Monthly Archives: November 2012

The implications of cooked or preserved meat consumption towards cancer!


Starting to spend more and more time in the library preparing for exams, in a weird way I actually enjoy final exams; despite the head ache of reading 100s of pages of notes and textbook material, I know I’m going to miss it when I’m done school. Planning on doing some major Christmas decorating as soon as my last class is over (this Wednesday!!); I am so excited for Christmas festivities and to make my way back home. I think I have a problem with how much I love Christmas, on Saturday I forced my co-worker to listen to Christmas music through our shift together- I’m sure she’s looking forward to getting more shifts with me as Christmas approaches: p.

Here’s a picture of me climbing at my favorite place (Kentucky) earlier this year!

Anywaysss, this post will be on the implications of cooked or preserved meat consumption towards cancer. Hope you enjoy!

Many cancers including colorectal, esophageal, larynx, gastric, bladder, prostate and breast cancer have been shown to have increased risks for development in association with cooked or preserved meat consumption, increasing with the level of ‘doneness’. Maternal exposure to preserved meats has also been linked with childhood brain tumors. These associations are obviously very controversial in terms of research findings and recognition.

The major dietary carcinogens present today are all secondary carcinogens that are very stable and usually formed during processing and cooking. The main categories are polycyclic aromatic hydrocarbons (PAHs), heterocyclic amines (HCAs) and nitrosamines (NAs). PAH results from smoking and requires cooking temperatures of 250 degrees Celsius or higher; fatty meats have the greatest concentrations. HCA is from cooking between 100-250 degrees Celsius and requires amino acids, creatine and sugar- therefore it is primarily from meat consumption (amino acid and creatine). HCA production is enhanced by dry environments and is seen at high concentrations in jerky, dried meat, gravy, etc. Nitrosamines occur from nitrate and amine combinations- nitrate as a preservative and amines from the meat. Nitrate preservation is a method used to decrease the risk for botulism. It can be formed from cultured celery or beet extract as well as many other methods. All of these secondary carcinogens help produce many tasty flavors we enjoy today.

So how do secondary carcinogens actually promote cancer? Bear with me for the science of it all… Secondary carcinogens have to be metabolized to avoid accumulation in fatty tissue or in the brain. This metabolism is done predominantly by an enzyme called cytochrome P450 (phase 1 metabolism of toxins) which essentially makes an ultimate, water-soluble carcinogen that can then be detoxified by phase 2 reactions.  While the phase 1 of toxin metabolism is essential in preventing the accumulation of secondary carcinogens, it does not need to be so quick since we typically aren’t exposed to high doses of carcinogens. When the activity of phase 1 is faster (by exposure to secondary carcinogens); more ultimate carcinogens will be formed that the phase 2 enzymes won’t be able to handle, resulting in an increased risk for cancer. The balance between both phase 1 and 2 enzymes are essential for the reduction in cancer risk, you want enough phase 2 enzymes to keep up with phase 1 (as well as the reduction of phase 1 activity). Diet and lifestyle have a big impact on the effects of secondary carcinogens through the regulation of P450 enzymes, and phase 2 enzymes.

Consumers remain poorly informed on the risks from meat preservation and cooking as well as the implications towards cancer. Current diets have a tendency towards an increased cancer risk due to meat processing and cooking as well as the reduction of phytochemical (via vegetables and fruit) intake, which is seen to both decrease phase 1 toxin metabolism and increase phase 2. A lot of the most common cancers are responsive to both diet and lifestyle; an estimated 60% of cancers are thought to be avoidable with a good diet and lifestyle.

So some concluding thoughts; be conscious of how you cook your meat (if you actually eat it) – although keep in mind, one over cooked steak is not going to give you cancer. Risks come from continuously eating these sources for secondary carcinogens. If you do eat over done meat; maybe pair it up with a plate of vegetables. And finally, the best way to reduce your risks would be to increase plant products and decrease cooked or preserved meats in your diet.

Jen

Heddle JA, Knize MG, Dawod D, and Zhang XB. (2001) A test of the mutagenicity of cooked meats in vivo. Mutagenesis; 16: 103–107.

Jian L, Zhang DH, Lee AH, and Binns CW. (2004) Do preserved foods increase prostate cancer risk? Br. J. Cancer; 90: 1792–1795.

Knize MG, and Felton JS. (2005) Formation and human risk of carcinogenic heterocyclic amines formed from natural precursors in meat. Nutr. Rev.; 63: 158–65.

Mirvish SS, Haorah J, Zhou L, Clapper ML, Harrison KL, and Povey AC. (2002) Total Nnitroso compounds and their precursors in hot dogs and in the gastrointestinal tract and feces of rats and mice: possible etiologic agents for colon cancer. J. Nutr.; 132: 3526S–3529S.

Xue W, and Warshawsky D. (2005)Metabolic activation of polycyclic and heterocyclic aromatic hydrocarbons and DNA damage: a review. Toxicol. Appl. Pharmacol. 2005; 206: 73–93.

Cancer risks related to caloric intake!


Starting to feel the stress of my upcoming finals, only about a week and a half before my first one!! Cannot wait to get them all over with and to have fresh classes for the next semester! Also am super excited for the holidays!!! Will be nice to head home for a bit closer to Christmas : ).

Here’s a pic of me, taken by my friend Dan, at ‘boulder night’ at the climbing gym yesterday night (fun!!)

So, my grandpa has cancer and my mom and sisters have been asking me for some suggestions on what he should eat- I’m no expert on the subject, so on my quest for research I came across a lot of really interesting stuff pertaining to diet and cancer. This blog post will be on Cancer, with emphasis on the effects of insulin and caloric intake. At some point I will most definitely follow up with a blog with more emphasis on nutrients and carcinogens… but for now, I’ll stick to the above. Hope you enjoy and find some of this information useful! : )

Cancer is simply uncontrolled and unregulated cell growth, eventually coupling with metastasis which leads to the spread of malignant cells to other tissues in the body. Throughout time there has been a steady increase in cancer rates, especially those which are associated with reproductive organs. Why are reproductive organs so special? I’d have to assume that it’s because hormonal imbalances but I’m not sure the answer to that one. In the US, approximately 20% of cancer deaths have been thought to be due to the rise in weight of Americans. We are at increased risks of cancer if we are overweight. Obesity is all around very expensive to tax payers, what if the government gave everyone gym memberships? Would free gym passes result in overall reduced expenses (and obviously healthier) for the country?

The Warburg hypothesis spawned in 1924 when Otto Warburg found that cancer cells had an increase in glycolysis and decrease in mitochondrial respiration, leaving them with an inefficient source for energy. It’s recently been found that tumor cells have fewer and smaller mitochondria, there’s an increase in mutations to mitochondria DNA and enzymes for beta-oxidation are decreased by 85%! Since cancer cells have to rely more on glycolysis, their source of energy is from glucose. This source, again, is very inefficient at meeting energetic demands.

What’s the big deal about the switch to glycolysis? It costs approximately 5ATP to make a single peptide bond; one protein can have thousands of peptide bonds. Without the mitochondrial respiration, cancer cells have a very inefficient means for making energy, especially to meet their increased energetic needs. Cancer cells can take pyruvate or lactate and use them for fatty acid synthesis to build new membranes for their descendant lineages. Essentially they swap an efficient source of energy for resources (pyruvate) to make new cells.

So what does insulin have to do with all of this? Studies have shown a correlation of circulating levels of both insulin and insulin-like growth factor 1 (IGF1) (important in regulating cell growth and death) with cancer risk. Insulin supplies the glucose  for growth and IGF1 supplies the signals to promote said growth. People with higher insulin levels due to a poor diet will therefore be at an increased risk for cancer. Exercise helps lower both IGF and insulin and also typically improves the efficacy of drug treatment.

While eating excess calories is associated with an increased risk for cancer, life-long calorie restrictions, as seen in many animal models, are associated with a decreased risk, possibly due to the decrease in reactive oxygen species. Using this information, it would be easy to jump to the conclusion that decreased calorie intakes in humans had the same benefits, unfortunately that is not the case as seen with the following example. During the Dutch famine, which occurred when a German blockade cut off food shipments, citizens had calorie restrictions from 30-50% of their normal intake for 8 months. These individuals were then followed with expectations of having lower risks of cancer (this included about 4.2 million people); they actually had an increase in breast cancer (the more restricted the diet, the higher the risk for cancer). Non-life-long restrictions have an increase in cancer (a good reason not to yo-yo diet!).

Another study found that if you follow a ketogenic diet with no glucose/carbs than the tumor will more or less be starved. Furthermore, if we can force cancer cells to use a mitochondrial source of energy, there will be decrease in tumor sizes. With all of this in mind, what do you think comes first? A switch to glycolysis or malignancy? Another question I definitely can’t answer.

Cancer cachexia, weight-loss despite adequate caloric intake, is a common occurrence in cancer patients. Essentially what happens is that our bodies rip ourselves apart in order to feed a growing tumor. Again, cancer cells have switched to a very inefficient source of energy (glycolysis) – this ultimately results in an increase in energy needs to supply the tumor. A few other issues are also associated with cachexia; insulin resistance and increased protein breakdown while there’s a decrease in its production. Insulin resistance has been shown to improve with exercise so should we promote activity in cancer patient? Probably not given the conditions of most cancer victims. Protein supplementation has been recommended to decrease the protein breakdown and thus decrease the loss of skeletal muscle mass- weight loss may then be reduced.

And so some concluding thoughts; healthy diets with fairly regular caloric intakes and active lifestyles are essential for cancer risk reduction.  Antioxidant consumption should be another major consideration when looking to reduce your risks, but we’ll get to that in a future blog! Any thoughts?

Hope you all have a splendid Friday!

Jen

Ford, N., Nunez, N., Holcomb, V., and Hursting, S.(2012) IGF1 dependence of dietary energy balance effects on murine MET1 mammary tumor progression, epithelial-to-mesenchymal transition and chemokine expression. Endocr Relat Cancer ERC-12-0329

Hursting, S., DiGiovanni, J.,Dannenberg, A.,Azrad, M.,LeRoith, D.,Demark-Wahnefried, W., Kakarala, M.,Brodie, A. and Berger, N.(2012) Obesity, Energy Balance, and Cancer: New Opportunities for Prevention. Cancer Prev Res 5; 1260

Hursting, S., and Hursting, M. (2012) Mechanistic Links Between Obesity, Metabolic Syndrome, and Cancer. Arteriosclerosis, Thrombosis, and Vascular Biology; 32: 1766-1770

Nogueira, L., Dunlap, S., Ford, N. and Hursting, S.(2012) Calorie restriction and rapamycin inhibit MMTV-Wnt-1 mammary tumor growth in a mouse model of postmenopausal obesity. Endocr Relat Cancer,19; 57-68

Type 2 diabetes- a pandemic in North America


So, another exciting week for me (and weekend!); worked a lot, had the bulk of my projects and presentations, and got my first paycheque! It’s amazing how nice it is to get a cheque more than the cost of rent for a change! Spent my Sunday outside climbing; the weather held up for us for the most part (although I turned into a sissy about the cold once we started climbing in the shade :p lol).  I desperately want to head back down south so I can climb comfortably again, I miss summer time climbing!!

Here’s a picture of me climbing in Kentucky about a month ago- hopefully I’ll be back soon!

And in ontario when the weather was still warm-

And so, on to my post…

Obesity has become a pandemic in North America, coinciding with a rise in type-2 diabetes, cancer and heart disease. What’s changed? Is or educational systems failing us in teaching proper eating habits? Is it the insanely higher prices of healthy foods? Or maybe the availability of junk food- it’s hard to resist when there’s a McDonalds on every main street right? This post will be focused on type 2 diabetes and some of the internal mechanisms that ultimately result in insulin resistance.

So what exactly is insulin resistance? Insulin resistance entails to the impairment in the mechanisms that uptake glucose into our cells (GLUT4); the first sign will be ‘hyperinsulinemia’ resulting in a loss of glucose tolerance. Eventually our pancreatic beta-cells will become defected and the secretion of insulin will decline (in early diabetes) and ultimately fail (in late diabetes).

How does insulin resistance happen?? As insulin sensitivity drops, fatty acid uptake is enhanced. Triglyceride formation is actually protective because that is how we are supposed to store fat.  Unfortunately, due to our westernized diets, lipid intermediates build up (our bodies can’t keep up with our diets) and decrease our insulin sensitivity.  These intermediates promote the formation of reactive oxygen species. An overload of food will cause an increased reducing potential at the mitochondria and ultimately an increase in reactive oxygen species. This increase will decrease insulin sensitivity- antioxidants can help quench the reactive oxygen species and help improve insulin tolerance. A side note- not only does reactive oxygen species production result insulin resistance, it also causes cancer! I can’t stress enough the importance of antioxidants (in their food forms as opposed to supplemental- I’ll get to that in a future post! Lol).

Adipose, the major fat storage unit, is the first to be insulted; we can no longer store fuel properly at this point and end up with dysfunctional adipose. As adipose tissue grows due to increased food intake, vasculature will decrease which will result in hypoxia (less oxygen available), inflammation, macrophage recruitment, impaired insulin signalling and ultimately insulin resistance. All very bad and unhealthy things! Chronic toxic fatty acid release will also occur, which goes to muscle, liver, pancreas, heart, vascular beds, etc. All around, it’s pretty easy to see how unhealthy it is to constantly overeat. In conclusion, in order to maintain insulin sensitivity, we need properly functioning adipose tissue.

Okay so fat is important, I get it, but why do I keep hearing that I need to lose my beer belly? Visceral fat (that surrounds the major organs in our bodies in the form of a gut) is pro-inflammatory and promotes insulin resistance, diabetes, and heart disease. On the other hand, subcutaneous allows enhanced storage and ultimately less pressure on other tissues. Subcutaneous fat has been found to improve glucose uptake at the adipose tissue. Subcutaneous fat is around the whole body and can be seen in the curves that us women are blessed with. So a wrap up of this paragraph; beer belly=bad, curves=good- too little body fat % bad? It seems to me that one could definitely argue that point, that too little body fat will not be advantageous for proper insulin sensitivity (along with proper hormone regulation, especially for women); but honestly, I really don’t know the answer to that one. If someone reading this does and wants to shed some light, feel free!

How can we improve our insulin sensitivity? One bout of exercise will actually prevent insulin resistance due to fat; it increases the partitioning of fatty acids and reduces their accumulation in our muscles. Short term starvation can also improve insulin sensitivity; a full blown type-2 diabetic will see a recovered insulin and beta-cell response in just 8 weeks. In 1919, Dr. Fredrick Allen actually used this idea and called it the ‘starvation treatment’.  I’m definitely not endorsing starvation, since it’s obviously not maintainable and comes with some other very negative consequences. It’s just very interesting how effective a lifestyle intervention can really be. Many drugs are on the market to decrease weight and improve insulin sensitivity but the most powerful method for improvements is a diet and lifestyle change.

And that marks the end of this post! Hopefully you enjoyed reading this! Questions, comments or concerns? I’m definitely open to any critiques, good or bad! And so to my American neighbors, happy Thanksgiving! To everyone else, hope you have a splendid Monday!

Until next time,

Jen

Bullo, M., Garcia-Lorda, P., Megias, I., and Salas-Salvado, J.(2012) Systemic Inflammation, Adipose Tissue Tumor Necrosis Factor, and Leptin Expression. Obesity Research, 11: 525–531. doi: 10.1038/oby.2003.74

Cameron, A., Magliano, J., and Soderberg, S. (2012) A systematic review of the impact of including both waist and hip circumference in risk models for cardiovascular diseases, diabetes and mortality. Obesity Reviews. doi: 10.1111/j.1467-789X.2012.01051.x

Monzillo, L. U., Hamdy, O., Horton, E. S., Ledbury, S., Mullooly, C., Jarema, C., Porter, S., Ovalle, K., Moussa, A. and Mantzoros, C. S. (2003), Effect of Lifestyle Modification on Adipokine Levels in Obese Subjects with Insulin Resistance. Obesity Research, 11: 1048–1054. doi: 10.1038/oby.2003.144

Ross, R., Janssen, I., Dawson, J., Kungl, A.-M., Kuk, J. L., Wong, S. L., Nguyen-Duy, T.-B., Lee, S., Kilpatrick, K. and Hudson, R. (2004), Exercise-Induced Reduction in Obesity and Insulin Resistance in Women: a Randomized Controlled Trial. Obesity Research, 12: 789–798. doi: 10.1038/oby.2004.95

GENETIC MODIFICATIONS! (+ a recipe for a carrot cake protein smoothie)


A very hectic week on my part! Lots and lots of projects and presentations, all conventiantly due within a four day span lol… And an obvious question from you guys would be “then why are you posting a blog?” One word- procrastination lol. Some people choose to watch tv, some to browse the internet; I do all of the above with the addition of nerdy research that counts for nothing in terms of grades lol.

So, I’ve gotten a lot of questions about my diet (grain free and vegan) so I decided I’d post a sample meal (my lunch yesterday lol): Spagetti squash (baked in the oven) with homemade pasta sauce and bok choy as well as my own smoothie concoction- a carrot cake protein smoothie!

Recipe:

1 cup almond milk (or any other milk)

1 frozen banana

1 scoop of natural Vega One (any protein powder will do- I often make this with just hemp protein)

1 slice of ginger

1 large carrot

Half a teaspoon of both cinnamon and nutmeg

Ice

Mix in the blender and you get this tasty treat!

Photo-courtesy of my amazing roommate Kaylyn :) .

And finally a pic. of my complete meal…

Yum!!

Anyways, onto my blog posting…

Genetically modified foods is a tricky topic… upon doing a little more research after I had decided to blog about it I quickly regreted my choice lol. There is A LOT of information out there, most of it is biased in either a pro or con direction, understandably. GMO foods is an issue that many people take to heart; its hard to separate that emotion from research you may be doing. I wrote the blog anyways but I’m really not sure what I think about the issue- I see definite advantages to GMO foods but personally would prefer not to eat something that has been engineered with very new technology. Anyways, here you are- hopefully you guys enjoy reading it (and don’t get mad that I really don’t have many strong views… mostly because of the lack of research- which really could be a result of Monsanto… again! Tricky!!).

So to start, GMO’s food are a result of the introduction of foreign DNA to enhance or deteriorate a given protein. As a result, DNA can be changed faster to improve growth, spoilage or the nutritional content. So here’s how it works: a gene is cloned, that sequence (or antisense sequence) can be incorporated into bacterial DNA (plasmid) that also has an antibiotic resistance gene. The plasmid is then stuck into plant cells, and if things go to plan, then into the plant DNA. Seeds of that plant will be screened for the desired gene product. The goal of GMOs is to produce proteins by bacteria that will be used for food processing, inactivate genes with undesirable protein products, produce new enzymes to promote nutritional availability, make enzymes to degrade commercial pesticides, produce endogenous pesticides, produce plant vaccines and add amino acids to make complete protein profiles.

GM foods will have greater pesticide resistance and therefore should we be concerned with more ‘natural’ pesticides? More residues? Increase in allergic responses due to unexpected protein expression? These are worries when creating GMO foods; they are thus reviewed more rigorously than new plant strains through normal breeding. Since GM foods use bacterial and viral DNA vectors, should we be concerned with the risk of a potential ‘unstoppable human pathogen’? The use of antibiotic resistance genes?

GMOs have the potential to solve world hunger and malnutrition, as well as protect the environment yet it has resulted in controversies and disagreements among both the scientific and public community. Biotechnology and genetic engineering are relatively new concepts that we are only beginning to understand, therefore we should definitely be treading more cautiously in terms of production and consumption. GMO foods have even brought about consumers ‘right-to know’ labelling.

The first GMO plant to be successful was in 1983, when an antibiotic resistance gene was stuck into a gene of the tobacco plant. The first GMO approved for consumption by humans was the ‘Flavr Sayr’ tomato by the company Calgene; it had rotting resistance and was sold from 1994 in the USA (even though the FDA claimed there was no evidence for risk) for only a few years. Calgene was later bought by Monsanto in 1996.

During 2007, GMO crops utilized about 114.3 million hectares- today crops are grown in 23 countries- crops are thought to double between 2006 and 2015. Herbicide resistant crops may be more environmentally friendly in terms of technology for weed removal resulting in decreased environmental contamination. Tillage practices can also decrease which protects the soil and also saves us from the expenses associated with tillage (e.g, financial, human labour, energy, CO2 emissions). Insect resistance has also allowed a decrease in insecticide use which means better health and safety for farmers and energy/financial savings. Although there are obvious benefits, GMOs remain to be highly controversial. Next generation GMOs will have increased vitamins, shelf life and pharmaceutical compounds (e.g. vaccines… not sure I want to be eating that…).

Genetic engineering is relatively new technology which will in turn raise consumer concerns. Most studies have shown no risk but a few have arisen that questioned risks for horizontal transfer of antibiotic resistance markers, ingestion of ‘foreign’ DNA, new nutritional composition, allergenicity, harm to other animals and reduced natural pesticide effectiveness. Regardless, there is currently no strong data to support adverse effects through GMO foods. Is this a product of the ‘evil’ Monsanto hiding new research? Who knows (not me obviously lol)?

Any inputs on this topic are encouraged, as is, I’m a little out of my depth. That said; I’ll get back into my comfort zone of nutrition in my next post lol.

Jen

Batista, R. and Oliveira, M.(2009)Facts and fiction of genetically engineered food. Trends in Biotechnology Vol.27 No.5

Neutraceuticals and public trust


This week has been going by pretty quickly! Getting lots of hours at my new job and keeping myself busy with school and climbing! Did another good workout last night, want to get tankin’ again!

Heres a recent picture of me climbing… Indoors : ( lol

And here’s a couple of me a year ago- my switch from bouldering to sport climbing has come with a bit of change in strength. Achievable for the next comp. in January? : ) lol

-I know, I know- easy problem… but very photogenic :p lol

So anyways, my toxicology professor brought up some interesting things over the last few lectures so I thought I’d share. This post is going to be about neutracuticals, marketing and public trust… some controversial views I’m sure; any commentary, good are bad, is always welcome!

Too start things off, heres the bare bones of his lecture in a couple of paragraphs…

When animal models with extremely high doses of a given compound show increases in cancer risk, results may ultimately make their way to the media. Public views are then molded with the biased results- if this compound gave rats cancer at an excessive amount, the public views may be that its going to promote cancer at any dose. Public perceived risk will than be much greater than the actual risk. Sometimes those compounds will even be beneficial in the animal models at lower doses.

On the flip side, when animals are given low doses of a compound and end up with positive effects, the public may end up believing that benefits will only increase with a higher dose. In reality, at high doses- anything super effective will be harmful. Neutracutical companies often take advantage of this fact and market different compounds at high concentrations as being a magic supplement for consumers to take. B-carotene is a prime example of this.

So, B-carotene has long been thought of as a powerful antioxidant- time and time again, people with higher carotenoids in their diet (e.g. higher vegetable consumption) have been shown to have lower risks for cancer. Scientists in the USA used this information to run trials on smokers with the proposition that since dietary carotenoids had cancer risk reducing properties, therefore higher doses would give even more benefits. Unfortunately they were wrong and, after subjects who were taking the B-carotene supplements started getting cancer and dying at drastically higher rates, the trial stopped and they were sued.

Maybe they should have, instead of testing on humans, tested on an animal model first. This is a perfect example of  a low dose benefits shaping the public, and scientists in this case, views and assumptions. There is much more to the B-carotene story, for example B-carotene acts as a pro-oxidant at a higher state of oxidative stress and that higher dietary antioxidants can decrease the effectiveness of enzymatic antioxidants butttttt, well go over that in an upcoming blog lol. Now even though there has been proven negative effects for B-carotene at higher doses, I still see it on the shelves of the neutracutical store (and almost any other) I work in.

Many neutracuticals will also be produced and distributed without actual human trials, trusting that since it was tested on mice and it worked for them it therefore must be both safe and effective for us! Mice have much different metabolisms than humans. Animal models typically overestimate results; failures in replicating those results occur often… I don’t know about you but I think that’s pretty shady for companies to do!

What makes it worse is when big names endorse these supplements as being miracle drugs. You have no idea how many times people have come to the store telling me about how Dr.Oz was telling them about raspberry ketones and how they are so eager to try it. Raspberry ketones, although its effective in animal models, has no human research! There are so many other supplements on the market that are sketchy and continue to be sold because there is a demand. All about the dollar, dollar bills? Right…

In the US, the FDA typically doesn’t review a product unless there are enough bad cases due to that product that come about. In which case, the FDA will review and ban the product- essentially these products are being tested on the people who are buying them. Supplement companies can legally put all of these amazing benefits on the packages and as long as they put a small disclaimer that the product wasn’t evaluated by the FDA, they can get away with saying it.

Now thinking back to what I’ve said so far in this post, I realize I’m being super negative- a product of me getting more and more heated lol. All of the above said, I am a firm supporter of certain supplementing companies; for example, VEGA products are absolutely amazing and I will always promote the company. When done right, supplements can be a powerful tool for promoting good health.

My whole point is that, since there are a lot of gray areas in neutracuticals- we should be very cautious when deciding to take a product. Do your research! Do the concentrations seem too high? Does any human research exist? What actually make the product beneficial? I seem to make this point a lot, but if you want to get the most out of both your diet and any supplements you take; you need to be an informed consumer (A hard task in this day and age due to all of the conflicting standpoints on nutrition).  Don’t jump on the bandwagon as soon as you hear some famous Dr. (who doesn’t specialize in nutrition) promoting it- look at all sides of the story!

Hope you enjoyed… and weren’t offended by my post :p lol.

Jen

Creatine and vegetarian athletes: do we need it to reach peak performance?


Hey all!

Continuing to trudge through my semester- final stretch before exams, cannot wait until christmas!! Still loving my job and have found a new love with kale chips :p lol. I’ve been a little unmotivated with training over the past month but after not being able to compete this past weekend (work :( ) I’ve gotten a little inspiration and am back full force :) . Did a pretty good workout today, I’m sure my shoulders will be wrecked tomorrow :p.

Also just trying to figure out the pictures on wordpress, if this works heres a pic of me climbing at the Red! :)

So on a related topic, and something I’ve been pretty interested in because I’m both a vegan and do a sport where power is important; todays post will be on creatine! Be warned, its a long one lol.

Vegetarians have been shown to have better or equal cardiorespiratory test scores but lower strength and explosive power test scores. Endurance does not seem to be a problem but there seems to be something missing that is necessary to build strength and power, this is seen by the domination of strength athletics at the elite level by omnivores. A reason for this may be due to the decreased levels of creatine in vegetarian and vegan muscles; endurance may not be affected since creatine aids more in anerobic and power exercises.

With the decreased concentrations that vegetarians and vegans have of creatine, are we doomed to always be restrained from reaching our peak athletic capacity? If we are athletes where power is vital for success, are we giving our omnivorous competitors a one up on us?

Once again, creatine stores in the muscles of vegetarians are lower than omnivores; dietary creatine is found in meats. Creatine supplementation can help correct this imbalance by increasing the content by about 30% (people with deficiencies are typically more responsive).  Vegetarian or vegan athletes are therefore more likely to see more gains through supplementation.

A lot of people have heard that creatine can be made in the body, why even bother for supplementing? Well your right, 50% of our creatine comes from endogenous sources and  is made with the help of the amino acids arginine, glycine and methionine (as well as the enzymes L-arginine:glycine amidinotransferase, guanidinoacetate methyltransferase and methionine adenosyltransferase) largely in the liver and kidneys (and also in the pancrease to a lesser degree). Endogenous synthesis provides about 1g/day, dietary intake also typically provides 1g/day so that there is a 1:1 ratio of endogenous and exogenous synthesis. Clearly, dietary intake is required to maintain normal creatine levels in our bodies.

About 90% of our creatine is located in the skeletal muscle as either free creatine or phosphocreatine; about 2/3rds of that creatine is in the storage form phosphocreatine. During intense exercise, phosphocreatine can be quickly broken down to release its phosphate (which is rapidly coupled with an ADP to produce energy)- it is broken down by an enzyme called creatine kinase.

Creatine plays an essential part in the transport of energy from the mitochondria. Since phosphocreatine is broken down so quickly, levels rapidly drop and ultimately results in fatigue. Increased concentrations of creatine can help increase the resynthesis of phosphocreatine during recovery.

Okay, so sure dietary creatine is important, but would supplements actually get into our muscles? Yes! Creatine is transported into cells and the mitocondira by Crea T1. As creatine levels drop, Crea T1 is activated in order to restore the balance. That’s why people who have deficiencies are more responsive to supplementation, therefore vegetarians and vegans will see greater improvements through supplements.

Now how would creatine help an athlete? Creatine supplementation enhances athletic performance, max strength, fat free mass and muscle hypertrophy when combined with resistance training. It is most effective for short duration exercises but there is some evidence to positive effects on endurance activities. It is effective for improving recovery, maintaining muscle creatine concentrations as well as acting as an antioxidant.

Creatine seems to have gotten a bad rep. throughout the years as so many gym rats take it in excess to get huge- water weight that will probably be lost after supplementation stops (which it should!). Creatine still remains to be one of the most powerful ergogenic aids on the market, you only need small doses to see a positive improvement in both muscle and power.

In a recent study on professional soccer players, after supplementation for only five days, there was a significant improvement in strength and power at the end of the trial (using a double blind randomised placebo-controlled trial). The difference between the placebo group to the creatine group was also staggering, while creatine muscle mass and power increased, the placebo group remained steady or dropped slightly. The fact that these results were seen only in five days is pretty crazy!

With all of that said, weight gain seems to be inevitable so if you compete in a weight dependent sport you should probably keep that in mind and tread cautiously if you’re considering supplementation. A good option would be making the doses much smaller and not doing the loading phase (studies indicate that creatine loading is not necessary). Expect to gain a few, but with that will come POWER!

Well that’s that, those are my thoughts on creatine supplements. Would I do that myself? I would definitely give it a try- but would 100% stop if I gained more than 5lbs. Body weights kindof important when you have to haul your body up a wall lol.

Hope you enjoyed :)

Jen

Cooper R, Naclerio F, Allgrove J, Jimenez A. (2012) Creatine supplementation with specific view to exercise/sports performance: an update. J Int Soc Sports Nutr. 20;9(1):33.

Gouttebargea, V., Inklaarb, H., Hautierc, C.(2012) Short-term oral creatine supplementation in professional football players: A randomized placebo-controlled trial. European Journal of Sports and Exercise Science, 2012, 1 (2):33-39. 

Venderley AM, Campbell WW. (2006) Vegetarian diets : nutritional considerations for athletes. Sports Med.;36(4):293-305.

Animal vs. vegetable based protein


Long time! Sorry guys! Midterm season caught me off guard and I had to take a bit of a break from blogging, but theyre done and over with! Wohoo!  Lots of change for me within the last month; my sister married her boyfriend of about a decade- so happy to have another brother in law annndddd I got a nutrition job!! :) :)  Climbing outside is getting hard given the temperature and my sissyness in the cold lol :p, I guess I’ll have to make do with indoor climbing for the time being until I can get some time off of work to head back south!

Annyways, my blog today will be about protein supplementation- in particular, animal based verses plant based… some controversial views- hope you enjoy! :p And let me know if you have any questions, comments or concerns! Negative or positive, I’m always happy to get feedback :)

Protein intake that exceeds the recommended daily allowance is widely used by athletes. Many athletes look to protein supplements in order to decrease recovery time and increase gains from their workouts; this in turn will increase their performance ability. Which protein source for a supplement is the best choice for athletes? Animal based or plant based? This is a question that has been hotly debated for years with factors such as absorption, completeness and alkalinity playing major roles.

Common sources of animal protein for supplementation include whey protein and egg protein; both are fast-absorbing. Casein protein is also an animal based product; it comes from beef and is slow absorbing.  Vegan options include soy and hemp (among others); both are of moderate absorption. Animal and plant protein supplements both provide complete amino acid profiles; animal based proteins have higher sulfur amino acid concentrations than plant based proteins, which may or may not be a good thing. Are the variations in absorption rates something we really need to concern ourselves with? Recent work has indicated that absorption rate of protein supplements is not of dire importance for a faster recovery in athletes. In my books, in terms of absorption and amino acid profile, vegan and animal supplements both serve their purpose well.

So what are some other considerations we should take in determining which source of protein is better for athletes? Drug Administrations allows certain concentrations of chemicals into our foods which have resulted in the allowance of many contaminants into protein powders including cadmium, arsenic, lead and mercury. The amounts may result in toxicity, predominantly in the liver, if users consume more than one serving per day, like many athletes do. Obviously an athlete who is straining their liver with toxin metabolism will not be able to reach a maximum performance. Animal based proteins show the highest concentrations of these chemicals, although that’s not to say that people who consume animal based proteins are on a path towards liver failure (just ones that are consuming way too much). With additives aside, how would an additive free animal based protein supplement compare to a vegan one?

Animal proteins are associated with higher saturated fats and cholesterol which may increase the risk for heart disease. Vegetable based proteins have no cholesterol, lower saturated fat and higher fibre content which are shown to improve glucose tolerance and risk for heart disease. That said, the above facts do not seem like something an athlete would have to concern themselves with. On the other hand, animal proteins also have higher amounts of sulphur containing amino acids, which contribute to increased acidity within our body. Our body must then waste energy to correct this! Enzymes cannot function at their full capacity when the pH is not that of a healthy, physiological pH and therefore athletes with acidosis will not be able to reach their full performance potential. On the flip side, vegan proteins are alkalizing which helps athletes remain at a normal physiological pH.

Alkaline diets promote recovery, decrease inflammation, and decrease muscle and joint pain and stiffness. That decreased recovery time means that athletes will be able to train more and as a result see quicker gains. The removal of stress from poor nutrition also means that athletes will be able to sleep better which is another factor for promoting recovery as well as managing sugar and caffeine cravings. A healthy athlete will be more likely to have a longer career and increased energy to train and compete.

Although vegetable based protein supplements may be a healthier option for athletes, they are deficient in a few things that would be beneficial to athletes. Heme iron for example is not present in vegetables, although non-heme iron is. Non-heme iron is not as bioavailable as heme iron and, since athletes require more oxygen delivery to their active muscles, non-heme iron may not be sufficient enough to sustain a healthy iron status. Iron deficiency anemia is a common problem, as well as anemia due to vitamin b12 (which is also only present in animals), in vegetarian and vegan athletes. Creatine is also lacking in vegetables, which is important in power during performance. With all of that said, the above can be supplemented into vegan athletes’ diets which will provide ample amounts of the above nutrients. Also, omnivore athletes will have these nutrients in their diets through other sources and therefore they wouldn’t be an important factor in which protein supplement is better for them.

Now it’s your turn to decide for yourself which protein source is better! Knowledge is power; instead of listening to mainstream marketing, take your health into your own hands and educate yourself to become the informed consumer we should all be.

Stay tuned for my next blog on creatine! :)

Jen