Overall Results

I have to say this journey was not at all what I expected it to be. But that is how science goes. You make a hypothesis, do unbiased experimentation, and report the results (regardless of whether or not your findings support your hypothesis). Unfortunately I did not support my hypothesis. With that being said, I am able to say that I have learned so much from my journey about my personal food sensitivities and how my body reacts to the low carb effect.

My Initial hypothesis was: If I adapt to a ketogenic state through low-carb dieting, then my performance as an endurance athlete will improve in terms of faster times.

Perhaps I should have included a more specific goal that included actual time trails. Overall however, my running workouts did not improve drastically enough to prove that ketosis / fueling through fat improves my own running performance. Although my workout times improved slightly over the months, this could have been due to physiological / mitochondrial adaptations from my training alone.

Overall, from a health aspect I began to feel very inflamed. I will enjoy eating leaner and lighter foods again such as high-carb fruits and vegetables while still staying away from low-nutrient carbs such as breads and white starches. I am interested to see how my training will be impacted from the switch off of low carb!

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Training Progress and Updates

I’ve decided to post about my progress since I’ve been on the low carbohydrate, moderate protein, high fat diet in January. I wanted to give a run down of my personal experience with low-carb and specifically the effects it had on my performance.

The specifics of my macronutrient restrictions included:
< 25 g of carbs / day
< 80 g of protein/ day
and unlimited fat intake depending on my training rigor

I did not change my training intensity nor volume so I could have a consistent comparison of the effects of my diet on my training.

Excerpts from my training journal :
Weeks 1-2:
"I can definitely feel a difference in my morning runs. After being on this diet for 4 days, I feel extremely sluggish and dazed during the first 2 miles of my easy runs. After 2 miles however I feel pretty normal and steady again. My workout days are pretty rough as well. I did an 8 x 1K workout that was miserable! My times were awful. Hopefully I will be adjusting soon.

Weeks 3-6:
“I am still a bit hungry on my morning runs when I first begin but I am getting used to it. On my interval training days (3x /week) I feel oddly stronger after my warmups than I did before low carb. I actually feel like I have more energy during the lasts repeats especially on mile repeats and longer intervals. I started hill sprints again and those have suffered a lot. After the first 20 seconds of the sprint I start to tank. It’s really crazy thinking about the text book pictures of the ATP-PC system during my workout and experiencing it crash. Since I have depleted my glucose supply glycolysis is lagging which is why the last 25 seconds of my hill sprints feel like I’m dying. Even though it is difficult for training, I am really enjoying applying/experimenting with all the science I have learned in my training.”

Weeks 7-10:
I believe I have pretty much leveled off with my low-carb tolerance. My training has both seen improvements and detriments. My longer runs (12+) are so much more enjoyable now! I don’t tank or hit that glycogen depletion feeling after 90 minutes any more! The only workouts that are still suffering are my shorter/anaerobic workouts. All workouts with hill repeats/ sprints under 1 minute still feel like death. It definitely makes sense coming from a scientific view of it. Being that I am training for aerobic races of 5k distance or greater, this really is only a detriment during my final kick of the race. All other endurance workouts have greatly improved! I don’t know if I will stay low carb indefinitely. There are still many other aspects to be looked at such as if it is healthful long term apart from running /performance. And I do miss my bananas and oatmeal!

Ketosis vs. Diabetic Ketoacidosis

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You have probably heard of the dangers of a low carb diet by now. You don’t need to google far to be warned of it’s complications. One critic to the low carb diet, is the dangers of diabetic ketoacidosis. Unfortunately many sources mistake ketosis for ketoacidosis. These two terms are erroneously intermixed. Ketosis is the bodies ability to effectively metabolize fat into ketones to be used as fuel by the working cells. While in diabetic ketoacidosis, insulin fails to reach working cells inhibiting glucose from entering. This diabetic then enters into starvation and as tries to break down ketones for fuel. This diabetic has no insulin however to allow the ketones to enter the cell. The ketones build up causing an extremely acidic environment where proteins denature and ultimately death ensues. This amount of ketone production is not possible for those with functioning pancreatic cells and insulin responses. Even the slightest insulin response will cause a halt to lowering acidity levels.

Let’s look at some graphs provide by Dr. Attia of Eating Academy.

This graph shows the advantage of ketosis when glucose stores are unavailable. The ketone, B -hydroxybutyrate, is able to compensate for the lack of glucose as glucose eventually stabilizes. (For more information on this study click here)

Our brains are built to be fueled by glucose and ketones and nothing else. And because the typical human can only store 24 hours worth of glucose, ketones allow a spare reserve when glucose isn’t available. Where do these ketones come from? Ketones are produced by the liver from fat (and some proteins) and allow our brains to function in the absence of glucose. When ketones are released the pancreas is signaled to release insulin to encourage ketone and glucose uptake by working cells. In ketoacidosis however there is no insulin released and so ketones continue to build up in the blood stream. The insulin feedback loop is broken so the cells believe they are starving and continuously break down more fat/protein with no cell uptake.

Here is a visual for the ketoacidosis feedback loop:

References:

Attia, Peter, M.D. “Blog – The Eating Academy | Peter Attia, M.D.” TheEatingAcademy.com. The Eating Academy, 26 Nov. 2013. Web. 13 Mar. 2014.

“The Difference between Ketosis & Ketoacidosis?” Diabetes Daily RSS. N.p., n.d. Web. 13 Mar. 2014.

O’neille, Michael. “Ketosis: Fear, Uncertainty and Doubt | KetopiaKetopia.” Ketopia. N.p., n.d. Web. 13 Mar. 2014.

Over-eating and under moving? Is it really that simple?

With obesity rates creeping yearly, the nation’s health and workforce is in crucial danger. Why has this problem been recognized for decades but not remedied. Could it be laziness, lack of caring, or just misinformation? Most people have been warned of the dangers of a low-carbohydrate diet and it’s extreme restrictiveness. What are the claims behind a low-carbohydrate diet? Why is a low calorie diet not enough? Why do some people seem to struggle with weight while others don’t? And most importantly, what does the research indicate?

Is the problem of obesity caused by over-eating and under-moving? Conventional wisdom tells us yes but the answer is not so simple. I believe the obesity problem is not an issue of fat intake but of glucose overdose. It is no new discovery that adipose tissue is an organ that actively functions and contributes to hormone secretions. Overweight people have excess adipose tissue which secretes insulin at an elevated rate due to insulin resistance. Being overweight is more than just an accumulation of fat but rather it is a growth disorder. It is an excess accumulation or growth of adipose tissue. This tissue alters the way we metabolize fat. Instead of mobilizing fat for fuel, the obese person stores it which only enhances the problem. Not only does this storage of fat increase stress on the cardiovascular system but it is actively contributing to the problem of insulin resistance and over-eating. Insulin is the most important hormone that influences fat cells to store more fat instead of utilize it. This is where a low-glycemic and low carbohydrate diet comes in. The goal of low carbohydrate diet is to minimize the amount of insulin secreted to minimize fat storage. Your body begins to utilize fats and proteins as its main source for fuel.

The bottom line is that an epidemic this fatal and widespread cannot just be ignorantly prescribed a one-size-fits-all diet or prescription. Every individual is different and just because Sam can lose weight by means of exercise only does not mean that Sue will have the same success.

References:

Attia, Peter, M.D. “Blog – The Eating Academy | Peter Attia, M.D.” TheEatingAcademy.com. The Eating Academy, 2 Dec. 2014. Web. 13 Mar. 2014.

Attia, Peter, M.D. “Blog – The Eating Academy | Peter Attia, M.D.” TheEatingAcademy.com. The Eating Academy, 26 Nov. 2013. Web. 13 Mar. 2014.

LatinWorks. Ads of the World. N.p., n.d. Web. 03 Apr. 2014.
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Does a high-fat diet contribute to heart disease?

Since the dawn of the 70’s, fats have become branded as a sort of evil villian among macronutrients. Many reknown and reliable nutritional sources (such as AHA and CDC) blamed an elevated fat intake for the rise in cardiovascular disease. They believed that dietary fat consumption could increase LDL levels thereby leading to a higher risk for artheriosclerosis. Along with this theory came a recommendation to boycott most fats for a healthy heart. However, since the rise of low-fat diets, our obesity rates have done the same! Here are some graphs I pulled from a Brittish nutrition journal and the National Center for Health Statistics.

The Obesity Epidemic in The USA Started at Almost The Exact Same Time The Low-Fat Dietary Guidelines Were Published



Source: National Center for Health Statistics (US). Health, United States, 2008: With Special Feature on the Health of Young Adults. Hyattsville (MD): National Center for Health Statistics (US); 2009 Mar. Chartbook.

Obesity Epedemic Increased as Butter and Lard Were Replaced With Vegetable Oils and Trans Fats

Source: Dr. Stephan Guyenet. The American Diet. 2012.

With the rise of low fat diets, the high carb diet nightmare began. Not only sending obesity rates soaring but also encouraging higher triglyceride levels. Higher triglyceride levels promote a higher risk for heart disease. So in essence, the very thing that low-fat diets try to prevent is the thing they cause… heart disease.

Shockingly, there has been absolutely no correlation between saturated fat intake and heart disease. This myth began after a poorly conducted and very biased study [Gunnars]. New research now shows that it is actually high sugar intake and high processed food consumption that does the most harm. In fact, the Journal of American College of Cardiology states that “Dietary cholesterol has an important effect on the cholesterol level in the blood of chickens and rabbits, but many controlled experiments have shown that dietary cholesterol has a limited effect in humans. Adding cholesterol to a cholesterol-free diet raises the blood level in humans, but when added to an unrestricted diet, it has a minimal effect.” It also goes on to say that low-fat, high-carb diets play a major role in the obesity epidemic.

So to summarize, now you can fry your bacon and eat it too!

References:

1. USDA Center for Nutrition Policy and Promotion. Nutrition Insights: Insight 5: Is Total Fat Consumption Really Decreasing? In; 1998.

2. “Fats and Cholesterol: Out with the Bad, In with the Good.” The Nutrition Source. Harvard: School of Public Health, n.d. Web. 25 Mar. 2014.

3. Gunnars, Kris. “Modern Nutrition Policy Is Based on Lies and Bad Science.” Authority Nutrition. N.p., n.d. Web. 25 Mar. 2014.

4. Weinberg, Sylvan Lee, MD. “Disease-heart Hypothesis: A Critique.” Journal of American College of Cardiology. JACC, Mar. 2004. Web. 25 Mar. 2014.

Why?

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To start this blog off, I wanted to describe in detail why I am doing this. I am an extremely active, young female with no outstanding concerns who eats a spotless diet according to the USDA recommendations (with the exception of a few glasses of wine). So why would I decide to venture away from a “healthy diet” to explore the effects of a low carb diet? In other words “if it ain’t broke, why am I fixing it?” The biggest motivator I have is curiosity. Even though I have an adequte supply of energy to get me through the day, what if I could tap into even more energy. I am a decently competitive runner, but what if I could increase my body’s ability to rely on lipolysis and increase my efficiency as an endurance athlete. I am tired of simply reading the science behind why or why not low-carb (because either way, their is no simple answer as you will read in my later posts). I want to know first-hand how ketosis feels and its effects personally. My grandmother used to tell me as a child, “figure it out yourself, thats what life’s all about”. In my opinion, there is only so much second-hand research that can be done without getting your hands dirty that can lead to an answer.

Sense & Science

Welcome! My name is Alyssa Allen and I am a current undergrad student of Exercise Science at UNCC. I am infatuated with the physiology of the human body as well as it’s capacity to exercise. This blog will follow my self-experimentation as I rebel against the conventional nutritional science of a balanced diet and explore the advantages or perhaps detriments of a low carbohydrate diet. I am mainly focusing on it’s affects on my endurance performance as I am a competitive runner. Many question my curiosity and stick to the adage “if it ain’t broke, don’t fix it”. As a lover of science however (and seeing our nation’s obesity rates rise to over 30%!), I am geared to question everything. As a child my grandmother taught me “figure it out yourself, that’s what life’s all about”. Keeping to this, I will lead you through my personal journey and discoveries on a low-carb diet as well the science behind it. Enjoy!

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