP, Yi CX, Schur EA, Guyenet SJ, Hwang BH, Dietrich MO, Zhao X, Sarruf DA, Izgur V, Maravilla KR, Nguyen HT, Fischer JD, Matsen ME, Wisse BE, Morton GJ, Horvath TL, Baskin DG, Tschöp MH, & Schwartz MW (2012). Obesity is associated with hypothalamic injury in rodents and humans. The Journal of clinical investigation, 122 (1), 153-62 PMID: 22201683

If you’re in good enough shape to read this post then I’m sure you’re just fine, but…well, it’s worth a look to see what the latest research says about all that refined sugar and/or alcohol you just consumed.

1. You might not remember stuff. You would think that this is because of the alcohol, but actually, this one’s about the candy. New research in Behavioral Neuroscience shows that when people are on a high fat and refined sugar diet, they have significantly impaired hippocampal memory. This means that the people in the study had trouble forming new memories about their experiences…like what they had even eaten. Depending on how many Skittles you’ve been popping, there’s a chance you might not recall as much as you would have if you’d opted for tricks instead of treats.

2. You might have ended up in the hospital. I don’t mean from alcohol poisoning, although that’s certainly the case for some, but I’m referring to alcohol-related injuries. A recent data analysis exercise estimates that a whopping 21% of hospitalized injuries are attributable to alcohol. A heavy drinker with alcohol in his/her system is anywhere between 4 and 7 times as likely to end up in the hospital with an injury when compared to someone who hasn’t hit the bottle. “But I’m not a heavy drinker!” you say. Turns out, moderate drinkers suffer more injuries per hour with alcohol in their systems than heavy drinkers do, and the occasional binge definitely raises hospital injury risk.

3. You might have had a fight with your significant other. A study in New Zealand found that alcohol was involved in more than 25% of altercations between intimate partners. Women were more likely to report anger, fear, and severity of aggression while feeling victimized, and the perceived severity was significantly greater if the male partner had been drinking. However, men and women claimed approximately equal rates of being the victim or the perpetrator of the aggression. You see, when alcohol’s involved in lovers’ spats, nobody wins.

4. You might have kick-started your heart disease. I hate to scare you, but a science journal called Atherosclerosis probably knows what it’s talking about. Researchers in New York took mice and divided them into three groups: group 1 had two drinks per day, seven days a week (“daily-moderate” drinkers; blood alcohol content 0.07%); group 2 had seven drinks per day, two days a week (“weekend-binge” drinkers; blood alcohol content 0.23%); group 3 had no alcohol (same number of calories, though). While good and bad cholesterol levels rose in both drinking groups, bad cholesterol went up significantly more in the binge-drinking mice. And although the researchers induced atherosclerosis (clogging of the arteries of the heart) in all groups, the moderate-drinking mice actually had smaller atherosclerotic plaques than the no alcohol group; plaque volume was significantly greater in the weekend-binging mice.

Don’t kill the messenger, folks! But do be safe the next time you’re out having your candy- and alcohol-fueled party nights. Your memory/uninjured body/significant other/arteries will thank you.

Stay nerdy! And look way over to the right hand side of the site – you can like us on Facebook, follow us on Twitter, and subscribe to our RSS. Everybody wins!

Francis HM, & Stevenson RJ (2011). Higher reported saturated fat and refined sugar intake is associated with reduced hippocampal-dependent memory and sensitivity to interoceptive signals. Behavioral neuroscience PMID: 22023100

Miller TR, & Spicer RS (2011). Hospital-Admitted Injury Attributable to Alcohol. Alcoholism, clinical and experimental research PMID: 22004026

Connor JL, Kypri K, Bell ML, & Cousins K (2011). Alcohol involvement in aggression between intimate partners in New Zealand: a national cross-sectional study. BMJ open, 1 (1) PMID: 22021745

Liu W, Redmond EM, Morrow D, & Cullen JP (2011). Differential effects of daily-moderate versus weekend-binge alcohol consumption on atherosclerotic plaque development in mice. Atherosclerosis PMID: 21930274

Though this blog has already featured insects more than I would have imagined (i.e. at all), this post is about something I really feel the need to share. Because, every so often, I come across something for which the research is so overwhelmingly positive, I’m shocked that it’s not more well-known.

If you want to know what bees are up to now that could significantly impact human health, click on.

In short, bees are collecting this stuff called propolis. They collect it from plants and it’s sort of like sap, but apparently way more awesome. Bees use it to patch up the smaller holes in their hives, but researchers are using it on…everything.

1. Propolis and diabetes. In China, researchers gave propolis capsules to rats with type 2 diabetes. At the end of the experiment, rats who received propolis had significantly less sugar and fat in their blood, and more insulin, compared to diabetic mice who didn’t get propolis. Not bad for bee spackle. Given that almost 10% of the U.S. has diabetes, we need all the help we can get against this condition.

2. Propolis and ulcers. Stomach ulcers are no fun; they’re painful and can cause a lot of vomiting. Although 60% of stomach ulcers are caused by bacteria in the stomach, some cases occur after a person receives radiation, as with cancer treatment. So some compelling work in Egypt found that if mice were given propolis orally one hour before receiving radiation, they were largely protected against the formation of stomach ulcers. In fact, propolis-treated mice developed a whopping 75% fewer ulcers than untreated mice.

3. Propolis and burns. Anyone who has had a second-degree burn probably wouldn’t wish it on his worst enemy. Interestingly, researchers are still exploring what the best dressing is for these burns. A few weeks ago, a team in Brazil tried propolis. You’ve probably caught onto this pattern, but applying 5% propolis to second-degree burns on rats decreased inflammation and increased the rate of tissue repair. Look at this graph:

Pessolato et al. "Propolis and amnion reepithelialise second-degree burns in rats." Burns. July 6, 2011. Figure 6.

See those black bars that are way taller than the other bars? That’s showing the fact that burns treated with propolis produced a lot more collagen than untreated (gray bars) or tissue-grafted (white bars) burns after 1, 2, and 3 weeks into the experiment. Impressive stuff.

4. Propolis and atherosclerosis. I don’t think I need to give much preamble about atherosclerosis, but basically it’s when arteries become blocked because of fatty deposits, and it’s a serious risk factor for heart attacks. Lo and behold, when a different group from Brazil gave propolis to atherosclerotic mice, the condition of the animals improved. These mice were genetically predisposed to have high cholesterol and they were fed a high cholesterol diet to induce atherosclerosis. After 4 weeks of being given extracts from various types of propolis, the mice were sacrificed and mice who received propolis treatment had better ratios of good to bad cholesterol, and had smaller areas of atherosclerotic build-up.

Finally, if you still need more convincing…

5. Propolis and cancer. Glioblastoma is the most common and most detrimental type of brain tumor in humans. People with glioblastomas tend to only survive 1 or 2 years with treatment (3 months without). That’s why it’s pretty exciting that researchers in Brazil (Brazil is really on top of propolis) found that propolis slowed the growth of glioblastoma cells in their lab. Propolis was effective alone, and even more so in combination with a standard brain tumor drug.

What can’t propolis do? Glioblastoma isn’t the only form of cancer against which propolis has proven effective. These five scenarios I’ve described aren’t the only conditions in which propolis has been a successful treatment. I encourage you to do your research if you’re interested:

And/or consider picking up a bottle of the stuff:

If the research didn’t back it up, I wouldn’t advocate for it.

Li Y, Chen M, Xuan H, & Hu F (2012). Effects of encapsulated propolis on blood glycemic control, lipid metabolism, and insulin resistance in type 2 diabetes mellitus rats. Evidence-based complementary and alternative medicine : eCAM, 2012 PMID: 21716678

El-Ghazaly MA, Rashed RR, & Khayyal MT (2011). Anti-ulcerogenic effect of aqueous propolis extract and the influence of radiation exposure. International journal of radiation biology PMID: 21745002

Pessolato AG, Martins DD, Ambrósio CE, Mançanares CA, & de Carvalho AF (2011). Propolis and amnion reepithelialise second-degree burns in rats. Burns : journal of the International Society for Burn Injuries PMID: 21741176

Daleprane JB, da Silva Freitas V, Pacheco A, Rudnicki M, Faine LA, Dörr FA, Ikegaki M, Salazar LA, Ong TP, & Abdalla DS (2011). Anti-atherogenic and anti-angiogenic activities of polyphenols from propolis. The Journal of nutritional biochemistry PMID: 21764281

Borges KS, Brassesco MS, Scrideli CA, Soares AE, & Tone LG (2011). Antiproliferative effects of Tubi-bee propolis in glioblastoma cell lines. Genetics and molecular biology, 34 (2), 310-4 PMID: 21734835

Because many complications can occur with any type of transplant, one example being immune rejection, stimulating the body’s own stem cells to make new heart cells would be ideal. This idea serves as the motivation for this entry’s article.

Title: De novo cardiomyocytes from within the activated adult heart after injury

Authors: Nicola Smart, Sveva Bollini, Karina N. Dubé, Joaquim M. Vieira, Bin Zhou, Sean Davidson, Derek Yellon, Johannes Riegler, Anthony N. Price, Mark F. Lythgoe, William T. Pu & Paul R. Riley

Date of publication: June 8, 2011

Direct link: ttp://www.nature.com/nature/journal/v474/n7353/full/nature10188.html

PMID: 21654746

Abstract: Knowing that there are several limitations to cell transplantation as a means of replacing damaged heart tissue following a heart attack, these researchers set out to try to identify a pool of stem cells in the adult heart that could potentially be utilized to restore damaged heart tissue from within. The authors ultimately found that these adult stem/progenitor cells could be identified by the expression of a gene called Wt1, which was turned on after treating with a peptide (essentially a small version of protein) called thymosin b4. These progenitor cells are suggested to have derived from the epicardium, which is the outer layer of the heart. Stimulating these adult stem cells with thymosin b4 caused them to integrate with damaged heart tissue and become mature cardiomyoctyes (heart muscle cells). Developing a way to utilize these inherent progenitor cells to help mend a damaged heart would be a powerful way to minimize the use of drugs or the need for transplanted tissue.

Methods: The authors made use of mice whose cells would turn green if the Wt1 gene was turned on – recall, the hypothesis is that if Wt1 is turned on in a cell, then that cell may be a heart stem cell. The fact that the cells would turn green when the gene turned on allowed for easier studying of those particular cells later. Mice were injected for 7 days with thymosin b4, because it had previously been shown to improve the function of heart stem cells, before being induced to have a myocardial infarction (heart attack). The researchers induced heart attacks by anesthetizing the mice and then sealing off a major artery of the heart (the left anterior descending artery).  At 2, 4, 7, or 14 days after sealing the artery, the heart was removed and those green progenitor cells could be studied within the heart tissue or isolated from the tissue. Additionally, the authors used some of these isolated stem cells to transplant them into other mice that had had heart attacks, to see if the stem cells could improve the condition of the mice.

Results: Mice pretreated with thymosin b4 before myocardial infarction had significantly more progenitor-like cells in their hearts after myocardial infarction, compared to mice that did not receive these injections. Although mice injected with a negative control did show an increase in progenitor cells following a heart attack, thymosin b4 significantly increased this response. The authors could see that these cells had traveled to the scar on the heart caused by the heart attack, and had started to express some of the genes specific to heart cells – meaning that the stem cells were turning into heart tissue and helping to heal. The progenitor cells isolated from one mouse and transplanted into the heart region of another mouse that had had a heart attack started to turn into heart cells and help to heal the injury in the heart of the recipient mouse as well.

Bottom line: In mice, which are clearly not humans but are the most closely related common lab animal, these researchers identify a pool of cells in the heart with the ability to generate additional heart cells following a heart injury, and this ability is significantly enhanced by the peptide thymosin b4. Although thymosin b4 treatment was not as efficient as an ideal human cell-based therapy would be, the work in this article justifies the search for other molecules that can similarly increase the response of progenitor cells in our hearts to heal and replace the damaged heart tissue that results from heart attacks.

Interesting fact: Working with mice is expensive. Maintaining a mouse cage costs $1-2 per day. Just 30 mouse cages, which this work seemed like it would have needed, at least, would cost $10,950-$21,900 for one year of research. And it is typical for the research in a major publication to represent at least a year’s worth of work, if not four or more.

Stem cells: To make a human, or most any other animal, the first step is sperm meeting egg. The two cells fuse and since each one contains half the genetic information for a whole animal, the fused sperm and egg are considered one cell, called a “zygote.” Obviously an animal is ultimately made up of more than one cell, so the zygote needs to divide to become two cells, then four, then eight, then sixteen, and so on. From that one zygote, there needs to be created a heart, skin, lungs, bone – many kinds of tissues. To get from one cell to many different kinds of cells, many of the early embryonic cells are stem cells or have varying potencies to divide and produce other types of cells (“other types of cells” can include heart cells, fat cells, kidney cells, and even other stem cells). Even as an adult, some of our tissues retain a small population of stem cells so that in the event of injury, for example, damaged tissue can be remade.

 
Smart N, Bollini S, Dubé KN, Vieira JM, Zhou B, Davidson S, Yellon D, Riegler J, Price AN, Lythgoe MF, Pu WT, & Riley PR (2011). De novo cardiomyocytes from within the activated adult heart after injury. Nature, 474 (7353), 640-4 PMID: 21654746