The role of nutrition on acne

I had my first climb in a bit over a week after being sick, man I feel weak! Hopefully I’ll be back to normal in a couple of climbing sessions; good to be back either way. Other than that, I’ve been spending most of the last couple of days working or watching Smallville lol :p. Good show!

2012 has been, so far, the year with the most personal changes for me. I doubled up my Zoology major with Nutrition (I’m so glad for that!). I spent almost every day between May-September climbing outside; I can now rough it like no one else (people who’ve camped with me in the tail end of the summer would definitely agree lol). I ended my first serious relationship, I think I learnt more about myself within the few months following than I have throughout all of university lol (another factor that led me to doubling up my major!). I quit my job at a restaurant where I hadn’t been treated fairly only to find a few amazing jobs! I worked with an ‘outdoor adventure’ company throughout the summer with some absolutely amazing people. After the warm season was up, I decided to apply for a nutrition job and was lucky enough to get it; another amazing work place where I continue to learn every day! And finally, I decided to start a blog; I`ve had some amazing followers who have continually encouraged me to keep writing. All around, a very exciting year! I can only imagine what 2013 will bring after I`m graduated! It`s scary to think that I have no idea where I`ll be come June, but I have faith that things will work out for the best like they have so far!

Anyways, here’s a picture of me using my rest on a ledge in Kentucky- photo cred’s to my friend Liz


Acne is an epidemic that effects 85% of teenagers and persists into adulthood for about half of us. Environmental acne promoters (including diet) persist after puberty and drive adult acne. It is a distressing condition that often comes with depression, anxiety and significant physiological disability. So with that said, this post will be about the role of nutrition in acne (something that dermatologists should 100% consider).

So why is there such a rise in acne? The western diet is characterized by a high caloric, high glycemic, high fat, high meat and high dairy intake. These high intakes stimulate an increase in insulin and insulin growth factor-1 which will lead to an over activation of nutrient-sensitive enzymes (mTORC1). The increased mTORC1 activation is one of the major contributors for the slew of common modern day chronic diseases (e.g. obesity, diabetes, cancer). The over-activated mTORC1 will result in an increase in both fat production and androgen hormones (e.g. testosterone) which ultimately result in acne (and other problems). Our skin is a good indicator for our internal health, which is why we should be addressing our overall health when dealing with acne (in my opinion anyways).

In recent research, the reduction of high glycemic foods has been confirmed to improve acne, the rate of sebum excretion and androgen hormone content. An example of this can be seen in populations following paleolithic diets (e.g. certain indigenous populations) that are lower overall in glycemic loads. Acne is virtually absent; they have lower insulin levels because of the low glycemic load of their diets and as a result have lower rates of mTORC1 driven diseases. Although there`s overwhelming evidence for the role of diet in acne, this role is highly controversial and as a result, dermatologists still turn to drugs before considering nutrition.

I’ll say it again to keep driving my point home; acne prevention can be achieved through a reduction of mTORC1 activation. So how do we do that? A dietary intervention for acne can include the following; decreased calories, decreased high sugar products, decreased dairy, increased fruits and vegetables and potentially decreased meat consumption. The above would effectively decrease the mTORC1 activation. Vegan and paleolithic diets that are high in vegetables and fruits and excluding refined sugar, high-GI grains and dairy have been shown to improve insulin sensitivity and are therefore good options for treating acne. I strongly believe that dermatologists should be responsible for providing appropriate advice, before pushing drugs, which may save patents from other mTORC1 diseases later in life (e.g. obesity, diabetes, cancer).

Unfortunately, nutrition is not a common prescription given by dermatologists. Many of us have turned to a dermatologist and were then prescribed chemicals, antibiotics, birth control or even Accutane; all come with health risks like any other drug and don’t necessarily confront the root of the problem. ”Pop this pill a few times a day and you’ll be cured”, a common theme in modern medicine. I have a particular issue with this system because I was one of those teenagers who turned to a dermatologist and ultimately went through a large period of health problems (which were solved, after seeing a number of medical specialists, by my own research and a change in my diet). Why are we putting ourselves at any risk at all when finding a healthier diet free of risk would potentially resolve our problems? This continues to confuse me and has led me to be extremely leery of certain health care professionals.

So a wrap up; if you are suffering from acne, before turning to a drug, try a changeup in your diet. Try to reduce the glycemic load of your diet, maybe take out milk and up your intake of fruits and vegetables. Although a diet change is much harder than just taking medicine, your body will thank you in no time! And that marks the end of my post, hopefully you enjoyed reading it! Hope all of you have an excellent day! :)

Cordain L. (2005) Implications for the role of diet in acne. Semin. Cutan. Med. Surg.24;84-91.

Melnik, B. (2012) Dietary intervention in acne: Attenuation of increased mTORC1 signaling promoted by Western diet. Dermato-Endocrinology 4:1, 20–32.

Reynolds R, Lee S, Choi J, Atkinson F, Stockmann K, Petocz P and Brand-Miller J. (2010) Effect of the Glycemic Index of Carbohydrates on Acne vulgaris. Nutrients, 2, 1060-1072; doi:10.3390/nu2101060.

Eating as a reward: why do we do it?

Hope you all had a merry Christmas!

A rough Christmas for my family and I, a stomach virus got us a couple of days before Christmas and is just starting to clear up. I guess I’ll have to find a way back home in the next few weeks so I can have a proper visit; I’m now on a train back to my home up north. Either way, I enjoyed having my sisters and parents, sick or not, around for the holidays :)

Also, I just wanted to thank you all for all of the support you`ve given me! I am astonished to have so much positive feedback from you guys, definitely positive reinforcement for me to continue blogging so often! I never expected to have so many followers, so again, thank you!

Oh and p.s., you can now follow me on facebook :D

Here’s a picture of me climbing in Ontario while it was still hot outside :)


Why do some people have no problems keeping their weight at a healthy range while for others it’s constant struggle? This post will be on eating as a reward and for pleasure, hope you enjoy!

There are strong regulatory mechanisms that maintain our body weight; we eat when our body needs the calories. In modern times though, many people eat not because they’re hungry but because of a hedonic drive; eating, when not hungry and despite large fat reserves, for pleasure. There’s a lot of controversy on whether food can be considered addictive with the neural component being a main argument in favor of food addictions. Readily accessible foods and sedentary lifestyles are major factors for obesity but the interactions between these factors and genetic predispositions are what are really important in the occurrence of obesity.

Food is often used as a reward or as a response to emotions or pain. This response is exaggerated through a lifetime of using food as a reward; when we give kids food for good behaviour we teach them bad behaviours for the future. The reward system will motivate us to eat tasty treats while the hedonic (pleasure) system will encourage us to keep eating. With our current surroundings with an increase in accessibility, advertisement and palatability, our brains react the way any animal’s brains would react due to our reward and hedonic systems. Many of our attitudes we have towards food comes from our childhoods, this makes it especially important for us to not reward kids with food.

So what do I mean by the reward system? In warm-blooded animals especially (like us), finding and eating food is a daily need that is high on our priority list even in a dangerous environment. Food as rewards is proposed to be the motivation needed to overcome difficult conditions. When seeking food, reward expectancy and effort as well as risk requirements will be accessed with the question ‘will I benefit overall?’ Seeing, smelling and finally tasting the first bite of food will give reward value feedback. Appetite is heightened by things like stomach acid and insulin secretion. Pleasure comes from olfactory (taste) sensations which drive consumption until satiety signals dominate (which can be down-regulated when we chronically over eat). Nutrient sensors in our digestive tract further enhance the reward interpretation after a meal (e.g. mice will learn to prefer sugar over water even when taste sensing is removed). Feelings of satisfaction linger after a meal; a number of sensory and emotional stimuli determine the rewarding experience derived from eating. Food as a reward is an adaptation in animals to enhance our survival.

Overeating can be explained by an over-activation of reward systems and decrease in satiety systems. There seems to be a reward deficiency with defective dopamine signalling in obese individuals (via genetics or non-genetic predispositions early in life or via diets high in sugar and fat or via obesity); increased food intake will occur in attempt to restore their set point for rewards. Obese individuals ‘like’ and ‘want’ palatable foods more than lean individuals (dependent on the effort necessary to get these foods). Obese individuals have a greater hedonic hunger along with a decreased perceived sweetness; ‘liking’ increases with increased sweetness as BMI increases. Clearly, overeating is multifactorial and hard to overcome especially in modern times.

Dieting has been shown to be difficult to adhere to by inducing strong feeling of hunger and cravings. Food deprivation will increase the reward value of foods. Higher-calorie foods will selectively increase the neural activity of the reward related areas of our brains and result in an increase in motivation to eat. A better method for weight loss would be not as restricting and therefore more prolonged; fast weight loss programs are definitely not the way to go when trying to achieve long term weight management.

So how can we overcome eating as a reward? Overeating can only be overcome by practicing self-control, which is hard in today’s day and age; allow yourself goodies every once in a while but limiting its amount. Creating healthy habits can be another powerful tool for reducing the use of food as a reward. Finding other rewards e.g. get a nice haircut or treat yourself to a spa day. Lastly, ensuring balanced meals and adequate calories throughout the day would help overcome overeating.

And some concluding thoughts; in normal circumstances, energy balance is tightly regulated but in modern times mental and emotional factors can overpower these regulations for energy balance. A greater understanding of these interactions can be a valuable tool in future therapies for obesity. Tasty foods are rewarding by the pleasure and satisfaction that is derived from them, which is an easy go-to relief from our increasingly stressful lifestyles. Hopefully this has been an eye opener for the reason we’re compelled to overeat!

Hope you all had a merry Christmas!


Avena NM, Rada P, Hoebel BG. (2009) Sugar and fat bingeing have notable differences in addictive-like behavior. J. Nutr.;139:623–628.

Berthoud H. (2002) Multiple neural systems controlling food intake and body weight. Neurosci. Biobehav. Rev.;26:393–428.

Berthoud H. (2011) Metabolic and hedonic drives in the neural control of appetite: Who’s the boss? Curr Opin Neurobiol.; 21(6): 888–896.

Berthoud H, Zheng H, and Shin A. (2012) Food reward in the obese and after weight loss induced by calorie restriction and bariatric surgery. Ann N Y Acad Sci.; 1264(1): 36–48.

Ravussin E, Bogardus C. (2000) Energy balance and weight regulation: genetics versus environment. Br. J. Nutr.;83(Suppl 1):S17–S20.

Gluten free diet: is it right for you?

And I’m home! Four days with my family before I have to make my way back to where I live now :). The presentation to the high school kids went really well! I’ll be going back again next semester to give another talk :)… hopefully by the time I graduate I’ll be a pro at public speaking!

My grandpa is in the hospital and so my family and I are doing ‘project clean grandpas house’ before he’s released; hopefully it will be a nice surprise for him! Should be a very busy day!

Here’s a picture taken of me at my climbing gym :)


Anyways…This post will be on gluten, gluten sensitivity and gluten free diets! Hope you enjoy :)

Gluten consumption has increased over time and as a result has led to an increased awareness of coeliac disease (CD).CD is characterized by an increased immune response to gluten in genetically susceptible people. Today, CD is thought to affect 1% of all adults; it is more common in adults than in kids. People with CD have a higher risk for deficiencies, reduced bone density, cancer and death; treatment consists of strict adherence to a gluten-free diet (GFD) which is shown to help reduce symptoms and improve mortality rates. Until recently, gluten was only associated with a wheat allergy or CD; for this reason, typical CD individuals who had normal antibodies and histology were advised to keep eating gluten foods (because gluten was ‘determined’ to not be the cause of their problems). The majority of people who seek medical attention for GI symptoms from gluten don’t have CD or a wheat allergy. Evidence is growing though that these individuals will still benefit from a gluten free diet since their symptoms are, regardless, associated with their gluten consumption.

There are now three gluten induced conditions: CD, wheat allergy and non-coeliac gluten sensitivity (NCGS). These conditions have a wide range of symptoms which indicates that gliadin (from gluten) is handled in many ways by our immune systems and that the mechanisms are still largely unknown. In CD, the small intestinal permeability is much higher and allows harmful invaders to pass through. An activation of both our innate and adaptive immune response occurs; ultimately there will be small intestinal wall damage and a rise in certain antibodies. NCGS patients on the other hand have normal intestine permeability and only trigger innate immune responses. NCGS is thought to be associated with intestinal symptoms (e.g. bloating and diarrhoea) and other symptoms unrelated to the GI-tract (e.g. depression, fatigue, pain and rashes). Current findings suggest that NCGS may be the most common gluten disorder seen by healthcare professionals; its prevalence is still widely unknown. Something to add, there seems to be an increase in antigliadin antibodies in patients complaining about gluten related symptoms despite the rule-out of CD.

There is uncertainty as to if gluten reduction is the specific cause of gluten-free benefits or if another component of wheat is the cause. Fermentable fructans may provoke irritable bowel syndrome; a reduction of gluten may indirectly reduce these fructans. There may be some overlap with the reduction of IBS symptoms with gluten sensitivity. More research is needed to separate glutan and fructan sensitivity.

Many doctors still refuse to accept that gluten sensitivity exists, some going so far as to claiming that it’s ‘a myth’. A doctor interviewed with the Annals of Internal medicine claimed that gluten free diets can be dangerous. He then went on to list the dangers as; resulting in a misdiagnosis of CD, taking out gluten for the wrong reasons and spending more money on gluten free products. Ok, I can definitely agree with the first statement, but wouldn’t it be better to take out gluten earlier rather than later anyways to reduce risks associated with CD (e.g. cancer)? Why is it so important for us to incorporate gluten in our diets? We in no way require that protein. And as for the money, I’m not really sure how that can be lumped into a ‘danger’. He went on to list the symptoms of gluten sensitivity as e.g. stomach cramps, diarrhea, headaches, etc., but said that these symptoms could be a lot of other things and can be treated with something other than a gluten-free diet. Although, yes, research is still in its infancy in regards to gluten sensitivity, that’s not to say that it should be disregarded by doctors, ESPECIALLY when there is growing evidence for benefits associated with the reduction or elimination of gluten consumption. Why should people not pursue a diet, regardless if gluten is the culprit, which reduces their symptoms and makes them feel better?

So, some concluding thoughts… Although humans have existed in some ancestral form for about 2.5 million years, we weren’t exposed to wheat until about 10000 years ago, originally in south western Asia; wheat and therefore gluten (in the endosperm (in wheat, barley and rye)) were novel introductions to our diets. Today wheat has become a staple in modern diets; along with a rise in many chronic diseases. People have been getting benefits from a gluten free diet despite not having CD; this has led researchers to consider the concept of non-CD gluten sensitivity. Non-CD gluten sensitivity may affect 20% or more of our population, these individuals may have positive results from a gluten free diet. As you may have read, I am a big advocate for a gluten-free diet based on an evolutionary perspective (a perspective I think should be considered more often); regardless, hopefully this post has shed some light on the rise in gluten-free diets and gluten sensitivity.

Happy Holidays everyone!


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Ferch CC, Chey WD. (2012) Irritable bowel syndrome and gluten sensitivity without celiac disease: separating the wheat from the chaff. Gastroenterology 20;142:664-6.

Jones, R. (2009) Easily Missed? Coeliac disease. BMJ;338:a3058.

Sanders DS, Patel D, Stephenson TJ et al. (2003) A primary care cross-sectional study of undiagnosed adult coeliac disease. Eur J Gastroenterol Hepatol 4, 407–413.

Sanders DS, Hopper AD, Azmy IAF et al. (2005) Association of adult coeliac disease with surgical abdominal pain: a case control study in patients referred to secondary care. Ann Surg 242, 201–207.

Sapone A, Lammers KM, Casolaro V et al. (2011) Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity. BMC Med 9, 23.

Zarkadas M, Cranney A, Case S et al. (2006) The impact of a gluten-free diet on adults with coeliac disease: results of a national survey. J Hum Nutr Diet 19, 41–49.

Bone health: Are you at risk for osteoporosis?

I started this week thinking I had all of the time in the world to write more blogs… the presentation power point took me a bit longer than expected (along with have to work more than I’m used to), but it’s looking good now :)! Just have to practise so I don’t embarrass myself in front of the 75 or so grade 12s lol… this should be a good learning experience!

Here’s a picture of me at a comp. last year :)


And as per request, here’s a picture of the Christmas tree I made :p lol


Osteoporosis is characterised by low bone mass, fragility and an increased risk for fractures. It’s estimated that one in three women and one in twelve men will suffer from osteoporosis! Menopause (as well as amenorrhea) put women at a higher risk for osteoporosis. Many of us stay unaware of the rise in osteoporosis and that’s why this post will be about bone health! Hope you enjoy :).

Bone is a living tissue with continuous cycles of bone formation (via osteocytes and osteoblasts) and breakdown (via osteoclasts). Our bone health in adulthood is primarily determined by: the maximum peak bone mass which is achieved during development to early adulthood, maintaining bone mass and by a reduction in the rate of bone loss in adulthood. Both peak bone mass and the rate of bone loss are determined by a number of factors that include genetics, exercise and nutrition.

So what do we need to keep healthy bones?

Calcium is the most abundant mineral in our bodies; 99% of that calcium resides in our bones and teeth. The other 1% is located in our body fluids and soft tissues. Calcium plays a role in both support and metabolic function, it is essential for e.g. cell structure, signal transmissions, contractions, nerve functions, blood clotting, enzyme activity, etc. The metabolic role of calcium (blood calcium) is much more important to our general health and functioning, because of this; blood calcium needs to be tightly maintained at 90-105mg/L. When we do not absorb enough calcium to fulfil the 90-105mg/L requirements in our blood, bone can be broken down in order to supply our blood with calcium.

Vitamin D (1,25-dihydroxycholecalciferol) is required to stimulate the absorption of calcium across our intestine (by inducing Ca-binding proteins). Vitamin D is mainly derived from sunlight but recent research has indicated that this source may not be adequate, especially in the winter. Vitamin D stimulates bone formation and, along with the parathyroid hormone, regulates calcium (and phosphorus) metabolism by promoting calcium absorption by our intestine and kidneys. There is a lot of evidence showing that even a mild vitamin D deficiency (especially in females and children) can lead to detrimental bone health effects. Vitamin D is clearly a very important consideration in terms of bone health and calcium absorption.

And now onto a less known vitamin in regards to bone health…

Vitamin K (‘koagulation vitamin’) was first described for its coagulating properties. Phylloquinone (K1) is derived from plants and menaquinone (K2) is derived from bacteria. In respect to bone health, vitamin k is a cofactor in several bone protein carboxylations (including osteocalcin). When our vitamin K consumption is not adequate, the result may be an under-carboxylation of osteocalcin which may ultimately result in a lower bone mass and higher risk for osteoporosis.

On a related note, vascular calcification happens when calcium builds up in our vessels (associated with atherosclerosis). Vitamin K has been proposed to prevent this vascular calcification because it activates the matrix GLA protein (MGP) which inhibits calcification in vascular tissue. Animal and cell studies support this idea but human studies are pretty inconsistent. The majority of human studies have relied on K1, yet growing evidence indicates that higher K2 (and not K1) is associated with less calcification (which may be the cause of inconsistencies in human studies). Without K2, we may not be able to move calcium out of our soft tissues (vessels) to our bones, ultimately leading to both osteoporosis and atherosclerosis. Consequently, calcium supplementation may actually lead to osteoporosis and atherosclerosis if there is a vitamin k (2?) deficiency. If looking to supplement, a good option would be a supplement that includes vitamin k2. This is a very new and controversial area of research.

A few other nutrients have gained more research indicating their importance in bone health including magnesium, silicon and boron. Magnesium can be found in e.g. potato skins and lentils, silicon can be found in e.g. carrots and green beans and finally boron can be found in e.g. prunes.

I’ll leave it at that… Take care of your bones! You’ll be happy you did 20 or so years down the road :).

Happy holidays!


Price C, Langford J, and Liporace F. (2012) Essential Nutrients for Bone Health and a Review of their Availability in the Average North American Diet. Open Orthop J.; 6: 143–149.

Eastell R (1999) Pathogenesis of postmenopausal osteoporosis. In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 4th ed., pp. 260–262.

Consensus Development Conference (1991) Diagnosis, prophylaxis and treatment of osteoporosis. Am J Med 90, 107–110.

van Staa TP, Dennison EM, Leufkens HG & Cooper C (2001) Epidemiology of fractures in England and Wales. Bone 29, 517–522.

Abrams SA (2003) Normal acquisition and loss of bone mass. Horm Res 60, 71–76.

Smith R (2003) Calcium and the bone minerals. In Human Nutrition and Dietetics, pp. 451–489.

Parfitt AM (1990) Osteomalacia and related disorders. In Metabolic Bone Disease and Clinically Related Disorders, 2nd ed., pp. 329–396.

Underwood JL & DeLuca HF (1984) Vitamin D is not directly necessary for bone growth and bone mineralization. Am J Physiol Endocrinol Metab 246, E492–E498.

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Leino AE & Viikari JSA (2002) Vitamin D and attainment of peak bone mass among peripubertal Finnish girls: a 3-y prospective study. Am J Clin Nutr 76, 1446–1453.

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Delmas PD & Meunier PJ (1992) Vitamin D and calcium to prevent hip fractures in elderly women. N Engl J Med 327, 1637–1642.

Szulc P, Chapuy M-C, Meunier PJ & Delmas PD (1996) Serum undercarboxylated osteocalcin is a marker of the risk of hip fracture: a three year follow up study. Bone 18, 487–488.
Weber P (2001) Vitamin K and bone health. Nutrition 17, 880–887.

Shea MK, and Holden RM. (2012) Vitamin K status and vascular calcification: evidence from observational and clinical studies. Adv Nutr.;3(2):158-65. doi: 10.3945/an.111.001644.

Gut microfloras and their implications for our health

I’ve definitely been enjoying the first few days of my break, I’ve been trying to write two blog posts a day to have them in my arsenal for the future… or maybe I could up to a few more than 2 posts a week during my winter break, what do you guys think?

My roommate drove down to Alabama for a climbing trip last night (I had to work :(); I am already feeling a little lonely at my place lol… although I am keeping pretty busy with work, blogs and climbing, I’m just a little needy apparently lol. I’m excited to go home this Saturday (and also to give that high school presentation on Friday :))

Here’s a picture taken of me at my climbing gym in the summer :)


Bacteria make up the bulk of the biomass in the human gut; identifying factors that control the diversity and health of our gut microflora has become an exciting area of research. So what’s the big deal? This blog post will be about our microbial inhabitants that reside in our large intestine. Hope you enjoy!

So let’s start from the beginning… Our guts are sterile at birth and rapidly develop as a result of environmental exposures and diet. Breast milk, for example, contains many antibodies and lactose which promotes the establishment of lactobacilli (which promotes a normal immune function).The first weeks, better yet, days is vital for gut colonization. Depending on our blood pH, nutrient availability and bacterial exposure, different floras will arise.

Microbe exposure results in a quickly changing gut flora in infants, it isn’t until about 3 years of age that the microbes stabilize. Since bacterial exposure is much different around the world, gut flora will consequently be much different in each individual. For example, people who live in poorer communities have drastically reduced incidence of allergies, autoimmune disorders and inflammation (even if they move to cleaner environments later in life); this is a result of many factors including their gut flora. Early development of our gut floras through infancy puts us at lower or higher risks for many disorders (including diabetes and obesity). Something to add, antibiotics may modify our gut microbiome and immune response, especially when taken in our early lives.

After weaning, fibre becomes very important- fibre, along with inulin and oligosaccharides (which are resistant to mammal food breakdown enzymes), pass into the large intestine where our gut flora resides. These non-digested carbohydrates become a major energy source for the bacteria; our diet determines which microbial species that will be successful. When there are lower carbohydrates and/or more refined carbohydrates in our diets, less undigested food will make it to the large intestine and thus less energy will be provided to the gut flora.

In animal models, gut flora can promote either extreme or minimal tendencies to gain weight. Furthermore, obese animals have microbiomes with a higher ability to harvest energy from high carb diets. The common north-American diet consists of highly refined carbs and fat and lower complex carbs; this has been linked to the rise of obesity. Fructose and artificial sweeteners have also been linked to this trend. These sugar compounds, particularly fructose, changes our microbiome with altered metabolic capacities. Furthermore, a procedure that replaces the bacteria in the large intestine of an obese individual with metabolic syndrome with that of a lean relative actually produces rapid improvements in insulin sensitivity (sustained for weeks!).

So you’ve probably heard of probiotics and prebiotics, what are they? Probiotics are microbial foods that are taken to correct our gut flora. Prebiotics provide suitable carbohydrates to preferentially stimulate a certain microbe. Effectiveness of pro and prebiotics is quite controversial and further research is definitely needed.

So some concluding thoughts; our gut microbiomes, largely determined by the first few years of our lives, puts us at different risks for many diseases including diabetes and obesity. Fibre is an important component to keep a healthy gut flora, as well as a reduction of refined carbs, fructose and artificial sweeteners. Although short term diet adjustments have been shown to improve gut flora temporarily, long term life style changes are the best way to support permanent beneficial changes. For this reason (and others), crash dieting is probably not the best way to get healthy but rather a permanent healthy lifestyle change.

Anyways, time to go to the library to do some more research :D, hope you all have a splendid Monday!


Backhed F, Ding H, Wang T, et al. (2004) The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci U S A.4;101:15718–15723.

de Vos WM, de Vos EAJ.(2012) Role of the intestinal microbiome in health and disease:from correlation to causation. Nutr Rev.;70(Suppl.). doi: 10.1111/j.1753-4887.2012.00505.x.

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Jackson AA, Gibson NR, Bundy R, et al. (2004) Transfer of (15)N from oral lactose-ureide to lysine in normal adults. Int J Food Sci Nutr.;55:455–462.

Ley RE, Lozupone CA, Hamady M, et al. (2012)Worlds within worlds: evolution of the vertebrate gut microbiota. Nat Rev Microbiol.;6:776–788.

Relman DA. (2012) The human microbiome: ecosystem resilience and health. Nutr Rev.;70(Suppl.). doi: 10.1111/j.1753-4887.2012.00489.x.

Omega 3 and omega 6: whats all of the confusion about?

And I’m done exams, wohoo!! No more classes until January 7th :D! I really want to focus on my blog this Christmas break; I’ve got a few topics in mind before I start researching the suggested topics from some of you guys. If any of you have any requests, feel free to ask and I’ll make a list and eventually get to it :).

My roommate and I had our Christmas party last night, couldn’t have asked for a better group of people who came; it was a really nice reward after all of our exams :). After spending most of the day climbing (obviously), we came home and decorated the house with Christmas lights, homemade snowflakes and a cardboard Christmas tree I taped to the wall :P. I definitely feel the holiday spirit now, ready to get onto some vegan holiday creations!

Here’s a picture taken of me in Kentucky from some of my American friends- Thanks Matt for the picture :)…


There’s a lot of confusion about the effects of omega 3 and omega 6 polyunsaturated fatty acids, so this post will be an attempt to make sense of it all for you guys. Hope you enjoy :)!

So first things first, what are polyunsaturated fatty acids? Polyunsaturated fatty acids (PUFAs) are just what their name describes, fatty acids that are unsaturated with multiple double bonds; the location and number of double bonds play a role in determining their properties. PUFAs are essential in mammal diets because we lack enzymes to put a double bond in either the 6th or 3rd position of fatty acids and therefore cant create them endogenously. Both omega 3s and omega 6s play an important role in altering cell membranes, signalling molecules, gene expressions, etc.

Omega 6s are abundant in modern diets, especially in corn and soy bean oils and grain-fed meat. Omega 3s on the other hand are less available, they should be actively incorporated into our diets. Omega 3s are found in only a few foods, primarily in fatty fish (increasing at decreased environmental temperatures for the fish in order to maintain membrane fluidity) and certain vegetables and nuts. Algae and phytoplankton make omega 3 which is eaten by fish, omega 3 increases up the food chain through bio-accumulation. Nut omega 3 typically comes in an alpha linolenic acid (ALA) form whereas fish typically has docosahexaenoic acid (DHA), but I’ll get to that later…

From an evolutionary perspective, we evolved on a diet with a PUFA ratio of omega 3s:6s at about 1:1. Today that ratio has shifted to over 15:1 commonly. The ratio of PUFAs are important for regulating homeostasis and growth.

Omega 3 has a counteracting action to omega 6; while omega 6s promote coagulation, angiogenesis and inflammation for example, omega 3s are anticoagulants, anti-angiogenic and anti-inflammatory. Omega 3 has been shown to have anti-tumor properties and a role in the protection against many chronic diseases including heart disease. In contrast, omega 6 was shown to promote tumor formation and growth as well as promote heart disease. Both are essential and required for optimal health (for example, in the case of clotting; the pro-coagulating and pro-inflammatory properties of omega 6 are very important).

Omega 3s and 6s compete for cell membrane incorporation; higher levels of omega 3s in our diets can help prevent adverse effects associated with omega 6s. Again, many chronic diseases, e.g. heart disease, cancer, diabetes, rheumatoid arthritis, depression, asthma, etc, are associated with an increased omega 6 intake. Risks can be effectively reduced by increasing your omega 3 intake. Since many chronic diseases start in utero, proper PUFA consumption is important in pregnancy (and before) (also important for normal brain development).

The primary omega 6 is linoleic acid (LA) which is converted to arachidonic acid (AA). The three primary omega 3s are alpha-linoleic acid (ALA) (the form in many vegan omega 3s), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA); ALA can be converted to EPA and DHA following consumption. This conversion is quite inefficient; consuming preformed EPA and DHA may be necessary to meet dietary requirements for omega 3. There are, however vegan DHA supplements out there derived from algae (but typically at lower concentrations than fish oil supplements).

So I’ll end things here, hopefully I got the point across for the need to up your omega 3 intake! Hope you all have an awesome weekend!


Cicero A, Reggi A, Parini A, and Borghi C (2012) Application of polyunsaturated fatty acids in internal medicine: beyond the established cardiovascular effects. Arch Med Sci.; 8(5): 784–793.

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Kang J, and Liu A. (2012) The role of the tissue omega-6/omega-3 fatty acid ratio in regulating tumor angiogenesis. Cancer Metastasis Rev DOI 10.1007/s10555-012-9401-9.

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Simopoulos A. (2006) Evolutionary aspects of diet, the omega-6/omega-3 ratio and genetic variation: nutritional implications for chronic diseases. Biomedicine & Pharmacotherapy 60: 502–507.

The implications of binge eating

Just trudging on with exams, got one tonight and my last one on Thursday- in the home stretch! I’ve also got some really exciting plans post-exams including giving a lecture to a group of high schoolers on metabolism, homeostasis, nutrition etc… am really looking forward to it :). I’m also excited for a Christmas party my roommate and I are throwing this Friday, and of course excited to a) deck our house out with Christmas decorations and b) make Christmas goodies.

Here’s a pic of me climbing earlier this year :)


So with the holiday season approaching, I figured I’d do a post on a common holiday problem: overeating. Hope you enjoy :)

The following will be a description of what should normally happen in a normal sized meal. As we eat, sugar and fat get pushed through our metabolic pathways and create substrates for our Electron Transport Chain (ETC) at the mitochondrial membranes of our cells. The ETC can take those substrates and, by passing electrons through a series of complexes, create energy in the form of ATP. That energy is then transported out of the mitochondria (via the ANT and phosphocreatine shuttle) so that the energy will then be available to our muscles. This is a pretty (maybe overly) simplified description of what happens during the metabolism of fat and sugar for fuel.
So with a little back ground information…

What happens after we binge? When we eat in excess, more substrates become available to the ETC- more than the ETC can handle; a back pressure will be created and the passing of the electrons from complex to complex will be slowed. Ions will spend more time at each complex and have a greater chance to combine with oxygen to form superoxide; more reactive oxygen species will be created. The ROS created, although it has a bad rep from a cancer perspective, serves a purpose in the cell to adjust the ETC to a healthier speed (and in turn result in less ROS produced).

So how does ROS help us then? In order to adjust the ETC to a more suited speed, a lower energy environment (i.e. more ADP: ATP) is required. The ROS inactivates a few enzymes in previous metabolic pathways and results in an increased storage of our fuel in fat (triglycerides), which also (via MalCoA) inactivates fat transporters that bring fat into the mitochondria for metabolism by the ETC. Less substrate will be available to the ETC and the speed will be able to adjust. Triglycerides are the normal and healthy way we should be storing fat. Take home point- one binge won’t kill you… the trouble comes from chronic binging.

Following a westernised diet with regular bouts of excessive calories, the concentrations of triglycerides are much higher; the path to create triglycerides will become saturated and less efficient. The inefficient production of triglycerides will result in more fatty acid intermediates in our cells which are where the big problems lie. The fat intermediates inhibit normal insulin signalling, the ANT at the ETC (leading to more ROS) and also MalCoA’s (from the pathway to store energy in the form of triglycerides) ability to block fat uptake by the mitochondria. Take home point- chronically overeating leads to chronically higher levels of ROS created from the ETC. If we want to protect ourselves from excessive ROS production from the ETC, our bodies need to divert fat and sugar away from the mitochondria. We can decrease the ROS from the ETC by either exercise (increased turnover) or smaller caloric intakes (less substrates).

So on a more macro level… fat is the first insult from chronically binging; we will have a harder time storing fat properly. Less subcutaneous (which is protective) and more visceral (pro-inflammatory) fat may eventually result. As fat cells increase in size, their vasculature decreases leading to hypoxia and then inflammation and macrophage recruitment. These fat cells will end up releasing both cytokines (which promote inflammation) and excess fatty acids (which promote an unhealthy fat distribution and toxicity to other tissues). Insulin resistance will soon also occur in the fat cells.

I could write a book about the negative effects from binge eating, but for the sake of keeping this (relatively) brief- I’ll end here. It’s easy to fall into a trap of constantly overeating, which is pretty well the norm in North America. One binge leads to two and so on and so forth. Hopefully this gives some of you guys more incentive towards sticking to a healthy diet, especially with Christmas around the corner.

Wish me luck on tonight’s exam!


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Martínez JA. (2006)Mitochondrial oxidative stress and inflammation: an slalom to obesity and insulin resistance. J Physiol Biochem.:303-6.

Medina-Gómez G. (2012) Mitochondria and endocrine function of adipose tissue. Best Pract Res Clin Endocrinol Metab.:791-804. doi: 10.1016/j.beem.2012.06.002.

Chocolate- a healthy treat? :)

Three exams down, two more to go! My week hasn’t been overly exciting; my days typically are consisting of me studying most of the day, climbing and occasionally working. My roommate and I have brought our kitchen table into our living room so we can study on our comfy couches with a table (best of both worlds :p). Less than a week left, cannot wait!!

Here’s a pic of me at a competition a couple of months ago :)


So anyways, with the holiday season approaching (and my exams looming) I figured I would talk about Chocolate! Hope you enjoy! :)

Historically, chocolate has been used for medicinal purposes; by the 1600s it was used for both taste (obviously) and to treat disorders including angina and heart pain. It was only within the last 50 years that its use has shifted to primarily a confectionary one.

Why is chocolate good for me? Chocolate is derived from the cocoa bean and has many health benefits which are associated with its flavonoid, a class of plant metabolites, content. The most abundant flavonoid in chocolate is flavonol; dark chocolate is one of the richest sources for flavonol (responsible for its bitterness) at about 510mg per 100g! Flavonol is known for its antioxidant capacity and has been shown to reduce risks for heart disease.

By 2030, an estimated 23.6 million people will die because of heart disorders according to the World Health Organization. Today, about one fifth of the world is thought to have metabolic syndrome, resulting in increased risks for diabetes and heart disease. Diet is the key factor for heart disorder development; again, flavonol in cocoa is shown to reduce the risks. In a meta-analysis, higher chocolate consumption was associated with a 37% reduction of heart disease risk, 31% reduction of diabetes risk and 29% reduction in stroke risk according to the studies analyzed. Flavonols have been shown to decrease LDL cholesterol oxidation, increase HDL cholesterol, and decrease blood pressure. They have also been shown to affect eicosanoids by increasing prostacyclin (which inhibits blood clotting) and decreasing leukotrienes (which increases vasoconstriction and inflammation).

So what are some factors for the flavonol content in chocolate? Processing is a major player; bean selection, fermentation, roasting and alkalizing are factors in the concentration. Increased time for fermentation and roasting (as well as increased temperatures) will result in more flavonols lost. Alkalization, which is a Dutch process and is also optional, also results in very large losses.

Some other things to take into account before mowing down on a box of chocolates; chocolate is high in calories (about 2100 kJ (500 kcal)/100 g). As a result, increased consumption will cause weight gain which is a factor for hypertension, diabetes, and cardiometabolic disorders. The high sugar content should also be considered, lower sugar chocolates would improve outcomes associated. Chocolate is also high in fat; stearic acid (the fat in chocolate) is unique though in that it doesn’t increase blood cholesterol like other short chain fatty acids.

Wait, chocolate isn’t vegan? Chocolate is actually vegan but the chocolate we see in grocery stores tends to have many additives including milk. A good quality one however will only have cocoa, cocoa butter, lecithin and sugar and therefore be vegan. Lesser quality ones tend to have a lot of filler ingredients (including milk). So there you have it, anyone can enjoy chocolate (but some may have to pay a bit more for it :p).

Anyways, that was my feel-good post of the day. Hope you all have a good rest of the weekend! :)

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Buitrago-Lopez A, Sanderson J, Johnson L, Warnakula S, Wood A, Angelantonio E, Franco O. (2011) Chocolate consumption and cardiometabolic disorders: systematic review and meta-analysis. BMJ. ; 343: d4488.

Corti R, Flammer AJ, Hollenberg NK, Luscher TF. (2009)Cocoa and cardiovascular health. Circulation;119:1433-42.

Sudano I, Flammer AJ, Roas S, Enseleit F, Ruschitzka F, Corti R, Noll G. (2012) Cocoa, Blood Pressure, and Vascular Function. Curr Hypertens Rep.(4):279-84.

World Health Organization. (2011) Cardiovascular diseases. Fact sheet No 317.

Antioxidants- whats the big deal?

Had my second exam this morning, I think it went pretty well; three more to go! In a weird way, I kindof like being in finals; studying all day (with the exception of a few climbing breaks here and there :p)- It makes me feel very productive and good about myself lol. I told this to my roommate… she openly told me that that made her hate me just a little bit :p lol. Either way, cannot wait until Christmas break! I’ve got some cute ideas for decorating our place (post exams as a reward lol), I’ll definitely share some pictures of the finished product!

Here’s a picture of me taken at devil’s glen in Ontario :)- photo cred to my friend Jess, awesome shot!



Everyone wants to get more antioxidants in their diet, what’s all the fuss about? So many people come to the nutrition store I work at asking for antioxidant supplements, stuck on the idea that these supplements will make them healthier. With all the interest, this post will be on antioxidants, with emphasis on beta-carotene, and the differences between dietary and supplemental forms.

So what do antioxidants do? Antioxidants work to quench free radicals and prevent the buildup of reactive oxygen species; this may reduce our risks for cancer and other chronic diseases. There are both enzymatic antioxidants, which scavenge hydrogen peroxide and superoxides and can be regulated based on our body’s requirements, as well as dietary antioxidants. Dietary antioxidants (non-enzymatic) include vitamin A, E and C as well as beta carotene and other nutrients. They are ‘chain breaking’ antioxidants and aid enzymatic antioxidants in reducing reactive oxygen species and reactive nitrogen species.

So before I move onto the question of whether supplementing with antioxidants are a good idea, I’ll discuss one dietary antioxidant followed by the results of this antioxidants supplementation. The antioxidant I’ll discuss is b-carotene…

Diets that are higher in carotenoids are thought to be protective through antioxidant activity; with beta-carotene in mind, lower levels are correlated to a higher incidence of heart disease and cancer. In 1981, beta-carotene was suggested to be the active carotenoid in vegetables that contribute to these healthy effects. This idea spawned from the fact that beta-carotene is the most abundant carotenoid in vegetables.

In 1996, the famous CARET study came around and changed the game in terms of beta-carotene. Smokers were given beta-carotene supplementation; the expected result was an improvement in cancer risk. Unfortunately, participants who were given beta-carotene had a 28% increase in lung cancer incidence and a 17% increase in death along with an increased rate of heart disease. The trial had to stop due to these adverse effects on participants.  A similar trial to the CAROT study used alcohol users as subjects. Beta-carotene was also observed to increase their risks of cancer. These studies confused a lot of people since beta-carotene has been long thought to be an antioxidant.

So what went wrong? Beta-carotene can have pro-oxidant effects at increasing oxygen tensions (from e.g. smoking) as well as increased beta-carotene concentration. This is an effect that we are only beginning to understand.  Breakdown products of carotenoids are formed when they interact with free radicals; these breakdown products present a risk for ’genotoxicity’. Since supplements have a much higher concentration of beta-carotene, they pose a risk firstly from their high concentration and secondly, if they are exposed to something that will cause oxidative stress (which is very common given modern lifestyles).

Something else to keep in mind, supplements do not have the same phytochemicals (‘plant chemicals’) that are present in actual vegetables- phytochemicals also decrease cancer rates, but through different pathways (e.g. toxin metabolism).In normal beta-carotene intakes (seen through the diet), it would be extremely hard to get adverse effects from the antioxidants present for a number of reasons including the lower amounts of antioxidants and higher amounts of phytochemicals. Take home points- dietary antioxidants=good idea, supplements=maybe not.

Something else to add is that, although fruits have a higher amount of antioxidants than vegetables, vegetables actually are more effective at reducing risks for cancer. What can we take away from that fact? Phytochemical content is very important for risk reduction (but I will get to them in a future post!), likely more so than antioxidants. Furthermore, the food matrix is very important for preventing risks associated with antioxidant breakdown products.

So to wrap things up, antioxidants and phytochemicals through our diet helps keep us healthy; we need to be cautious when we move out of a food matrix and into a neutraceutical. Research on antioxidants is both complex and hard to follow; e.g. one day it’s good, next day it causes cancer. Personally, I think the best way to eat for your health is through a proper diet with lots of vegetables (and fruits).

Anyways, gotta start studying for my next exam (on Friday); hope you all have a good day!


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Leo, M. and Lieber, C. (1999). Alcohol, vitamin A, and b-carotene: adverse interactions, including hepatotoxicity and carcinogenicity. Am J Clin Nutr. 69(6):1071-85.

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Why should YOU exercise? :)

Done all my classes, now I’ve just got exams in the way of my Christmas break! Spent most of my day studying… then came home and made myself cauliflower mash (delicious) and the tastiest desert I’ve made in a long time! Lol I mixed 3 tablespoons of hemp hearts, 1 mashed banana,1 cut up apple, half a tablespoon of coconut oil, cinnamon and a teaspoon of coconut sugar and baked it… soooooo indescribably good :p.  I ate this feast while giving into my guilty pleasure (and procrastinating) of ‘the vampire diaries’ lol.

Here are some more pictures of me climbing in Ontario, cannot wait for the spring!



And a showcase of extreme flexibility :p…



Exercise is something that everyone should actively incorporate into their life; the benefit of even a single bout of exercise has huge implications towards our health. Exercise has been linked to lower rates of chronic diseases such as diabetes, cancer and cardiovascular disease. Physiological function, fitness and health are improved through regular exercise which ultimately leads to significant beneficial adaptations. So what’s going on here? This blog post will briefly discuss the implications of exercise to our health and well-being. Why should you exercise? Here are some good reasons for ya lol…

So you’ve probably heard that people who have more muscle burn more calories and fat, how does that work? Well, there are a number of reasons that include the following…Exercise increases the activity of an enzyme called hormone sensitive lipase (HSL); this enzyme ultimately increases the breakdown of triglycerides to fatty acids for fuel.  Exercise also increases mitochondrial content (necessary for aerobic metabolism) of our adipose tissue; fatty acid oxidation is seen to rise approximately four-fold. The rate of ‘futile cycling’ also increases; futile cycling is essentially us wasting energy, i.e. burning more calories. Our bodies respond to low energy environments by giving them more fat than is actually required (fat is an incredibly rich source for energy); the unused fat needs to then be re-esterified which takes energy. Futile cycling is associated with improved insulin sensitivity. Take home point- our muscles get better at burning fat through exercise.

How can exercise make us healthier? This is also multifactorial but I will primarily focus on the implications towards the electron chain transfer (ETC) at the mitochondria (a huge source of aerobically derived energy) (beware, this is about to get even techier- bear with me, I’ll sum things up at the end!)…

To paint a better picture, I’ll describe the implications of over-eating. When our food intake increases, more substrates are sent to the ETC resulting in more ions being pushed through. Our metabolism cannot keep up with this and eventually the ETC will slow down and a back pressure will be created. Ions will spend more time at each complex in the ETC and as a result have a greater chance of combining with oxygen to form superoxide. More reactive oxygen species are then created which is very bad news for our health (e.g. ROS can be linked with cancer risk). Typically when our body use the energy created by the ETC, the energy available will decrease. The lower energy environment will help dissipate this membrane potential and in turn decrease the ROS production.  At increased food intakes, the energy will still be too high and the membrane potential will not be dissipated. During exercise, the low energy environment in the mitochondria will decrease reactive oxygen species (ROS) by dissipating the above membrane potential and ultimately allowing hydrogen ions to flow through. Take home point- exercise decreases the ROS from the ETC.

Exercise also decreases our risks for diabetes. Exercise increases glucose uptake by our cells by stimulating more GLUT4 (glucose transporters) to membranes, this helps improve insulin sensitivity. Improved lifestyles, following the American food pyramid and exercising 150 minutes per week, has been shown to improve risks for diabetes by 58%! Just one bout of exercise is able to prevent lipid-induced insulin resistance. Furthermore, exercise can decrease insulin and insulin growth factor and effectively reduce risks for cancer (which requires glucose for growth). Exercise has also been shown to improve drug efficacy.

Not only is exercise good for our well-being, it also allows us to get strong (duh lol :p)!Our bodies adapt to high stress exercises in order to make them easier the next time. Exercise stimulates protein synthesis and breakdown; we need positive nitrogen balances to build muscles (otherwise we will lose muscle mass). Exercise improves the efficiency of amino acid conservation and protein synthesis during training. Furthermore, resistance training has been shown to enhance elderly sit to stand strength.

Exercise may have been an essential ingredient for the evolution of human intelligence! The hunter gatherer lifestyle of our ancestors required large increases in aerobic activity which altered the human physiology to enable the utilization of new resources in their changing environments. Recent studies suggest both acute and long term exercise increases brain size and improves cognitive performance in humans as well as other animals. Recently, work suggests that the rise in exercise may have been a factor for increased brain sizes and overall intelligence in our ancestors.

So a summary of everything we’ve discussed; exercise makes us better at burning fat, improves insulin sensitivity, helps us avoid ROS formation AND makes us smarter. There are soooooo many other positive effects derived from exercise, but for the sake of keeping this post (relatively) reader friendly, I’ll end it here. In future posts I’ll delve more into other topics surrounding exercise including implications on cardiovascular disease. Now that winter weather is in full swing, hopefully this will give some of you guys the motivation to keep at your workout regimes!

Hope everyone has a good weekend!


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