Sunday, July 31, 2011
Sunday, July 24, 2011
Ok, what is insulin resistance and how does it make me fat? Here’s my interpretation of Taubes’ hypothesis.
When I eat a meal, the carbohydrates are broken down into glucose and enter my bloodstream. Glucose, a form of sugar, causes my blood sugar to increase. Since high blood sugar is toxic, my body instantly responds. First, any fat in my meal isn't immediately used for energy. Rather, it is shuffled to fat storage, at least temporarily, until the high blood sugar is reduced. I temporarily get a little fatter. Second, my pancreas secretes the hormone insulin. The secretion of insulin is in direct response to the increase in blood sugar. Insulin's job is to tell my body's cells to take in this glucose from the blood stream to reduce my high blood sugar.
Muscle cells will take in this glucose and burn it for energy and store some for future fuel as glycogen. Liver cells store some as glycogen and convert some to fat. Fat cells convert the glucose to fat for storage. As the cells in my body use up the glucose in my blood, the blood sugar will drop, and so the insulin will also drop. As the process occurs, fat is released from my fat cells so that they can be burned for fuel in place of the reduced glucose levels. I temporarily get a little leaner. My fat cells are acting as a temporary buffer for energy until my body deals with the toxic sugars.
Understanding the mechanism for how insulin communicates with my body's different cells is the key to understanding how I get fat. Insulin works through two enzymes on the cell: lipoprotein lipase (LPL) and hormone sensitive lipase (HSL).
LPL is on the outside of cell membranes and pulls fat from the bloodstream through the cell membrane. In muscle cells, this fat is used for fuel. In fat cells, it is simple stored and makes the cell fatter. LPL does its job by breaking up the fat from a triglyceride form (glycerol + 3x fatty acids) into individual fatty acids. When insulin is secreted due to high blood sugar levels, it activates LPL on fat cells resulting in fat being diverted from the bloodstream to the fat cells. Conversely, insulin suppresses LPL on muscle cell, so these muscle cells cant burn fat for fuel, but rather the muscle cells will burn the gluclose from the bloodstream to lower my blood sugar level.
HSL breaks down triglyceride fat in the fat cells into their individual fatty acids. Unlike the large triglyceride fat, the fatty acids are small enough to go through the fat cell membranes to be liberated into the bloodstream and eventually used for fuel in muscles. Insulin suppresses HSL. When insulin is secreted due to high blood sugar, it doesn't allow the HSL to liberate fatty acids so muscle cells need glucose for energy. When the blood sugar levels drop and insulin drops, then HSL activates the release of fatty acids into the bloodstream to be used for fuel by the muscles.
The reason why some of us seem to fatten more easily is that our body's muscle cells are less sensitive to insulin. Said another way, some of us are insulin resistant. And the reason why some of us fatten as we grow older is that our muscle cells become less sensitive to insulin. When our muscle cells are less sensitive to insulin they do not adsorb glucose as readily from the bloodstream. This makes our blood sugar levels higher which makes us secrete more insulin. More insulin secretion activates more LPL on fat cells so that they accumulate more fat. More insulin secretion suppresses more LPL on muscle cells so that they will not burn more fat. More insulin secretion suppresses HSL in fat cells so that fatty acids are not released for fuel. With more insulin secretion more calories will be stored as fat, fewer calories will be available to fuel the rest of the body, the more we will eat to replace those lost calories in the fat (or become more sedentary) and the fatter we will get.
Insulin resistance leads to metabolic syndrome, which is a condition with several signs besides fattening, including high blood pressure, high triglycerides, low HDL levels, glucose intolerance (trouble controlling blood sugar) and becoming sedentary (from caloric drain into fat tissues).
Taubes argues that there is a way to break this cycle. Reduce the quantity of carbohydrates and improve the quality of the carbohydrates in a meal. These two factors drive insulin secretion and the accumulation of body fat. Not all foods that contain carbohydrates are equally fattening. The most fattening carbohydrates are the ones that have greatest effect on blood sugar and insulin levels. The glycemic index is a measure of how our blood sugar responds to certain foods. If the glycemic index of food is minimized, then the secretion of insulin and fat stores is minimized. Foods with high glycemic index include refined flour (bread, cereals, pasta), liquid carbohydrates (beer, fruit juices, sodas) and starches (potato, rice, corn). Leafy green vegetables are an example of low glycemic index foods. They have more water and digestable fibers that make up their weight. They have low concentrations of carbohydrates.
My only criticism of Taubes' book is that it is easy to get lost in his argument against "calories in, calories out". He argues consistently that a positive caloric balance (eating more, moving less) is not the reason why we get fat. This seems illogical, and it is at face value. Taubes' argument is merely that a positive caloric balance is a side effect of getting fat, not a cause. The real cause for fattening is the loss of calories to fat cells caused by high insulin levels from too many carbohydrates in our food. An appreciation of this book requires an open mind and patience to follow a unique point of view.
Saturday, July 23, 2011
What a deal! Since I parted ways with my Garmin 205 (no heart rate monitor), I kinda missed the toy, and the new low Amazon price was too much to pass up. I wanted to share my first run with the Garmin 305, a 2 mile time trial on TTU's track.
The purpose of the time trial was to benchmark my performance for future time trials and to try to determine my maximum heart rate. The time trial was preceded by a 1 mile warm up (at average heart rate 133 bpm and average pace 11:21 min/mile)and succeeded by a 1 mile cool down (at average heart rate 148 bpm and average pace 12:07).
My average pace during the 2 mile time trial was 6:48 min/mile. My fast pace was at the very end at 5:36 min/mile. My maximum heart rate was also at the very end of the time trial at 192 bpm. The max heart rate age formula for a man is "220-age". Based on my age, my max heart rate should be 178 bpm. Does this mean my heart is 14 years younger than my chronilogical age, or perhpas the formula is too general?
I love to run on tracks. It brings back memories of my more competitive days and gets my juices flowing. But my main reason for wanting to run the time trial on a track is for consistency with future time trials, and for the consistency of elevation. I wanted heart rate response to be only affected by effort and not by elevation changes. Curiously, the graph below shows the track elevation isn't as level as I presumed it would be. Maybe it's just the scaling factor of the graph, but 10 ft. of elevation change (east side 10 ft. higher than west side) seems not very level. I suppose this is a characteristic of Tennessee hilly tracks.
Sunday, July 17, 2011
But Brian's store wasn't our first stop. When we were in Florida last month, Victoria found a cute pair of yellow Merrell shoes at a touristy shop on the boardwalk. I think they were called Pace Gloves. She liked them, but I was really hesitant to buy them, so we didn't. I can't recall how much they cost, but it was too much, like $110. One of my pet peaves is the non-minimal price of minimal shoes. It's not just Merrell either, Terra Plana and Vibram have high prices among others. Even the small guys like Luna and Soft Star have high prices. Aqua socks are one of the few reasonable alternatives for minimal footwear at minimal prices.
So back at Foothills, Victoria was trying on shoes for cross country. The only thing that these shoes seemed to have in common with the minimal shoes category were the high prices. The spikes and flats came close, but even those seemed to me from my barefoot perspective to have a lot of cushion. The shoes in this store were just like the shoes that I wore running for 25 years, off and on in between injuries. After years of chronic achilles tendonitis, not finding a shoe solution and after reading "Born To Run", I opted for an alternate solution. I suppose it could be called the Null Hypothesis, not wearing shoes. In two years since adapating this hypothesis, I haven't found a reason yet to go back to those cushy shoes.
But this was about Victoria's experience. Brian was watching her walk in several pairs in the store and also watching her jog outside the store. One thing that I read on his website and liked was that the shoe fitting process was not an exact science. He pointed out that Victoria's left foot kinda dropped inward when she landed. I couldn't really see what he was referring to. He was guiding her into shoes that had more support with that grey material under the arch. She wasn't digging the feel of them. Finally, he brought out a pair that she settled on, Saucony Kinvara. I think these were a good choice for her. They were one of the closest to minimal shoes in the store. Brian even pointed out that they have a minimal heel-to-drop of only 4 mm. There were also some of the cheapest at $85 (imagine that, the shoes most like minimal were the cheapest, the irony).
My food scale weighing the shoe (yes, I can get that anal about food)
Running and Rambling offered this review of the shoe. Under 8 oz. the shoes are relatively light. There's very little rubber on the sole, only on the high wear locations. This really shouldn't be much of a durability concern for Victoria because most of her running will be on the grass of the cross country course. Another advantage of the minimal rubber on the sole appears to be good flexibility, as you can do the burrito roll up test on them (sorry, no pic). Anyway, if the shoes give her problems running, as Brian said, they'll look good wearing them to school. I suppose the best part about the shoes are that their purchase supported our local running store.
Victoria and Sylvester on the Porch
Friday, July 15, 2011
This cause and effect is really hard for me to get my head around, as I suppose it is for most folks, at least before considering Mr. Taubes’ arguments or evidence.
For example, as mentioned in a previous post, in a study on mice those that had their ovaries removed got fat, either by eating more or if starved, then moving less. Estrogen, the sex hormone that’s produced in ovaries, was injected back into these mice, they ate less and they became leaner. When estrogen was removed, the mice stored more calories than they burned. Those stored calories in fat were not available for energy in the rest of the body, so the mice had to consume more food energy. When estrogen was replaced, the mice burn more calories than they stored, so energy was readily available and more food consumption was not necessary. The hormone was the cause of the obesity, and the caloric imbalance was an effect.
Another example given by Taubes is that children don’t grow taller because they eat more. They grow taller due to growth hormones. The growth causes a caloric imbalance, so they eat more. We don’t say that a 4’6’’ person is short because they ate too little, or that a 7’6’’ person is tall because they ate too much. Caloric imbalances are the result of growth hormones causing the body to grow and consume calories doing so. The effect is that children eat more.
Taubes is not saying that a fat person is not in positive caloric balance. Taubes is saying that a fat person is in positive caloric balance, but it’s irrelevant. It’s an effect of getting fat. So what causes us to be fat? I’ll give my understanding of Taubes’ hypothesis next.
Tuesday, July 12, 2011
Bryan Adams sang about it:
Hippies came together for Woodstock, the first one:
Neil Armstrong took one small step:
The Manson family went on a killing rampage:
The Stonewall riots sparked the gay right's movement:
It was also the summer I boarded Mothership Earth:
This is what 42 years can do:
Sunday, July 10, 2011
One example in the book is a study on rats. The ovaries were removed from female rats and they ate a lot and got fat. Some of these rats were calorie restricted. They too became fat by becoming sedentary. It would seem that the rats got fat because they either ate too much or moved too little. But Taubes says that this is simply stating the obvious and doesn't describe the underlying cause of the obesity. It's like asking why a room becomes crowded. A smart-ass would say because more people entered than left the room. Certainly, but why?
In the rat study, they also injected some of these rats with estrogen, a sex hormone that would have been produced by the ovaries. The rats with the supplemental estrogen did not eat more food and did not become fat. The explanation for these results is that the hormone estrogen has an inhibitive effect on fat absorption. Fat cells have an enzyme whose job is to absorb fat from blood into fat cells. Estrogen regulates or inhibits how effective these enzymes are, like a traffic cop. The role of this hormone also explains why it is common for menapausal women to gain weight when they produce less estrogen.
So, the rats didn't get fat simply because they ate too much or moved too little. They got fat because estrogen was removed from their bodies which allowed their fat cells to hoard fat from their bloodstream. This removal of fat from their blood caused a caloric deficit that would have otherwise been utilized by other cells in the body. These rats needed to offset this loss of energy by either eating more food or moving less. They ate more because they became fat.
Friday, July 8, 2011
"...None of them alone can fully explain the phenomenon of the body ignoring insulin's signal. Part of this problem lies with how we do science. This is the reductionist approach to discovering scientific truth. This is straight forward and relatively easy to do, so lots of scientists swear by it. But what if a clinical problem like insulin resistance is not due to a single domino, but rather a number of dysfunctional proteins or other structural materials in combination? The answer - the reductionist approach can't deliver an answer in this situation. If multiple steps in a pathway, working in varying combinations, eventually compromise that pathway's action, the reductionist paradigm fails. But if one takes a more holistic or cosmopolitan approach to assessing the problem, the cause of the problem might be better appreciated."
Simply said, studying a system one factor at a time doesn't necessarily tell the whole story. To really get the big picture, you have to do several trials where several factors are changed at one time, in a designed way, and analysis the average effects of those changes. This method, referred to as design of experiments (DOE), allows for determining the effects of several factors in a set of trials and the interactions between them.
Wednesday, July 6, 2011
In part 2 I was curious if a low carb-high fat is optimal for my endurance running.
Dr. Stephen Phinney's low carb exercise research could shed some light. He summarized his low carb exercise studies in 2004 article in Nutrition and Metabolism. It was based on two of his previous studies in 1980 article of weight loss and exercise and 1983 article of professional cyclists. Below I give a summary of Dr. Phinney's perspective on low carb endurance performance and my interpretation of his studies.
Clinical research evaluating the effects of physical performance by high carbohydrate versus low carbohydrate diets has historically supported a high carbohydrate diet. Danish researchers Christensen and Hansen in the 1930s measured endurance time to exhaustion on a stationary bicycle after one week on each diet. The endurance time on a low carb diet was 81 minutes compared to 206 minutes on a high carb diet. Swedish researcher Jonas Bergstrom in the 1960s assessed fuel stores in muscles. This research led to the strategy of carbohydrate loading to replenish the limited fuel of muscle glycogen for high intensity exercise.
It's an easy assumption that grain-based carbs are nutritionally superior to meat-fish-based fat and protein since agriculture has competitively dominated over the hunter-gatherer cultures. The development of modern society was supported largely by the shift to agriculture with the ability to grow and store grains, build permanent dwellings and communities and develop infrastructure for transport and trade. And yet, those hunter-gatherer cultures had physical stamina without carbo-loading. What gives?
Dr. Phinney conducted his clinical trials on low carb exercise based on the lessons from explorers living among one of the last of the hunter cultures, the Inuit, more than a century ago.
First, Frederick Schwatka's expedition in 1879-80 covered over 3000 miles in the Artic on foot. After a month's supply of food, the expedition's only source of food was hunting and fishing. Schwatka said that initially a diet of only reindeer meet seemed inadequate as he felt weak to perform long journeys, but those feelings passed away in about 2-3 weeks. At the end of the journey, he walked the last 65 miles in under 48 hours to make a scheduled rendezvous with a whaling ship. Dr. Phinney refers to this change as keto-adaption.
Second, Vilhjalmur Stefansson, a Harvard trained anthropologist, lived and traveled among the Inuit for a decade in the early 1900s while speaking their language and living on their diet without impairment. Stefansson's writings on his adaptation to the Inuit culture and functioning well on only the products of hunting and fishing caused enough controversy that Stefansson agreed to be scientifically observed along with a collegue at Bellevue hospital for the calendar year of 1929 while reproducing his Inuit diet of 80-85% fat and 15-20% protein. Dr. Eugene Dubois supervised the experiment and concluded that both subjects survived the 12 months in apparent good health with no signs of deficiency diseases.
Dr. Phinney recognized that previous clinical trials on low carb diets were only 1 week long, not enough time to allow for adaptation. His first study on the exercise effects of a low calorie ketogenic diet was 6 weeks long on overweight subjects. He evaluated treadmill performance by measuring peak aerobic power (VO2 max) and endurance time to exhaustion at 75% VO2 max. Peak aerobic power did not decline in 6 weeks. Endurance time to exhaustion declined in the first week of the ketogenic diet from 168 to 130 minutes, trending in the same manner as previous studies, but increased to 249 minutes after 6 weeks. It would seem that keto-adaption greatly improved endurance, but the results were confounded by the fact that the average test subject lost about 10 Kg of body weight. Despite wearing loaded backpacks to equal their weight loss, the subjects had greatly improved exercise efficiency as measured by oxygen consumption decrease.
A second clinical trial was conducted by Dr. Phinney on trained professional cyclists to remove the confounding effect of body weight loss and improved exercise efficiency. The cyclists were put on a ketogenic diet for 5 weeks similar to the Bellevue study with the intention that the subjects would be in ketosis without weight loss. On average the subjects lost less than 1 Kg of body weight in the first week on the diet and then stabilized for the remainder of the study. Endurance time was measured at 65% of VO2 max. There was essentially no change in peak aerobic power, exercise efficiency no endurance time.
Both studies show that a person's physical performance is fully restored after a few weeks to adapt to a low carbohydrate diet. Performance levels were measured around 70% of VO2 max. According to David Swain (1994), 70% of VO2 max correlates approximately to 80% maximum heart rate.
There were two other important variables that Dr. Phinney took note of based on Inuit culture. First, he made sure that his subjects had adequate amounts of sodium and potassium supplements. The Inuit people consumed much of their meat in a soup or broth made from coastal ice, a brackish source of water. It was also common for Inuit to add caribou blood to their soup, a rich source of sodium. Second, the protein ratio of the diets was about 1.5 g per Kg of body weight. Too far below this target will result in muscle loss and reduction in VO2 max. Too far above this target will result in suppression of ketogenesis. In Stefansson's writings he noted that the Inuit were careful to reserve higher fat portions of meat for themselves and feed lean meat to the dogs.
Despite the apparent success of Dr. Phinney's studies, I am still nagged by the effect of exercise intensity on the bodies ability to burn fuel from fat. In the middle of the 2004 paper he states:
"...high carbohydrate diets might be more effective in short-term tests of high-intensity exercise..."And Dr. Phinney's concluding statement includes a caveat:
"...anaerobic (ie, weight lifting or sprint) performance is limited by the low muscle glycogen levels induced by a ketogenic diet, and this would strongly discourage its use under most conditions of competitive athletics."This raises a question for me. What is the optimal nutrition for an amateur runner (thinking of myself here) that wants to competitively run a long distance race, such as a full marathon with a goal to qualify for Boston? Is this amateur runner performing at an intensity far and above the subjects in these studies or hunter-gatherer cultures? If so, is low-carb-high-fat an inferior fuel source for such an event?
In my 2004 Chicago marathon charted in part 1, that was the only time I qualified for Boston. I have no idea what my exercise VO2 levels were, or even my heart rate. I was running at a pace that I perceived throughout at least the first half that I could maintain until the end. I wasn't breathing hard. It wasn't until around mile 17 or 18 that I could feel the energy draining from my body, which became progressively worse until I could barely stand to run by mile 23. All else being equal, could I have avoided hitting the wall if I was keto-adapted, or was the pace too fast to keep muscles from glycogen depletion despite an ability to better utilize fat as fuel?
What have other runner's experienced? Kent of Atkinsdietgeek.com ran the Green Bay Marathon in 2011 without hitting the wall. His pace is shown in the chart below. He set a PR of 4:09. Not knowing Kent, I can only assume with a moniker like "Atkins Diet Geek", he is marathon training and racing on low-carb-high-fat nutrition. His pace appears to be at an intensity level similar to Dr. Phinney's trials. It would be interesting to know if Kent has run previous marathons in a keto-adaptive state, but initially at faster paces until hitting the wall near the end of the marathon.
Another low carb endurance runner's account of bonking is on Rambling Outside the Box. In the post by Cynthia and David, they describe running without impairment on several occasions distances up to 50K in a timeframe of about 7 hours without refueling (only water). This pace is in the range of 13 minutes/mile. Again, these experiences seem comparable to Dr. Phinney's research.
Jonas Colting is an example of a very competitive, professional triathlete who embraces low-carb-high-fat nutrition. He has been interviewed by Jimmy Moore and posted on Mark Sisson's site. It's clear though that he doesn't strictly follow low-carb-high-fat nutrition. As he said, all rules are thrown out on race day. He calls it "train low, race high", in reference I think to muscle glycogen. He even is sponsored by the sugary drink manufacturer "Red Bull". However, he does say that his carbohydrate consumption is "a far cry" from the typical amount recommended by Swedish nutritionists for athletes, about 10 grams per Kg of bodyweight, or about 800 grams per day.
Mark Sisson, the former marathon/triathlon "mileage king" doesn't recommend endurance exercise exceeding 80% maximum heart rate to maximize fat burning capacity on training runs. For low-carb-high-fat athletes that choose to compromise some level of fat burning for competitive efforts, he recommends consuming 10-20 grams sugar every 15 minutes after the first 60-90 minutes.
So it seems that some low carb runners like Kent, Cynthia and David correlate well with Dr. Phinney's research, as long as intensity levels are low to moderate. And Dr. Phinney isn't the only researcher to clinically show fat-adaptation doesn't impair endurance. Scientists at the University of Cape Town have published similar results. But it also seems unavoidable that competitive endurance relies at least partially on carbohydrates as per Jonas and Mark. I expect there will be more to say as I do personal experimentation. Til then.
Sunday, July 3, 2011
Although the pace slowed 10% over the first half the run, it stabilized in the second half, as seen by the trendline in the graph. The distance was shorter than I had planned. I wanted to run at least 60 laps (15 miles) but the temperature was getting into the 90s and I could feel heat exhaustion setting in. There was no discomfort in my abs, so the muscle pull has healed. I stopped due to heat exhaustion (I couldn't keep my body cool enough), but the heat was also effecting my feet. Whenever I stopped to get some water, my feet started to burn. The rubber track was really hot. It was tolerable when I kept moving. Blisters formed on the edges of my feet, I believe due to the hot surface. See the video.
So its time to incorporate regular long runs, and I'm thinking I need a GPS/HR monitor. I sold my GPS to Barefoot Josh, and I'm missing it. Prices have dropped alot on Garmins. I can hear them calling my name.