Tuesday, December 4, 2018

Vegetable Oils are Bad: Tucker Goodrich, Peak Human podcast review (Part 1)

The Peak Human podcast with host Brian Sanders and guest Tucker Goodrich is my favorite health podcast episode of 2018. In the podcast, Goodrich makes a persuasive case as to what he believes is the primary cause of the diseases of civilization (diabetes, coronary heart disease, autoimmune disease, cancer, etc). In this 94 minute podcast, he strongly posits that one type of food is at the root of the health problems of our times.

What is the primary cause of these health issues? Vegetable oils. Or seed oils, as they are more accurately but less commonly known.

These seed oils are industrially-processed oils containing high levels of Omega-6 fatty acids, which break down into toxic products in our bodies. These vegetable oils (corn oil, sunflower oil, canola oil, soybean oil, safflower oil, etc.) are cheap and therefore ubiquitous in our modern food supply. Tucker Goodrich postulates that these oils, even more than refined carbohydrates, are driving the diseases that plague most of the civilized world.

Goodrich makes the case by looking at the effects of consuming vegetable oils from several valid perspectives. In my view, he approaches the modern disease problem from all the correct angles. Some of the perspectives from which he approaches the problem are:
  • Evolutionary perspective
    • Why are we now getting these diseases of civilization at greatly increased rates?
  • The Weston A. Price perspective
    • Did the healthy populations visited by Price eat these vegetable oils?
    • Were the unhealthy populations visited by Price eating these vegetable oils?
  • Epidemiological perspective
    • What happens to disease rates when a population begins eating these oils?
  • Engineering/"IT guy" perspective
    • Populations have not always had high rates of these diseases. What changed?
  • Mechanistic perspective
    • Do we have a legitimate mechanism for why these oils would cause these problems?
    • Have we seen this mechanism show up in animal models?
    • Have we seen this mechanism show up in human interventions?
  • Personal perspective
    • What happens when an individual increases these oils in their diet?
    • What happens when an individual cuts these oils out of their diet?

This podcast episode is intriguing to me because the idea that these oils are harmful unites many diverse dietary strategies. Paleo, Well-Formulated Keto, Whole Foods Plant Based, Carnivore, Ray Peat, Potato Hack, Weston A. Price Foundation: all of these ways of eating shun the consumption of vegetable oils. I think that commonality is a large part of why people can find success with such wildly different approaches.

This podcast (along with following Goodrich’s and dozens of others’ writings, podcasts, and research) helps convince me that seed oils are the worst part of the modern American diet. While I also think there are benefits to limiting carbohydrate intake, cutting down on consumption of linoleic acid (an Omega-6 polyunsaturated fatty acid that is highly concentrated in vegetable oil) is potentially even more critical for health. Wheat products also seem to cause a lot of health issues, so limiting or completely removing them would be wise. This podcast with Goodrich touches on all of these points. It is a valuable listen for anyone who would like to improve their health or gain a better context as to why vegetable oils should be avoided.

In Part 2, I will post my takeaways from the podcast. And in Part 3, I will include a podcast listening companion post in which I provide notes and many of the citations referenced by Tucker in the episode.

Do yourself a favor and check out this podcast. And if you're feeling really generous, do yourself another favor and cut vegetable (seed) oils out of your diet.

Here is an incomplete list of oils you would be wise to avoid: soybean oil, corn oil, canola oil, cottonseed oil, rice brain oil, peanut oil, safflower oil, sunflower oil, rapeseed oil. (Avoiding motor oil consumption is also a good choice.)

If you enjoy this episode, consider checking out all the rest of the episodes of Peak Human. It is a really terrific podcast. And after meeting host Brian at a conference a few months ago, I can vouch for him as a kind, sincere, passionate guy.

Monday, November 12, 2018

My Five-Day Fast

Or, how not eating taught me that I really can not do anything I put my mind to


The Highlights


  • I fasted for five days, consuming nothing but water and salt. It was an amazing experience.
  • I consistently felt more fully present, more energized, and more mentally sharp than I do on typical days. (For what it's worth, I was also engaged in a "Twitter fast" during this time, which I think also helped me be focused/present. But due to the tangible difference in how I felt, I attribute it mostly to the actual fast.)
  • On top of my mind feeling sharp, my body felt terrific. Felt light, fluid. Joints felt looser (in a good way), pain-free. Skin felt very strong (there's even a specific patch of skin on my face where I got shingles a couple years ago that I swear I think the skin got stronger. Hard to articulate, but I think some healing took place there), although the skin on my hands and elbows still got very, very dry. (My hands and elbow skin get very dry every year when it gets cold)
  • I didn't notice negative side effects this time (I had digestive issues on a previous 3-day fast. I didn't even poop once during this fast); I think adding sufficient salt may have been the key.
  • I was able to work out every day of the fast at usual intensity. I might have dropped a bit of strength on the back half of the fast, but the difference was minor.
  • I work as a software developer; I was able to work every day of the fast at (at least) normal capacity.
  • My body was cold. Digestion seems to heat the body up. I even get cold when I fast for 16 hours or so on typical days, so being cold was not a surprise.
  • I got a lot less sleep than normal. The last 3 nights of the fast, I got 6, 5, and 4 hours of sleep, but I still felt very energetic. I just woke up really early and was ready to get after it!
  • With a couple exceptions, hunger was not a major issue.
  • Not eating for a few days made me realize that a lot of time, thought, and bodily processing is tied up in eating.
  • The human body is incredibly adaptive.

The Details


Two weeks ago, I decided to complete my longest fast to date. My previous longest fast was 78 hours, so just over three days. I began this fast just wanting to hit a new mark, maybe hit 100 hours, and, if I felt good enough, potentially max out at five days (according to the work of Dr. Valter Longo, five-day fasts can have some beneficial regenerative, health-building effects on the body). Did I feel good enough? You better believe it! I did the full five days.

Five days of consuming nothing but water and salt. To many people, that sounds crazy. Maybe it even sounds like torture. I assure you, it was anything but. It was a remarkable experience and overwhelmingly positive. It was truly one of the most memorable five-day stretches that I have experienced; at the risk of sounding grandiose, it truly felt like I was living on a different level.


Sunday, October 28

I woke up early and worked out: farmers walks, kettlebell swings, and burpees. My wife and I went to our favorite Indian buffet for lunch, around noon. That being said, I was done eating by 12:30 PM on Sunday October 28. When I got home, I weighed myself: 210.5 pounds. I didn't eat the rest of the day. After the Indian meal, I had nothing but water the rest of the day (not even salt).

Monday, October 29

Monday, I dropped my wife off at the airport around 5:30 AM (she travels for work), went to the gym at my office and worked out (approximately 17 hours fasted). Solid weight lifting workout. I had nothing but water all day (not even salt). After my workout, I went to work. I weighed myself when I got home: 206.5 pounds. I did 100 burpees at home after work. I went to bed at 10:30 PM, weighing in at 203.5 pounds. I felt good all day. I had a great visit with one of my best friends that evening and felt very mentally clear and energetic all day. My legs were twitchy, though-- that happens to me a decent amount even when not fasting. Normally I treat that with some combination of salt, magnesium, or mustard. I thought I'd give it a little more time, so I didn't have salt, magnesium, or mustard Monday night. (I didn't have magnesium or mustard at all during the fast.)

Tuesday, October 30

I woke up at 2:30 AM with calf cramps. I do get this occasionally anyway, and generally try to mitigate this with salt and/or magnesium. To this point in the fast, I had not consumed any salt. So I walked around, went back to bed, and got up at 5:30 to go work out before work. I weighed in at 201.5 pounds before work. I felt energized but dehydrated.

I initially wanted to get to at least 48 hours without even having salt during the fast, but during my workout I was feeling a little light-headed (and had twitchy/crampy legs). As I learned from The Salt Fix, consuming sodium helps with these symptoms, and that was very true in this case. So at 6:10 AM in the middle of my farmers walk/kettlebell swing workout, I had some salt with water (I was not going to mess with hyponatremia, anyway). I finished the workout (41 or 42 hours fasted), then I went to work and had another good day. I continued feeling sharp and alert. I didn't record whether I did my 100 burpees before or after work that day. Anyway, I did them. I was worried that I was going to have some gastrointestinal issues (read: diarrhea) Tuesday, but I upped my salt intake and no issues came to pass. (On my previous 3-day fast, I did have some GI issues starting around the 48-hour mark.) Throughout the rest of the fast, I made sure to consume salt in plentiful amounts to replenish the sodium lost via exercise.

I experienced very little hunger all day. Occasionally I would get slightly hungry but it quickly passed.

Wednesday, October 31

I woke up at 3 AM Wednesday and felt raring and ready to go (and weighed in at 203 pounds). I did some comedy writing exercises for a couple hours, then I went in to the office gym and worked out. I felt amazing and, 66 hours fasted, set a new personal best for weighted pull-ups. This improvement in pull-ups was very unexpected. The thing I was most worried about with the prolonged fast was breakdown of muscle mass. After my lifting workout of pull-ups, machine rows, rear delt pulls, and barbell upright rows, I went to work. During the work day, I wrote in my phone notes: "10/31 continue to feel terrific, so much mental clarity, elevated mood. It's amazing how much energy the body must use to digest food based on the increased clarity I feel." Seriously, I felt amazing. Even compared to my baseline, which I tend to think is pretty good/energetic.

I talked to my mom on the phone Tuesday evening. And then I talked to my wife on the phone while waiting for trick-or-treaters to come. No trick-or-treaters came, and that's probably just as well (they would have been disappointed coming to the lame house handing out toys instead of candy).

I don't remember if I did 100 burpees after my morning lifting workout or after getting home. Probably after I got home. Anyway, I did them. Also, I weighed myself at 7 PM: 204.5 pounds

Just like the day before, I experienced very little hunger all day. Occasionally I would get slightly hungry but it quickly passed.

I went to bed around 9:00.

Thursday, November 1

Once again, I woke up really early (2:00 AM) and felt energized. More comedy writing exercises. I had a great time doing this. And I was excited-- I was preparing to do open mic stand-up that night (for just the second time in my life).

Then, around 6 or 6:30 AM, it was time to hit the gym. Time for some hex bar deadlifts, 90 hours fasted. Two quick warm-up sets, then one set of trying to pull 365 pounds as many times as I could. I got 12 reps that day, basically in line with where I was when I last did that workout five days earlier. Afterwards, I tried to test out my vertical jump (my legs typically feel springy after hex bar deadlift), and I was an inch or two below my typical jump. That made sense, as my legs did feel a bit fatigued; some combination of no food and low sleep was likely the cause. But I felt terrific overall.

Then, it was time to shower up and head to another day at the office. At the start of the work day, I had my strongest hunger signals of the week. My body was craving food, especially for about the first hour after working out. But. . . even then, it passed. Throughout the work day, I took notes in my phone saying things like "Fasting is the truth" and "Felt chipper as fudge all week" (only I didn't say fudge). So. . . I was feeling goooooood.

After work, 100 hours fasted, I did 100 burpees.

Then, I prepared a little more for doing open mic comedy. . . I went up at about 9:30 PM (105 hours fasted) and did five minutes of stand-up. Compared to my first time doing it about two months earlier, it went really well. I had a great time; I got some decent laughs from a way-too-friendly crowd. Don't worry, I still bombed on some of my punchlines. I'm just glad my fast wasn't broken by crowd members launching tomatoes at me. Anyway, I was really, really excited about how well it went. It capped off a great day. I got home and went to bed around 11 PM.

Friday, November 2

Up at 3 AM: 204.5 pounds. More comedy writing exercises. I was still amped from my positive experience the night before. Around 5:30 AM, time for the gym. Farmers walks, kettlebell swings, and burpees. I did fail a few steps early on my final set of farmers walks, so maybe I was losing a bit of physical strength by this point. But anyway, I got the workout in. Then I went to work, had a normal work day until lunch time, at which point it was my turn to help on my company's Meals on Wheels delivery route. We finished the route at about 12:30, basically the exact 5-day mark of the fast. I drove towards my house, grabbed some food from the grocery store, and went home to cook it.

Friday I never got as hungry as I was on Thursday after my morning workout, but I definitely felt hungry from time to time and I was looking forward to eating. I was so excited to chow down that I forgot to weigh myself one final time. Plus, I had to quickly get my lamb chops cooked to avoid cast iron sizzling being a distraction on a 1:30 PM conference call. You know, work responsibilities and stuff.



Yum. The lamb chops (and a couple cans of sardines) were delightful. They tasted great, they didn't interrupt the work call, and the fast was complete.

I ended up eating a lot that night. I didn't think to weigh myself until the next morning (after probably eating about 5000 calories since breaking the fast and after an hour or so of open gym basketball Saturday morning): 205 pounds.

A Few More Notes to Recap

Even compared to baseline, I just felt so alive and in-the-moment that week. My mood was very elevated. It was a very memorable week. To my knowledge, no one I talked to even knew I was even fasting except for a few friends at work who I talked to about it (and my friend who I hung out and talked about it with that Monday). I think my performance at work and my social interactions were at least as good as normal, probably better.

I talk about these types of energy, mental clarity, and body-feel-good benefits from my typical way of eating (largely carnivorous, ketogenic, Paleo-ish, low-carb, low-omega-6, intermittent fasting) a lot and I believe they are real. But I'll be damned if there wasn't a marked difference going from that to how I felt during the fast.

I found the weight changes interesting, as it goes to show how weight on a scale isn't always that meaningful. It fluctuates a lot. Despite eating 0 calories between 10:30 PM Monday and 3 AM Friday, I gained 1.5 pounds. A lot of this likely has to do with hydration, sodium intake, and water retention.

I did my first 24-hour fast about a year prior to this 5-day fast. That experience (and the resulting mood elevation, lessening of joint inflammation, etc.) was one of the key moments that made the power of nutrition feel real to me. It shaped how I thought about food and and it helped get me interested in learning more and more and more about health and nutrition. I now know I have a lot more to learn, but this five-day experience was another incredibly powerful experience for me. All of my experiences fasting: from starting out with 12-hour eating windows, to 1-day, to 3-day, to 5-day fasts. . . have been very good for building self-confidence and self-discipline. Being able to control my intake of food made me feel like I could establish self-control in other areas of my life as well. (Somehow, it helps build self-control despite the fact that the self-discipline didn't feel difficult once I decided to fast because the fasting felt so good.)

Admittedly this experience was better than my previous three-day fasting experience (which I also found overwhelmingly positive). During my three-day fast (about six months prior), I got pretty antsy waiting for the fast to end; I went to bed early the last night so I could fall asleep and then wake up and eat a steak-and-eggs breakfast. Plus I got diarrhea during the 3-day fast but not during this 5-day one. This time, I had no intense desire to rush to break the fast and no diarrhea.

With that, I'm done writing about diarrhea. Anyway, fasting was fun. Do you have comments? Questions? Do you have any experiences with fasting? Let me know in the comments section. Thanks for reading.

Note 1: Despite my positive experience and reflections, I am not encouraging anyone to try any kind of prolonged fasting without proper medical supervision. Especially if taking any medications and/or if one struggles with disordered eating. Not everyone is metabolically ready for fasting; it is not risk-free.

Note 2: I record my weight throughout this week because I found the fluctuations to be interesting, not because I had a goal to lose weight. I did this to see what it would be like, to build up a little self-discipline, and to potentially kick off some healthful regenerative processes in my body; I had no desire to lose weight (although I knew that some weight loss would occur).


Monday, October 15, 2018

Book Review: Tripping Over the Truth

Summary


Tripping Over the Truth is a book about one of the most dreaded words in the world. Cancer. Because we have all known and loved people affected by cancer, it’s not a topic to be brought up in polite conversation. And because we have all known and loved people affected by cancer, it is a critically important topic. Throughout his book, author Travis Christofferson weaves together history, science, personal drama, and level-headed criticisms of the status quo in cancer research. This attention-demanding book is likely to make any reader take a step back and consider viewing the disease differently.



Christofferson suggests that the last several decades of cancer research have approached cancer from the wrong angle. Viewing cancer as a genetic disease has led to billions of dollars (and thousands of research careers) being spent on relatively uninspiring results. Despite many claims of breakthroughs, statistically, cancer rates have barely budged since the 1950s. A gripping anecdote: Senator Ted Kennedy signed the National Cancer Act in 1971, and the nation was optimistic that cancer would soon be overcome. Nearly 40 years later in 2009, despite having access to world-class oncologists, Kennedy died from brain cancer. His treatment induced toxic side effects and provided no life extension.

For the last several decades, cancer research has been conducted under the dominant paradigm of the somatic mutation theory (SMT). The SMT postulates that cancer is caused by DNA mutations. However, in practice, cancer is proving to be more complex than the SMT predicted. Some cancers have no driver gene mutations, whereas the SMT predicted that all tumors require sequential genetic alterations. Beyond that, mutations between different tumors and even within tumors are usually too variable to treat. Targeting specific mutations via pharmaceuticals ends up being like playing “Whac-a-Mole”; as soon as one mutation is targeted and destroyed, another mutation pops up. During this time, toxic side effects accumulate for the patient. With all of these moving pieces and parts, it is no wonder prominent oncologist Bert Vogelstein questioned, “Is it possible to make sense out of this complexity?”

The book is certainly critical of the dominant cancer research paradigm, but it does more than simply criticize the SMT. It provides another view for what causes cancer; in this view, DNA mutations are side effects rather than causes. A small group of scientists have been approaching cancer from this other perspective, based on the research of the late Otto Warburg. Warburg said “the prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar.” His theory states that cancer is a problem related to cellular energy production (metabolism). Cancer cells producing energy via sugar fermentation rather than via aerobic respiration is now known as the Warburg Effect.

After Otto Warburg’s 1970 death, Pete Pederson may have been the only researcher still approaching cancer from this metabolic perspective. Pederson made discoveries and published work consistent with Warburg’s theory. He discovered that tumors form when mitochondria (cellular energy producers) become so damaged that they cannot provide enough energy via aerobic respiration, so they send out a distress signal. This distress signal leads to a retrograde response which tells cells to start fermenting sugar for energy.

Decades into his research career, Tom Seyfried (who holds a master’s degree in genetics and a PhD in classical genetics) discovered that caloric reduction could have antitumor effects. Intrigued by this idea, Seyfried then discovered some of Pederson’s research. He also discovered research from Jerry Shay and Warren Schaeffer. Shay and Schaeffer, completely independently, found that inserting malignant cytoplasms (i.e. damaged mitochondria) into healthy cells led to tumor formation. And inserting a healthy cytoplasm into mutated cells led to mainly tumor-free results (only 1 in 68 mice developed tumors in this scenario). Looking at this research, despite never having heard of the metabolic theory of cancer until the 2000s, Seyfried became convinced that cancer is not genetic, but that it is a metabolic disease. He has since become an outspoken advocate of that view, and he published the 2010 paper Cancer as a metabolic disease and the 2012 book of the same name.

Once the metabolic theory of cancer is accepted, ketosis becomes a potentially therapeutic cancer treatment. If you fast, or if you have a very low intake of carbohydrates, your liver will produce ketones. Your normal cells with healthy mitochondria are fueled by these ketones in the absence of glucose. Cancer cells cannot utilize ketones for fuel, so a ketogenic diet can work to “starve” the cancer cells. At the same time, the ketones help the healthy cells deal with the stresses of radiation. So ketosis has a double benefit in cancer treatment. Because of this, Seyfried (building off the work of many other researchers) has become a major proponent of the restricted ketogenic diet for cancer patients. So far, the ketogenic diet’s success in cancer therapy is relatively small in scope: preclinical experiments, case studies, some trials, and many anecdotes. Many more clinical trials are needed. However, in the meantime, it shows tremendous potential as a non-toxic adjunct therapy. And the ketogenic diet’s early success could help reframe how cancer is viewed. Perhaps cancer could be more effectively battled if viewed as a single metabolic disease and not as one of thousands of indecipherably complex mutations. Nothing is certain; like the book says, “only time will tell.”

The Book's Afterword


This book was initially published in 2014. The version I read is the revised version published in 2017, and with it comes a very enlightening Afterword section. In this section, he provides some tidbits showing that the metabolic view of cancer continues gaining momentum and that the ketogenic diet is currently being used successfully as part of a cancer treatment strategy. But the most interesting part of the Afterword is the story how the author’s mother was diagnosed with endometrial cancer in July 2015, just nine months after the book’s publishing. It is a true “skin in the game” moment: how would his mother choose approach her own cancer treatment? At the age of 73, she underwent surgery to remove her tumor, followed by localized radiation treatment, the adoption of a ketogenic diet, and twice-weekly sessions of hyperbaric oxygen treatment. Christofferson’s mother “felt good and recovered remarkably fast from the radiation.” Actions speak loudly.

Other Topics Covered by Tripping


  • The FDA approving drugs based on tumor shrinkage despite that not being correlated with prolonged survival
  • History of how cancer came to be known as a genetic disease
  • Short history of chemotherapy and details of how controversial it has been to essentially poison cancerous and healthy cells indiscriminately
  • The struggle of Pederson’s lab partner Young Hee Ko to bring potential breakthrough cancer drug 3BP to human clinical trials
  • The success of chronic myeloid leukemia drug imatinib (Gleevec)
    • What it means in the big picture of cancer research
    • Whether it truly supports the somatic mutation or metabolic theory of cancer
  • The difficulty in getting funding for research of ketosis as a cancer treatment
  • The regulatory difficulties impeding the testing of cancer drugs in combination
  • The building momentum for metabolic approach to cancer research and treatment even from luminaries like DNA structure discoverer James Watson
  • Press-pulse strategy: constant stress on cancer cells (press) via ketosis, periodic acute cancer stress (pulse) via hyperbaric oxygen treatment
  • Notes about scientific consensus being overturned including the story of how Barry Marshall went from “quack” to Nobel Laureate by drinking bacteria juice and giving himself an ulcer


My Thoughts


Two concepts were constantly flowing through my mind while reading this book.
  1. Baseline beliefs and assumptions matter.
  2. The Pareto Principle is important.
Baseline beliefs and assumptions matter. I believe that, like other wild animals, humans evolved to be naturally healthy and largely free of chronic disease. The “primitive” populations studied by Weston A. Price did not eat white flour, sweetened goods, or vegetable oils. Those same populations had nearly nonexistent incidence of cancer. (For what it’s worth, other studies of traditionally-living hunter-gatherers also show the same low incidence of cancer.) This makes me skeptical of approaching cancer research in a gene-centric way*. The metabolic theory of cancer just explains the sudden increase in cancer rates upon Westernization better than the somatic mutation theory.

The Pareto Principle is important. The Pareto Principle states that the 80% of benefits come from 20% of causes. Lots of brilliant, caring researchers have dedicated their entire careers to studying cancer. But Tripping causes me to wonder whether many of these researchers are simply looking at the wrong cause. Perhaps DNA mutations are not the cause (as suggested by Somatic Mutation Theory), but the effect of mitochondrial damage (Metabolic Theory). Perhaps focusing more on mitochondrial damage and reversal of the Warburg Effect would be the “20%” that provides “80%” of cancer research benefit. 80/20 probably actually undersells the Pareto distribution in this case, as 95% of cancers are PET-positive. PET-positive cancers are cancers that feed off of sugar, making cancer cell sugar starvation (reversal of the Warburg Effect) a potentially fruitful approach.

All of that being said, I think the ketogenic diet is likely to be a very important non-toxic approach for cancer treatment. It’s a simple idea: cancer cells feed off of glucose, so don’t ingest glucose. Starve the cancer cells while your healthy cells can still feed off of ketone bodies. Your body being in a ketogenic state (via fasting, a ketogenic diet, or a combination thereof) will help mitigate the nausea and weakness brought about by other cancer treatments such radiation and/or chemotherapy. Periodic hyperbaric oxygen treatments could be beneficial as well. Doing this could lead to a more effective and less toxic cancer treatment than standard of care**.

Cancer is often seen as something that just randomly happens to people, based on genetics. I do not share this view***. Seeing how much impact lack of nutrition had in previously healthy peoples in a single generation in Weston A. Price’s studies makes me a firm believer that what we eat is far, far more of a driver of cancer than genetics. (In other words, the people studied by Price were genetically healthy but their diets changed and they became afflicted by chronic diseases. Similarly, every single day I see anecdotal reports online of modern people making radical health improvements via diet. These observations significantly impact my view here.) Diet is not the only environmental factor that can cause cancer, but I find it likely to be the most prevalent one. I also find diet likely to play an important role in treating the disease.


*I am not saying there is nothing about cancer that is related to genetics. As the book says, about 5-7% of cancers are related to germline mutations (passed from parent to offspring). But even those inherited mutations interfere with mitochondrial function, consistent with the metabolic theory of cancer.


**I am not claiming that ketosis will cure cancer, nor that there are no possible negative side effects. Ketogenic diet cancer researchers at the OSU Low Carb conference in August mentioned the existence of a reverse Warburg effect in some types of cancer cells (where cancer is fueled by ketones), so ketosis is not a panacea. But ketosis has a lot of potential for improving cancer treatment in a large percentage of cancer cases.

***I also do not mean to blame anyone suffering from cancer. But I do want to provide the perspective that you don’t need to resolve yourself to the idea that “maybe I’ll get it, maybe I won’t, not much I can do”-- there may be steps you can take to lower your risk (steps mentioned in How to Improve Your Insulin Sensitivity here would be among steps that deserve consideration). And if you do suffer from cancer, perhaps you could find therapeutic benefits from fasting, ketosis, or other treatments targeting cancer metabolism (certainly, there are no guarantees, but it might be worth researching further).

Tuesday, September 18, 2018

My Favorite Podcasts

Here is a running list of my favorite podcast episodes.

It's already over 100 episodes. Shout out to the Tim Ferriss/Jocko Willink podcast that got me started down the rabbit hole. It's phenomenal.

Special shout-out to the Comedy Bang Bang podcast. . . I don't list its episodes here (most are more around health/nutrition/mindset), but it's so good it deserves its own separate mention.

Thursday, September 13, 2018

Don't Resist. Be (Insulin) Sensitive

Overview

Just take me to the bullet points. . .

Basics About Insulin

Insulin is a protein and hormone produced by the pancreas and released into the bloodstream; one of its primary functions is to reduce elevated blood glucose levels.
  • Insulin resistance: cells in the body are resistant to the effects of insulin. This is metabolically unhealthy.
  • Insulin sensitivity: cells in the body are sensitive to the effects of insulin. This is metabolically healthy. 
Insulin resistance is tightly coupled with hyperinsulinemia, a condition in which excess levels of insulin are in the bloodstream relative to the levels of blood glucose. Because the insulin-resistant cells do not properly process insulin, the pancreas is forced to secrete additional insulin in order to stabilize blood glucose levels. And those cells may have become insulin-resistant because of chronically elevated insulin. The cause-and-effect relationship between insulin resistance and hyperinsulinemia is a difficult puzzle to piece together, but as a general rule: where there's insulin resistance, there's hyperinsulinemia. And vice versa. And they're both very bad news.

Why are Insulin Resistance and Hyperinsulinemia Relevant?

Insulin resistance and hyperinsulinemia are connected to most of the major health problems that plague modern humanity: type 2 diabetes, cardiovascular disease, polycystic ovary syndrome, erectile dysfunction, Alzheimer's, certain cancers, osteoarthritis, atherosclerosis. . . the list goes on and on.

In general, the higher your fasting insulin is, the higher likelihood you have of getting a chronic disease.

Most people today are on the path to a chronic disease. That is harsh, but likely accurate. A 2015 JAMA study found that in 2012, 49 - 52% of American adults have either prediabetes or diabetes. And that number undersells the true scale of the metabolic problem, as the measurements used in the study are plasma glucose or HbA1c levels. Elevated insulin levels precede elevated glucose levels by up to 24 years. If half of American adults have elevated glucose levels, significantly more than half of American adults have elevated insulin levels and are therefore headed towards chronic disease.


How to Know if You Are Insulin Resistant

There are several ways to test out how insulin resistant you are.

Two Hour Insulin Glucose Challenge Test

You can ask your doctor if he/she will prescribe the test for you. Otherwise, you can order it without a doctor's orders from WalkInLab. Fasting insulin levels are checked at fasting, then one hour after ingesting 75 or 100 grams of glucose, then two hours after the glucose.

The lower your insulin levels are, the better, at all three measurements.

HOMA-IR Score (Fasting Insulin and Fasting Glucose Levels)

HOMA-IR stands for Homeostatic Model Assessment of Insulin Resistance. It is composed of two tests: fasting glucose and fasting insulin. You can ask your doctor if he/she will prescribe these tests for you. Otherwise, you can order them without a doctor's orders from WalkInLab (fasting glucose and fasting insulin). It is relatively inexpensive. You can then plug your fasting glucose and fasting insulin numbers into this calculator to figure out your HOMA-IR score. Or calculate it yourself: HOMA-IR = (insulin uIU/mL * glucose mg/dL) / 405

Generally speaking, the lower your HOMA-IR score is, the more insulin sensitive you are. Definitions for insulin resistance are slippery, so different groups define insulin resistance at different levels. It is likely wise to use the ranges from The Blood Code: 0.5 - 1.4 is optimal, 1.9 - 2.89 is early insulin resistance, and 2.9+ represents significant insulin resistance.

LP-IR Score

LP-IR stands for Lipid Profile Insulin Resistance. You can get it tested without doctor's orders from WalkInLab. The lower your score, the more insulin sensitive you are. The lab report should provide decent reference ranges so you know how your insulin sensitivity compares to other people's.

Triglyceride : HDL Ratio

You may be able to get an idea of what your insulin sensitivity is through a standard lipid test. A lipid panel can be ordered inexpensively without a doctor's orders here. Lipid panels return basic information about your cholesterol (total, HDL, and LDL) and your triglycerides.

A high ratio of triglycerides to HDL cholesterol (>= 3.5) has been found to be a straightforward way to identify insulin resistant people. Triglyceride-to-HDL ratio is not a perfect measure of insulin resistance. But if all you have are results from a standard lipid test, the results are useful. You want a low ratio-- the lower, the better.

How to Improve Your Insulin Sensitivity

Now you know how crucial it is to be insulin sensitive and how to measure whether or not you are insulin sensitive. With that in mind, how can you improve (or maintain) your insulin sensitivity?

Six ways to improve insulin sensitivity are nutrition, exercise, sleep, reducing stress, not smoking, and sunshine.

Nutrition

There are multiple ways to improve your insulin sensitivity via diet. Whichever dietary approach you follow, make sure you avoid processed foods that were never eaten by healthy traditional peoples studied by Weston A. Price. Exclude white flour, sugary products, and vegetable oils!

Low Carbohydrate Diet

A low-carbohydrate diet is a terrific way to improve your insulin sensitivity. In a controlled study, Type 2 Diabetes patients treated with a low-carbohydrate ketogenic diet improved their HOMA-IR scores by an average of 55% (measured by insulin levels, 29% measured by C-peptide). Fasting insulin levels themselves dropped by 43% in the same study. [Note: That study is groundbreaking and amazing. 60% of the patients reversed their diabetes in the first year. (!!!!!!!!!!!!!) Check out more about it here.]

Results from a continuous glucose monitoring device before and after adopting a low-carb diet. Notice how there is no blood sugar "rollercoaster" in the "After Low Carb" section. This is one reason low-carb diets are effective for treating insulin resistance. This image comes from the Twitter account of RD Dikeman, who is a prominent partner of Dr. Richard Bernstein.


One of the driving ideas behind a low-carb diet is that it keeps your blood sugar levels relatively stable. When your blood glucose levels stay stable, your pancreas does not have to produce much insulin in order to lower your blood glucose. Keeping the insulin levels consistently low helps avoid insulin resistance and hyperinsulinemia.

General idea: Low blood sugar -> low insulin levels -> better insulin sensitivity

Intermittent Fasting

Intermittent fasting involves deliberately shrinking the window of time during the day in which you eat. Some people consider it intermittent fasting to eat within 12 hours (e.g. eating occurs between 7 AM and 7 PM), while others do things such as One Meal A Day (OMAD). No matter what eating window an intermittent faster uses, their general idea is to spend more time in the "fasted" state as opposed to the "fed" state.

There is a lot of research on intermittent fasting in animals, and slightly less in humans (but there is some). But anecdotal and clinical experience shows terrific results. Intermittent fasting leads to improved insulin sensitivity. This may be partially because shrinking your daily eating window leads to a shrunken window of time during the day where insulin is elevated.

General idea: Shrink your eating window -> shrink number of blood sugar spikes -> shrink number of insulin spikes -> better insulin sensitivity

Caloric Restriction

Caloric restriction involves consistently eating significantly less than what you would eat naturally. Caloric restriction can also improve your insulin sensitivity. The mechanism by which it does this is not clear, but it is consistent with the idea that losing weight leads to improved insulin sensitivity.

Caloric restriction is difficult to sustain, especially for the long term. However, it can be a viable option for improving insulin sensitivity. Some research even shows that it can be very beneficial for quality of life.

General idea: Caloric restriction works for improving insulin sensitivity, but it may be tough to deal with the rather consistent hunger.

Exercise

Exercise to improve your insulin sensitivity!

Sleep

Not getting enough sleep increases insulin resistance in as little as two days! Get plenty of sleep to improve your insulin sensitivity!

Reducing Stress

Stress hormone cortisol is negatively associated with insulin sensitivity. Stress reduction is beneficial for improving insulin sensitivity. Find something that brings you joy. Have meaningful social interactions, meditate, hug a puppy... whatever it takes, reduce that stress!

Not Smoking

Smoking is bad for you. It's bad for insulin resistance. Don't smoke.

Sunshine

Low Vitamin D is associated with increased insulin resistance. The sun is the most natural source of Vitamin D there is. Get adequate sunlight to improve your insulin sensitivity!

Summary

  • You want to be insulin sensitive. You don't want to be insulin resistant. You don't want hyperinsulinemia.
  • Insulin resistance and hyperinsulinemia are intertwined; they are associated with diseases such as type 2 diabetes, cardiovascular disease, male and female reproductive problems, Alzheimer's, certain cancers, atherosclerosis, and many more.
  • Insulin levels are better markers of disease than blood glucose levels; elevated fasting insulin levels can be detected years or decades before elevated fasting glucose levels.
  • If you aren't already being intentional about your nutrition, there is a good chance that you have elevated fasting insulin levels and are on your way to developing a metabolic disease.
  • You can easily and inexpensively get your insulin resistance tested. Everyone should do this; generally speaking, learning your insulin resistance levels lets you know your disease risk years or decades before it will be detected by mainstream medical checkups.
  • There is good news; you can do something about your insulin resistance! Diet and lifestyle play a huge role. Dietary approaches effective in improving insulin sensitivity are low carbohydrate diets, intermittent fasting, and caloric restriction. Other interventions effective at improving insulin sensitivity are exercise, getting sunshine, getting enough sleep, and stress reduction.

References that Dig Deeper

It's the Insulin, Stupid - blog series by Amy Berger
Hyperinsulinemia: A Unifying Theory of Chronic Disease? by Catherine Crofts et. al. - narrative review of hyperinsulinemia and chronic disease
Hyperinsulinemia: Best Management Practice by Catherine Crofts et. al. - narrative review of best ways to manage hpyerinsulinemia
Hyperinsulinemia and Insulin Resistance: Scope of the Problem - editorial by Jason Fung, Amy Berger
The One Test Your Doctor Isn't Doing That Could Save Your Life by Mark Hyman
Why a Low Insulin Lifestyle is Essential for Health by P.D. Magnan
Low Carb Cardiologist Podcast Episode 27 - Bret Scher and Jason Fung
BioHackers Lab Podcast Episode 42 - Gary Kirwan and Ben Bikman
A Guide to Intermittent Fasting - Ted Naiman

Tuesday, August 28, 2018

OSU Keto Conference, Day 2 (Part 3)

Continued from Day 2, Part 2

Gary Taubes: Quality of Calories (Lunch Keynote)

Gary Taubes, prominent journalist and author of books such as Good Calories, Bad Calories, Why We Get Fat, and The Case Against Sugar, detailed some of his research for his lunch keynote speech.

He talked about meeting with Swiss Re, a global reinsurer, in Zurich. Whereas most of the processed food and pharmaceutical industries have little to gain financially from people improving their health via diet, reinsurance companies do stand to gain from it.

He detailed the state of affairs in the timeframe of 1998-2002. At the time there were maybe a dozen MDs across the country who utilized Low-Carb High-Fat (LCHF) as treatment. [He noted that he has since learned that number might be a little low, but regardless it was nearly unheard of.] Authorities (Gerald Reaven, someone named Flatt) used low-carb to lose weight but it was assumed that low-carb would lead to deadly cardiovascular consequences. Low-Fat diets and Calorie Restriction were dogma.

He then talked about an article written by Malcolm Gladwell in 1998 investigating the obesity epidemic in the Pima Indian tribe on a reservation in Arizona. Gladwell raised some interesting points and questioned the nutritional advice being given by groups with authority, but he also implied that Atkins was B.S. advocated just to make big money.

Taubes referenced the work of Daniel Kahneman (author of a terrific book, Thinking, Fast and Slow) by saying that the whole nutrition and medical industry were under the cognitive bias of WYSIATI (What You See Is All There Is).

Taubes fast-forwarded to the state of affairs now in 2018. He said tens of thousands of MDs now prescribe LCHF worldwide. He referenced that the Canadian Women Physician LCHF Network, a closed Facebook group of Canadian women physicians who prescribe LCHF. This group of doctors is at 3290 members.

He said that the conventional wisdom still says that LCHF is dangerous. He showed a 2018 U.S. News ranking that placed the ketogenic diet in last place of all diets. He said this was decided by a committee of establishment nutritionists using groupthink.

However, the tide is turning. In the media, now the argument is turning to whether Low-Fat is as good as LCHF/Keto. This is progress from where things stood a couple decades ago.

Taubes recalled an anecdote of his trip to Switzerland to point out the changing narrative. After a Swiss customs agent learned Taubes was there for a nutrition meeting, the agent said "I should give up carbohydrates, right?"

Taubes referenced the DIETFITS trial of Healthy Low-Fat vs. Healthy Low-Carb. He noted the progress, as both diets restricted refined carbohydrates.

Taubes said many doctors now prescribe by hypothesis and questioned: what about clinical experience?

He said that energy balance (calories in/calories out, AKA "Eat less, move more") does nothing to predict whether an 18-year-old lean person will continue to be lean or whether they are pre-obese. He said that eating "not too much" is a lean person's diet advice (as in, it worked for the lean person, but they might just happen to be lean. More helpful to have advice of someone who at one point was not lean.)

Taubes then talked about the limitations of nutritional epidemiology. That cannot establish causation. What epidemiology does is looks at what healthy people eat vs. what unhealthy people eat. (And thanks to the unreliable data collection methods, it does not even really do that well.) He said that it's not helpful-- compared it to saying that rich people eat at expensive places and buy fancy cars. . . so if you want to be rich, that's what you should do.

Taubes made reference to the DIRECT Diabetes Remission Clinical Trial. He said during the sustained weight loss phase, there was 2/3 energy intake.

Taubes talked about the hyperinsulinemia phenotype. He talked about the hypothesis that to put obesity and/or diabetes into remission, you need to minimize insulin secretion. He said you need low insulin to get fat out of fatty tissue.

He talked about Insulin Resistance vs. Healthy: he said the more time you spend below the insulin threshold, the leaner and healthier you are. He then referenced carnivory, intermittent fasting, and time-restricted feeding in relation to this idea.

He said the key is commitment. And then he showed a quote from Dr. Eric Westman:
"If you do this, it will work. But I can't make you do it. Word on the street is I'm too strict, but maybe strict is the answer."

He also showed this quote from Peter Foley: "Rather than going to the gym, think about the 84 meals a month you're eating."

Taubes referenced someone named Pennington in the 1950s who noticed his weight loss stopped if he ate a single apple.

Taubes asked about plateaus-- does it have to do with not enough fat? Too much fat? Do we still need caloric restriction? Too little/too much protein?

And he also showed this interesting quote from Dr. Evelyn Bordua-Roy:
"Many diabetic patients tell me they can't go low carb because they love pasta and bread too much. I say 'Imagine if you were allergic to almonds and could eat them with an epi pen, would you?' They say, 'Of course not.' So why eat pasta and bread when you can eat them only with an insulin shot?"

It was a wide-ranging, entertaining keynote speech, delivered over a delicious lunch (yes, that is steak, bacon, bleu cheese, and salmon on top of that salad).



Tim Noakes, PhD, MD: Sports Applications and Beyond

Day 1's lunch keynote speaker, Dr. Noakes, returned for a more technical speech on LCHF for performance.

He initially wrote a book titled Lore of Running in 1985. It talked about the need for runners to increase their carbohydrate intake. Noakes believed it from his research and utilized that dietary approach in his own life. Then, he was diagnosed with Type 2 Diabetes several years ago (despite lots of exercise). Throughout his career, he had been funded by industry to study carbs. His old goal was to eliminate all fat oxidation.

Noakes actually produced the world's first squeezy. "I apologize for producing that."

Noakes told Paula Newby-Fraser (multi-time world Ironman champion) to use High-Fat diet, but was still studying for High-Carb.

Noakes mentioned something about being able to store 4 days worth of energy in fat, but only 2 hours worth in glucose.

After one Ironman competition, Noakes was hard-pressed to explain (in a High-Carb context) how physiologically someone could run a 2:40 marathon after the other two legs of the marathon. "Ironman impossible" because there would not be enough glucose available. He listed off some statistics of why that would be impossible, including something about how a 2:40 marathon would require 1.15 grams/minute of fat burning. But despite depleted muscle glycogen, those marathoners kept them going. How long could they go?

Noakes said that fat-adapted athletes can oxidize fat at 1.2 g/min during exercise.

He mentioned some research about carb-loading (what his Lore of Running book promoted) not improving performance, which led to Noakes suggesting carb ingestion during exercise.

Other studies came out, and Noakes now promotes a LCHF approach for endurance athletes. (Note: He does not promote it for performance in all forms of exercise.)

His conclusions:


Stephen Phinney, MD, PhD, DSc and Jeff Volek, PhD, RD: Keto-Adaptation and Physical Performance

Dr. Phinney opened up by asking what we can learn from "modern Stone Age peoples". (A great question! As a reader of Weston A. Price's work studying such peoples, it becomes very clear that such peoples have lots of wisdom we can benefit from today. Related posts from this blog: here and here)

Phinney mentioned The Friendly Arctic, which he noted as the first recorded example of keto-adaptation. He talked about how from 1878-1880, Schwatka traveled with two Inuit families. These families survived nearly exclusively off reindeer meat. Initially they had weakness and became exhausted, but this soon passed. Then they had strength and endurance-- this is why he says it was keto-adaptation.

The quote: "When first thrown wholly upon the diet of reindeer meat, it seems inadequate to properly nourish the system and there is an apparent weakness and inability to perform severe exertive, fatiguing journeys. But this soon passes away in the course of 2-3 weeks." (He cited where that is from, but my screenshot was too blurry to read the citation.)

Phinney talked about the work of Vilhjalmur Stefansson (author of the aforementioned The Friendly Arctic). Stefansson was a Harvard anthropologist who claimed, based off his studies of the Inuit people, that you could live healthfully off of only meat and fat. The nutrition establishment called him a liar. He allowed himself to be studied for a year, in which he only ate meat and fat (and he was locked up for the first several months to ensure no foul play). At the end of the year, he was fine. He ate nose-to-tail of the animals, so his diet included muscle meat, organs, and fat. The energy composition of his diet was approximately 15-20% protein, 80% fat, and 2% carbohydrate.

A 1939 study is what led to the expansion of the high-carbohydrate diet. 3 subjects showed increased exercise capacity by consuming high-carb diets.

Keto-adaptation was mentioned in regards to an early Phinney study. It discussed how after one week of the ketogenic diet, performance is diminished. But after six weeks, performance is enhanced. So by the six-week mark, you are keto-adapted (AKA fat-adapted).

Phinney worked on a 1983 study where subjects adopted the Stefansson diet. Four weeks were allowed for adaptation. In those subjects, there was a minor improvement in Time To Exhaustion. Initially energy was provided about 50/50 by carbs and fat. Eventually it was mostly provided by fat.

Between the six subjects in this study, there was variability.

Uric acid competes with BHB (this is interesting to note for anyone with gout curious about the ketogenic diet).

In my notes, I have something about Phinney saying minimum adaptation is 9-12 weeks. . . I'm not entirely sure how that squares with the above mentions of keto-adaptation at 4 and 6 weeks. I'm sure I missed some of the detailed context in my notes.

This was a study of the metabolic characteristics of keto-adapted ultra-endurance runners. They had 10 subjects in keto-adapted group and 10 in a high-carb group; they were well-matched outside of dietary differences. The subjects ran for three hours staring at a brick wall. They took muscle biopsies, blood draws, urine and feces samples of all runners. The glycogen was the same between low- and high-carb athletes. They don't know exactly why. The low-carbers had increased LDL and HDL cholesterol (for LDL, they had increased "large fluffy" LDL particles and decreased "small dense" LDL particles).

They referenced that 71% of young people today are ineligible for military service today, largely due to obesity. They transitioned into a TANK (Tactical Athletes in Nutritional Ketosis) study. n=30. Average ketones of participants were 1.2 mmol/L. Despite this not being a weight loss study, and despite the subjects eating ad lib (e.g. their portions were not rationed out), the keto subjects lost body fat and increased lean mass.

They finished with the following image to display why an athlete might be wise to use a ketogenic diet:



Brianna Stubbs, PhD and Dawn Kernagis, PhD: Role of Ketone Supplements

Dr. Stubbs and Dr. Kernagis came to discuss exogenous ketones. The devil is in the details.

Stubbs was a member of the British international rowing team.

Differences between exogenous (taken externally) and endogenous (produced by body) ketone generation was discussed.

Exogenous ketones have a rapid onset effect, but they require a top-up once the ketone energy begins running out. Exogenous ketones are not fat-burning; they are anti-lypolitic. Low plasma free fatty acids.

The commonality between the Ketogenic Diet (KD) and exogenous ketones is beta hydroxybutyrate (BHB).

There are different types of exogenous ketones: MCT (not technically an exogenous ketone, but readily converted to ketones), ketone salts, ketone esters.

Ketone salts: D- and L- BHB

Ketone esters "taste like jet fuel"

They talked about differences between ketone bodies BHB and acetoacetate.

They talked about GI tolerance of exogenous ketones; they said exogenous ketones get a bit of a bad rap.

They talked about adding exogenous ketones to a carb-filled diet, including a sub-elite athlete study. In that study, muscle mass was spared with exogenous ketones. Intra-muscular fat burning was increased with exogenous ketones.

In a time trial, distance exercised (I don't have notes on whether this was rowing, running, or biking) was increased by 1.3% in the exogenous ketone group.

Carnegis is the co-host of the Florida Institute for Human Machine Cognition's podcast STEM-Talk.

IHMC is DOD-funded work testing ketone esters against military stressors. Can it help with muscle recovery? Inflammation? Core body temperature?

SOCOM-funded: is there protection against hypoxia? Does it help in altitude training? Grip strength? Cognition? Could ketone esters be useful for high-intensity missions?

Results are mixed on exogenous ketones. Below is a summary slide:


Brendan Egan, PhD: Exogenous Ketones and Athletic Performance

Egan, from Ireland, had a lot of information to get through in a short amount of time. I didn't keep up too well with it.

He started off talking about how little separates elite competitive athletes. The difference over 26.2 miles in the 2016 Olympic marathon 1st and 2nd place finishers was less than a 1% difference: just 70 seconds.

He showed the broad spectrum of types of athletes and where different sports fall: aerobic vs. resistance vs. both.

Power is improved a bit more by carbohydrate oxidation compared to free fatty acid oxidation (advantage: high carb)

High intensity exercise runs off carbs, but as you go longer, you start using more and more fat.

We are 50 years under the influence of "carb loading".

In 2015, exogenous ketones for biking were investigated (for the first time, I think). In 2018, seven Tour de France teams use them.

In rats, we see an increased capacity to use ketones with exercise.

Ketone esters improved time trials by approximately 2% in cyclists in one trial.

Ketone salts showed no benefit in repeated high intensity exercise trials.

Ketone diesters lead to gastro-intestinal (GI) problems.

Finger pricks often overestimate blood ketones vs. serum ketones.

Ketone esters for recovery? Maybe.

Steve Tashjian: LCHF in Soccer (for the Columbus Crew)

Tashjian is the High Performance Director for the Columbus Crew (Columbus' Major League Soccer franchise).

"When we all think alike, no one thinks very much." -Albert Einstein

We need to be willing to live in the margins, make mistakes, and learn from them.

Soccer players need a robust aerobic base with repeated sprintability. How could the volume of available energy be increased? How to more quickly resynthesize energy? Enter LCHF.

In the preseason, the Crew get 6 weeks for fat adaptation. Their players and staff eat 40-80 g carbohydrates per day. They do it as a team together and bond over it. The staff participates alongside the players in glycogen-depleted bike sessions.

They do this for wellness, lifestyle, and performance.

Players and coaches are now taking low-carb back to their families.

The team eats approximately 60% fat, 25% protein, and 15% carbohydrate. Their lipid panels are monitored.

Anonymous surveys find that compliance is pretty good but not perfect. On training grounds, compliance is 93%. At home, 80% (although 98% if you average it out over player minutes). When eating out, 88% comply with LCHF.

Since adopting this in 2015, the team's distance covered has increased each year. Anecdotally, players want less and less carbs even on match day. They are seeing intermittent ketosis from voluntary keto dieting.

In 2015 (the last year the MLS released all team's data), the Crew led the league in distance covered.

A subjective soreness rating two days removed from match day shows lowered inflammation and increased recovery from LCHF.

2014 (pre-LCHF) = 6.5
2015 = 4.8
2016 = 5.1
2017 = 4.4

Players are eating approximately 70 g carbs per day, down from approximately 400 g per day a few years ago.

A new Crew player: "I just feel better. I can't tell you why."



Peter Brukner, OAM: What Should the Team Be Eating?

Brukner, author of A Fat Lot of Good, is from Melbourne, Australia.

He has experience with Liverpool soccer. He was their Head of Sports Medicine and Sports Science.

He said LCHF for high-intensity interval sports has only anecdotal evidence.

Initial studies showed high-carb better for soccer distance covered. He now promotes "train low, compete high" (low and high related to carbs).

He said there is no one diet. He sees three general scenarios with low-carb athletes:
1) athlete full-time LCHF diet
2) Athlete LCHF/keto during week, top up carbs on match day or heavy training day
3) Athlete generally low carb

Advantages of LCHF/Keto: weight loss, which increases power:weight ratio. Metabolic health: what are the long-term effects of high carb? Recovery. Reduced inflammation. Reduced need to refuel during activity. Increased fat oxidation.

Anecdotally, endurance athletes' performance is enhanced. Anecdotally, high intensity athletes' performance may be diminished. There are responders and non-responders.


Q&A Session, Physical Performance Speakers

Finally, there was a Q&A session.

The first question was about epidemiology. A study had just been released, making headlines saying low-carb was dangerous. How do the panelists respond to that? They say it is based on flawed epidemiology. Epidemiology cannot establish causation. There have been lots of very valid criticisms of that study.

How accurate is the Ketonics breathalyzer vs. Precision Extra? No data on breath meters, but blood meters are typically more accurate. Stubbs said that the higher ketones get, the less accurate breath meters typically are.

Dave Feldman, software engineer extraordinaire and creator of cholesterolcode.com, asked about LDL in Columbus Crew players. He and Tashjian talked lipid values for a little bit. Tashjian said they take lipid panels very seriously and worry more about making sure Triglycerides are going down and HDL up, and on "large" LDL rather than "small dense" LDL (as opposed to focusing on total LDL count). Dave said he would love to get a hold of player data; I'm sure he would like to see how many fit his Lean Mass Hyper Responder profile.

A Type 1 Diabetes researcher from USF asked a question but I didn't follow it unfortunately. I think it was above my head.

Dr. Mark Cucuzella got up to give some of the reasons the aforementioned "low carb is dangerous" epidemiology is not very useful: at baseline, the "low-carb" subjects of said study were overweight, diabetic smokers who didn't exercise. So it's no surprise that they would have increased mortality.

A team physician at a small Boston school asked how he should go about implementing Low Carb at his school. I think it was Tashjian that responded saying it would have to be incremental.

A Michigan grad student asked if fat adaptation sticks around once carbs are consumed again. The panel didn't know.

And with that, I've exhausted my notes from the conference! It was a very enlightening conference. I learned a lot, had a lot of good conversations, and met a lot of great people.

Monday, August 27, 2018

OSU Keto Conference, Day 2 (Part 2)


continued from Day 2, part 1


Day 2, part 2

During this part of the day, the speakers were discussing the effect of ketosis on the brain-- specifically, the effects of ketosis on Alzheimer's and epilepsy.


Stephen Cunnane, PhD: Brain Glucose and Ketone Metabolism (Alzheimer's)

Cunnane talks about how ketones are an essential fuel for infant development. Breast-fed babies spend time in ketosis. There are medium chain triglycerides (MCTs) in mammalian milk.

Glucose is pulled into the brain, while ketones are pushed into the brain.

Alzheimer's sufferers have inhibited glucose uptake into the brain. And glucose uptake deficiency precedes cognitive decline. However, the ketogenic diet shows promise as an Alzheimer's treatment because when brain glucose uptake is impaired, brain ketone uptake is fine.

Cunnane mentioned cerebral metabolic rate. Interestingly, the ketone uptake rate into the brain is not as variable as blood ketone levels. People with Alzheimer's can still uptake ketones!

Cunnane talked about the BENEFIC trial (n=39) where cognitive performance was improved with MCT supplementation (MCTs are easily converted into ketones in the body) ("Conclusion: Ketones from MCT compensate for the brain glucose deficit in AD in direct proportion to the level of plasma ketones achieved.")

The more MCT consumed, the less the brain energy gap there was (glucose was still low, but ketones make up the difference). Also, exercise helps get both glucose and ketones to the brain in Alzheimer's patients. Cunnane noted the difficulty of doing such trials; it took 7 years to get 5 Alzheimer's patients through this protocol.

Summary bullet points (from Cunnane's slides):

  • Pre-symptomatic, glucose-specific brain energy deficit.
  • Brain energy rescue by ketones is feasible in MCI [Mild Cognitive Impairment] and AD [Alzheimer's Disease].
  • Recapitulates role of ketones in infant brain.
  • Cognitive benefits and mechanism of action need further evaluation.

Eric Kossoff, MD: Ketogenic Diet and Seizure Management (Epilepsy)

Kossoff is the Director of the Child Neurology Residency Program and a Professor of Neurology at Johns Hopkins. He covered the ketogenic diet's (KD) history in its use as a treatment for epilepsy. We are beyond the tipping point using KD for epilepsy. It is now a mainstream-accepted treatment.

Kossoff noted that in Mark 9:14-29, Jesus recommended prayer and fasting for seizure cure.

In 1921, Dr. Wilder at the Mayo Clinic learned that Low-Carb, High-Fat (LCHF) mimics fasting.

Fasting and ketosis work for epilepsy via different mechanisms.

There was an anticonvulsant drug explosion in 1938, then in the 50s, 70s, and 90s, all of which led to decreased usage of the KD for epilepsy; drugs were now an option, seems easier.

Kossoff mentioned that medical marijuana is now an alternative to the KD (he says it probably won't work).

In the early 1990s, the KD was rarely used. It was a last resport. There was no interest in it at the American Epilepsy Society. Then, in 1993, enter the Charlie Foundation (side note: The Charlie Foundation was started by one of the creators of the best movie of all time [Airplane!] when he went outside the mainstream to use the KD to cure his son's epilepsy. He actually teamed up with Meryl Streep for a related movie titled ...First Do No Harm.)

The number of KD studies has gone up exponentially since the late 1990s.

The Cochrane Collaboration, published in 2012, stated that the KD shows good results for epilepsy.

Today, the KD is usually used after 2 drugs have failed. It is one of the 4 major treatments. Mainstream!

Now, in 2018, the Charlie Foundation has been around for 25 years. 2018 will mark the 6th Ketogenic Diet symposium in South Korea. There is something called KetoCollege and KetoUniversity. The American Epilepsy Society, which showed no interest in the KD in 1993, is holding a symposium on the KD in 2018. Furthermore, the international guidelines are being revised!

Kossoff said we need to know how to make the KD easier and safer.

The traditional KD started with a 24-hour fast. 4:1 ratio of fat to other macronutrients. Kids seen every 3-6 months. After 2 years, they try to wean the kids off the KD.

Now. . . they don't need the 24-hour fast to initiate. Kids often don't need admission to the hospital for treatment. Kids can be gradualized in to the KD.

Kossoff detailed 4 ketogenic diets and said they are all equally valid (slight differences in macronutrient ratios-- Ketogenic Diet vs. Medium Chain Triglyceride Diet vs. Modified Atkins Diet vs. Low Glycemic Index Treatment).

Can the KD be replaced with a pill? People are trying. Certainly not definitive. Maybe as a supplement.

History of: "Can KD help infants?"
1963: No. Not helpful.
2002: Yes. Safe and effective.
2015: Yes. Kids under 2 do even better than older kids.

Johns Hopkins started an Adult Epilepsy Diet Center in August 2010 (previously there had been issues where it was tough to get treatment after turning 18 and no longer being eligible for pediatric care). There are now over 300 adults in the clinic. About 20% were already on the KD. 80% were not doing keto; they get put on the Modified Atkins diet (10-20 g carbohydrate per day, approximately 25% protein, 70% fat).

Outstanding questions to look into: How to improve compliance? What are the implications when patients see elevated lipids? Is the diet safe in pregnancy? (He says he thinks it probably is. In the Q&A below, he touches on this further)

Q&A Session, Cunnane and Kossoff

Is there any research on ketosis for Multiple Sclerosis since it may be an inflammatory brain disease like Alzheimer's? Kossoff said there is not much, although he noted there is some work looking at intermittent fasting for MS.

Dr. Scheck asked about people going off the KD. . . why wouldn't the epilepsy symptoms come back after going off the diet? Kossoff said the mechanism is debated. Said there is some evidence that the KD can alter underlying brain. Cunnane said that with AD patients, going off the KD leads to immediately diminished cognition.

Could the effects of ketones partially be an autophagy effect? Cunnane said they are trying to get funding to study just this.

Someone asked about the APOE4 gene allele-- that tends to lead to problems with saturated fat. . . my notes are slightly confused here. What I jotted down was that the APOE4 gene dampened cognitive benefit and metabolic benefit. But his study saw no difference between APOE4 and non-APOE4. So maybe the dampened benefits are what is typically thought, but his results did not support those.

Is there trouble getting trials for kids? Kossoff said institutional review boards (IRBs) are definitely keto-friendly for epilepsy now. But there are pregnancy exclusions for trials (hence, why he listed "Is it safe for pregnancy?" as an outstanding question in his speech). Just can't do pregnancy trials. Cunnane said the problem is that IRBs are scared of ketoacidosis (toxically high ketone levels) in those cases.

A sports medicine physician from Georgia asked about brain blood flow. Cunnane said you can get the acute effect with exogenous ketones. Cunnane then asked whether it is a desirable effect to get increased blood flow. He answered his own question by saying he's not sure that is a requirement.

A health coach from Detroit asked what the mechanism from exercise is for getting increased glucose and increased ketones to the brain in AD patients. Cunnane said he was not sure. Increased ketones because of increased capacity. Increased glucose: open question.

Someone asked abot children with autism (as approximately 30% of autistic children experience seizures). Is there any research of the KD for autism? Kossoff said the autism community is desperate for answers and treatments. He said a 2003 Greece study showed a very modest benefit. A 2017 Hawaii gluten free modified Atkins beneft also showed a very modest benefit. The mechanism is a hot topic. He said there is some work being done in animal models.

A functional registered dietician asked what may change after long-term KD adherence. Kossoff said only 5% of patients use the KD for > 2 years. He said there are very few long-termers. He said the results of long-termers have been "not great but not bad". He referenced that bone density and bone fractures have been issues. Growth has been an issue. He has seen good lipids and good GI results.

A family doctor from Canada asked about Alzheimer's studies with Metformin, as it can sometimes be helpful with insulin resistance. Cunnane said there are two schools of thought with Metformin. One says it is beneficial because it decreases insulin resistance. The other says it increases the risk.

A neuroscientist asked about nasal insulin as an AD treatment. And about nasal ketones. Cunnane said getting ketones to the brain is the goal. Unknown for both, but I thought Cunnane seemed skeptical.