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No, Skipping Breakfast Doesn’t Lead to Heart Disease

When reading through a list of headlines from one of my favorite health news sites, there was an article titled “Could Skipping Breakfast Feed Heart Disease?” I had to click it. Typically, I don’t eat breakfast (stay tuned for a future post for reasons why) so scientific evidence showing that it could put me at risk for one of the biggest health demons of our time meant that a change of habits may be due. Did the science show that there was truly something inherent with skipping breakfast that could do this? It didn’t despite the seemingly straightforward title.

Another breakfastThe title of the study itself was “The Importance of Breakfast in Atherosclerosis Disease” and they concluded that skipping breakfast could serve as a marker for atherosclerosis (heart disease). It’s no secret that authors will use bold article titles to draw in viewers, but consequently, these titles can be very misleading. I recommend that everybody read the study thoroughly to learn a lesson about why headlines can be misleading. While there were many problems with the study, I will be highlighting a few that I found to be most significant.


First, the sample size of the study was incredibly limited. The researchers were able to acquire a fairly large number of participants, but those participants were all employees of a single company located in Madrid, Spain. In order to extrapolate a study’s findings to all people, it is necessary to examine a more diverse population. With diversity aside, another issue is the lack of uniform distribution among the participants. Of the 4,052 participants, only 2.9% skipped breakfast while 69.4% ate a low-calorie breakfast and 27.7% ate a high-calorie breakfast. This means that although the sample size was fairly large, the researchers came to their conclusion based off of 118 individuals that skipped breakfast. Statistically, a sample size of 118 isn’t enough to make any definitive conclusions.


Another problem with the study is how they classified the skipping breakfast group. They classified skipping breakfast as consuming less than 123 calories, which could constitute 300 mL of orange juice or coffee with 20 grams of added sugar still counted as skipping breakfast. This means that someone could immediately start the day with an unhealthy intake of refined sugar and still be counted as not eating breakfast. This is concerning because it is common knowledge that consuming too much refined sugar causes inflammation and may lead to various chronic diseases. The researcher’s definition of skipping breakfast leads to a predisposition for the condition they are testing for, which makes it even more difficult to trust their conclusion.

These grounds alone are enough to doubt the conclusions found in the study, but there is another, more disturbing flaw in their research. As stated by the researchers, the group that skipped breakfast proportionally had the highest rates of smoking, alcohol consumption, and highest amounts of processed food consumed. All of these habits are commonly linked with heart problems and further diminish the ability of the study to specifically correlate skipping breakfast to heart disease. In order to come to a conclusion, it would be necessary that all of the individuals in the study have similar habits related to health.

Science is one of the best vehicles for driving the advancement of knowledge, but it can sometimes fall victim to misinformation. The original article I clicked on and the study discussed above serve as a perfect example of this fact and shows why every study must be evaluated critically. While participants who skipped breakfast were more likely to show early signs of heart disease, the problems with how the study was conducted don’t allow for a conclusion to be made.

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Uzhova, Irina, et al. “The Importance of Breakfast in Atherosclerosis Disease.” Journal of the American College of Cardiology, vol. 70, no. 15, 2017, pp. 1833–1842., doi:10.1016/j.jacc.2017.08.027.

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The New Frontier for Urban Health

When approaching a large city, you might see a monstrous, brown plume surrounding it. You could take a guess that whatever it is would consequently be considered the opposite of a healthy environment. That would be correct. This is alarming given that the United Nations approximated 82% of North Americans live in urban ecosystems[3]. Fortunately, there have been significant steps taken to reduce the amount of engine exhaust emissions, which has already drastically improved the air quality in most urban areas. Unfortunately, one aspect of air pollution which may be even more detrimental to public health has not received nearly enough attention. City pollution

On average, non-exhaust(NE) emissions from vehicles and roads may contribute up to 50-85% of total emissions that come from vehicles[1], depending on location. The category of NE emissions is broad, containing brake dust, tire breakdown material, road dust and much more [2]. Unlike engine exhaust emissions that come out of the tailpipe, NE emissions have received just a fraction of the awareness, which directly correlates to the amount of research being done on health implications and technology advances.

A notably alarming aspect of NE emissions is the potential damage that could be done to human health. The particulate matter from this source, in contrast to engine exhaust emissions, is very large and often contains heavy metals [1]. Some of these chemicals are known carcinogens and/or reactive oxygen species, which are known to cause many other diseases (heart disease, Alzheimer’s, atherosclerosis, etc.) and inflammation of the lungs [2]. One of the only changes to curb the damage done from NE emissions have been outlawing the use of asbestos [2] which is significant but doesn’t come close to solving the problem.

While it may be overlooked, even living near a freeway can contribute to serious adverse health conditions. Data from 5 randomized double-blind studies were used to show associations between developing cardiovascular disease and living near highways. In a study of 1483 people who lived within 100 meters or 328 feet of a Los Angeles highway, researchers used ultrasound to measure the thickness of the carotid artery every 6 months for 3 years. They found that those who lived within 100 meters of the freeway had accelerated thickening of the artery, double what the other participants had[4].


As time marches on, the population living in urban areas worldwide is projected to reach 66% by 2050[3]. This isn’t all bad. It means that many countries are furthering their development and thus acquiring new technologies. As a result, there will be an inundation of opportunity and better quality of life, but this is accompanied by threats that cannot go unaddressed. In developed regions, moving to a city enhances your ability to reach a substantial amount of people, unlocks many forms of new entertainment, and simply gives you more options for your life. For now, there isn’t much that can be done besides being conscious of the potential risks posed by living near busy streets or highways. We must also stay optimistic, hoping that an increase in research and technology will reduce these NE emissions so that living in an urban environment can be done sustainably and with good health.

If you liked this article, follow us to get notifications when new posts are published! Also, if you have anything you’d like to let us know about, feel free to contact us.


[1] Amato, Fulvio, et al. “Urban Air Quality: The Challenge of Traffic Non-Exhaust Emissions.” Journal of Hazardous Materials, vol. 275, 2014, pp. 31–36., doi:10.1016/j.jhazmat.2014.04.053.

[2] Grigoratos, Theodoros, and Giorgio Martini. “Brake Wear Particle Emissions: a Review.” Environmental Science and Pollution Research, vol. 22, no. 4, 2014, pp. 2491–2504., doi:10.1007/s11356-014-3696-8.


[4] 3 Mar 2010: Künzli N, Jerrett M, Garcia-Esteban R, Basagaña X, Beckermann B, et al. (2010) Correction: Ambient Air Pollution and the Progression of Atherosclerosis in Adults. PLOS ONE 5(3): 10.1371/annotation/21f6b02b-e533-46ca-9356-86a0eef8434e. View correction

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Sulforaphane: A Real, Scientifically Backed Superfood

With all the buzz circulating around “superfoods” on the internet and in health shops, the topic can get a bit confusing. What even is a superfood in the first place? How did these foods get their title? What evidence is there to support that the superfood at hand would be a good incorporation into your daily diet? I know it used to confuse the hell out of me, to the point where I gave up on trying to find “the one”.


Many articles that I read would start off with some version of how the new superfood would cure all of your diseases, make you live twice as long and give you the body you’ve always wanted. Then, somewhere near the end, there would be a convenient link to buy this new superfood or supplement. This is unfortunate because there are some real foods out there that could possibly yield incredible benefit.

Despite the fog when it comes to superfoods, one can find their way to the truth through using real scientific evidence. There are actually foods out there that can significantly reduce your chances of getting cancer, protect your cells from harm, lower your chances of developing conditions like heart disease and diabetes, all while decreasing your rate of aging. Currently, a growing body of scientific evidence supports these claims along with a host of other benefits through the incorporation of foods containing a compound called sulforaphane(SFN) just 3-5 times per week!


This may sound a bit technical, but a simple overview of where SFN comes from and how our bodies process it will be useful to help you get the most out of this article. First, we don’t obtain much sulforaphane from food itself, but rather a compound called glucoraphanin(GRA) from food along with the enzyme myrosinase (fun fact: your gut bacteria actually make some myrosinase as well!). Once inside your body, GRA is turned into sulforaphane by myrosinase. Then, SFN is free to run around your body fixing stuff!

SFN diagram

GRA and myrosinase are found in many cruciferous vegetables (broccoli, cauliflower, cabbage, etc…), but they are most abundant in broccoli and exponentially more abundant in broccoli sprouts [14].


So now you know a little bit about SFN, but you are most likely reading this to find out how SFN can actually help you. Lucky for us, there are literally too many studies to read that have been done on SFN, but there are some common themes. Below you will find some of my most interesting findings.

Cancer Prevention

Cancer is one of the biggest public health fears of our time, and SFN is here to help! There are many recent studies relating SFN to reduced cancer incidence, so you don’t just have to trust the internet. One such study showed that eating 3-5 large portions was correlated to a decrease of 30-40% in cancer development. Even consuming as little as 1 portion was shown to help [16]. In accordance with this amazing benefit, SFN was also able to reduce cancer progression through gene regulation and by limiting the amount the unwanted cells are able to grow [17].

Furthermore, another interesting way that SFN helps prevent cancer is that it can protect against UV light from the sun or other unnatural sources. In mice, a SFN cream was applied to their skin, which was able to decrease damage and slow tumor progression by 50% [18].  It does so by directly repairing DNA that was deformed by UV light [11] and enhancing cellular defenses [2]. The next time you feel a sunburn coming on, instead of grabbing the aloe you might be better off reaching for the broccoli sprouts! On a related note, SFN was also shown to repair DNA damage caused by pesticides [11], which we inevitably encounter on a daily basis. Many forms of cancer stem from DNA damage, so repairing it is crucial.


When SFN was administered to mice, there was a significant decrease in proinflammatory markers [1]. SFN was actually able to change how our body’s DNA creates inflammatory responses. Keeping inflammation in the body under control is crucial to defending yourself from various unwanted conditions like heart disease, joint pain, and aging. It was also shown to reduce inflammation in the brain, which may help lower your chance of developing diseases in the brain such as Alzheimer’s and Parkinson’s [7].  As a part of this process, SFN was also able to directly protect neurons from damage in mice [8].

Antioxidant Properties

Look at any fruity drink and you will likely see it being marketed as containing super antioxidants. There are good reasons for looking for antioxidants, but unfortunately, the juice concentrate you are about to drink will most likely have negligible effects. SFN, on the other hand, gets many of its favorable properties from being a very powerful antioxidant that can rid our bodies of reactive oxygen species and many other pollutants.

Reactive oxygen species (ROS) are detrimental to cells and DNA which can then lead to disease and faster aging. Because of this, getting rid of them is important. Luckily for us, many studies have shown that SFN is VERY good at getting rid of these ROS in the body [3].  Regarding ROS, there was also a study done on mice that shows specifically how SFN protects cells from damage [4]. This was shown to be especially important for improving liver function in humans[9].

As a powerful antioxidant, SFN can also help your body rid itself of harmful toxins, specifically airborne pollutants. If you live in a city or anywhere near one, this is important. It has been shown that an increased intake of SFN was linked to inhaled air pollutants leaving the body 20-50% more than the baseline [10]. This is essential because the harm that they are able to do is greatly limited. SFN was also correlated to a decrease in the severity of many allergenic diseases such as asthma by protection from airborne pollutants [13].


Maintaining a healthy cholesterol profile is common knowledge in the process of keeping your heart in good condition and regulating hormones, among other things. SFN, once again, can help us out in this category. One study found a correlation between participants who consumed 10 grams of broccoli sprout powder and a significant reduction in LDL (the bad stuff) while raising HDL (the good stuff) [5]. In addition, the same findings have also been demonstrated in other studies in as little as a week of consuming broccoli sprouts[6].

Immune System

As we age, there is an increased risk of falling victim to pathogens and other problems that occur with a weakened immune system. SFN was also able to slow the degradation of immune cells that occurs with age from oxidants in mice through being a powerful antioxidant as discussed earlier. It also helps by increasing the hormonal messengers that activate the immune system [4].

Sexual Health

This aspect of SFN is less studied, but still important nonetheless. In mice that had testicular cancer and other reproductive damage from environmental toxins, high doses of SFN were able to significantly increase testosterone, sperm count and sperm quality [12].


By this point, I hope that you have been convinced to include more cruciferous veggies into your diet, specifically broccoli and broccoli sprouts (my preference). Even throwing a handful into a smoothie in the morning could lower your risk of cancer and many other diseases. Don’t forget an increased immune system and slower cellular aging as well.

While there are a lot of studies and implications above, there are numerous studies that could have been chosen accompanied by a much deeper analysis. For this reason, if you want a more in-depth approach to the mechanisms and pathways affected by SFN, I encourage you to check out where I was first introduced to SFN: Dr. Rhonda Patrick’s blog and podcast at

If you liked this article, follow us to get notifications when new posts are published! Also, if you have anything you’d like to let us know about, feel free to contact us.


[1] Townsend, Brigitte E., and Rodney W. Johnson. “Sulforaphane Reduces Lipopolysaccharide-Induced Proinflammatory Markers in Hippocampus and Liver but Does Not Improve Sickness Behavior.” Nutritional Neuroscience, vol. 20, no. 3, July 2015, pp. 195–202., doi:10.1080/1028415x.2015.1103463.

[2] Benedict, A. L., et al. “The Indirect Antioxidant Sulforaphane Protects against Thiopurine-Mediated Photooxidative Stress.” Carcinogenesis, vol. 33, no. 12, 2012, pp. 2457–2466., doi:10.1093/carcin/bgs293.

[3] Tortorella, Stephanie M., et al. “Dietary Sulforaphane in Cancer Chemoprevention: The Role of Epigenetic Regulation and HDAC Inhibition.” Antioxidants & Redox Signaling, vol. 22, no. 16, 2015, pp. 1382–1424., doi:10.1089/ars.2014.6097.

[4] Kim, Hyon-Jeen, et al. “Nrf2 Activation by Sulforaphane Restores the Age-Related Decrease of TH1 Immunity: Role of Dendritic Cells.” Journal of Allergy and Clinical Immunology, vol. 121, no. 5, 2008, doi:10.1016/j.jaci.2008.01.016.

[5] Bahadoran, Zahra, et al. “Broccoli Sprouts Powder Could Improve Serum Triglyceride and Oxidized LDL/LDL-Cholesterol Ratio in Type 2 Diabetic Patients: A Randomized Double-Blind Placebo-Controlled Clinical Trial.” Diabetes Research and Clinical Practice, vol. 96, no. 3, 2012, pp. 348–354., doi:10.1016/j.diabres.2012.01.009.

[6] Murashima, Megumi, et al. “Phase 1 Study of Multiple Biomarkers for Metabolism and Oxidative Stress after One-Week Intake of Broccoli Sprouts.” BioFactors, vol. 22, no. 1-4, 2004, pp. 271–275., doi:10.1002/biof.5520220154.

[7] Holloway, Paul M., et al. “Sulforaphane Induces Neurovascular Protection against a Systemic Inflammatory Challenge via Both Nrf2-Dependent and Independent Pathways.” Vascular Pharmacology, vol. 85, 2016, pp. 29–38., doi:10.1016/j.vph.2016.07.004.

[8] Schachtele, Scott J., et al. “Modulation of Experimental Herpes Encephalitis-Associated Neurotoxicity through Sulforaphane Treatment.” PLoS ONE, vol. 7, no. 4, 2012, doi:10.1371/journal.pone.0036216.

[9] Kikuchi, Masahiro. “Sulforaphane-Rich Broccoli Sprout Extract Improves Hepatic Abnormalities in Male Subjects.” World Journal of Gastroenterology, vol. 21, no. 43, 2015, p. 12457., doi:10.3748/wjg.v21.i43.12457.

[10] Kensler, Thomas W., et al. “Modulation of the Metabolism of Airborne Pollutants by Glucoraphanin-Rich and Sulforaphane-Rich Broccoli Sprout Beverages in Qidong, China | Carcinogenesis | Oxford Academic.” OUP Academic, Oxford University Press, 1 Nov. 2011,            

[11] Topè, Avinash M., and Phyllis F. Rogers. “Evaluation of Protective Effects of Sulforaphane on DNA Damage Caused by Exposure to Low Levels of Pesticide Mixture Using Comet Assay.” Journal of Environmental Science and Health, Part B, vol. 44, no. 7, 2009, pp. 657–662., doi:10.1080/03601230903163624.

[12] Yang, Shu-Hua, et al. “Sulforaphane Prevents Testicular Damage in Kunming Mice Exposed to Cadmium via Activation of Nrf2/ARE Signaling Pathways.” International Journal of Molecular Sciences, vol. 17, no. 10, Nov. 2016, p. 1703., doi:10.3390/ijms17101703.

[13] Heber, David, et al. “Sulforaphane-Rich Broccoli Sprout Extract Attenuates Nasal Allergic Response to Diesel Exhaust Particles.” Food Funct., vol. 5, no. 1, 2014, pp. 35–41., doi:10.1039/c3fo60277j.

[14] West, Leslie G., et al. “Glucoraphanin and 4-Hydroxyglucobrassicin Contents in Seeds of 59 Cultivars of Broccoli, Raab, Kohlrabi, Radish, Cauliflower, Brussels Sprouts, Kale, and Cabbage.” Journal of Agricultural and Food Chemistry, vol. 52, no. 4, 2004, pp. 916–926., doi:10.1021/jf0307189.

[16] Jeffery, Elizabeth H., and Anna-Sigrid Keck. “Translating Knowledge Generated by Epidemiological And in-Vitro studies into Dietary Cancer Prevention.” Molecular Nutrition & Food Research, July 2008, doi:10.1002/mnfr.200700226.

[17] Singh, Shivendra V., et al. “Sulforaphane-Induced G2/M Phase Cell Cycle Arrest Involves Checkpoint Kinase 2-Mediated Phosphorylation of Cell Division Cycle 25C.” Journal of Biological Chemistry, vol. 279, no. 24, Aug. 2004, pp. 25813–25822., doi:10.1074/jbc.m313538200.

[18] Dinkova-Kostova, Albena T., et al. “Protection against UV-Light-Induced Skin Carcinogenesis in SKH-1 High-Risk Mice by Sulforaphane-Containing Broccoli Sprout Extracts.” Cancer Letters, vol. 240, no. 2, 2006, pp. 243–252., doi:10.1016/j.canlet.2005.09.012.