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).

OSU Keto Conference, Day 2 (Part 1)

continued from Day 1

Day 2, Part 1 (Ketosis, Clinical Applications for Cancer)

I was excited heading into Day 2. . . the first five speakers were all going to speak towards ketosis as a potential cancer treatment.

Also, in case I don't get back around to mentioning it. . . the food at this conference was phenomenal, and all keto-friendly. Eggs and bacon for breakfast one day (and some kind of dairy/berry combo), eggs and sausage the next day. Salads with protein and dressing options for lunch. Delicious. Many people at my table agreed that it was the best conference food they'd ever been served. Also, I wasn't even the only one at my table who brought their own salt! (I brought Redmond Real Salt, someone elese brought pink himalayan salt.)

Other note: I was surprised that a couple people at the conference still balked at mentions of the carnivore diet. I thought the keto crowd would be all on board for it! Most people I talked to were on board, but a couple people seemed thrown off by the idea.

Colin Champ, MD: Dietary Recommendations for Cancer

He didn't call this out, but if you want to read more from Dr. Champ on cancer, check out his website. Specifically, on keto and cancer.

Champ is a clinician and researcher at the University of Pittsburgh. He founded and runs the Cancer Prevention Project. Warburg metabolism was discovered 70 years ago-- this is where cancer cells rely on sugar. This is why ketogenic seem promising for (some) cancer treatments (no sugar for the cancer cells to feed on). This has something to do with faulty mitochondria.

With increased glucose, there is increased cancer cell growth, and with that there is increased fatality.

In a pancreatic cancer study, people who showed blood glucose levels > 200 had low survival. As blood glucose goes up, survival at 2 years decreases.

A 2014 study of ketogenic diets on glioblastoma showed that the ketogenic diet brought blood glucose down.

Exercise, fasting, carb restriction, ketosis are all ways to activate AMPK which decreases cancer growth.

Champ discussed a study where women who formerly had cancer had higher recurrence when eating a high-carb diet when compared to a low-carb diet. This may have something to do with IGF-1 stimulation.

Champ referenced a 1913 (yes, 1913!!!) study published in the Journal of Medical Research that showed a lack of carbohydrates leading to resistance to tumor growth in animals.

Champ said the ketogenic diet is not a miracle cure. He said it is often effective before cancer. And that it can be effective during treatment-- the ketogenic diet works synergystically with radioactive treatment, not by itself.

Interestingly, Champ mentioned a study about statins improving survival in pancreatic cancer patients. (Interesting because low-carbers often are anti-statins for other conditions)

Excess adipose tissue has been shown to be associated with increased cancer recurrence.

Champ, from Pittsburgh, took some pot shots at Cleveland and Cincinnati sports teams. Then he related that to the competition between low-carb and low-fat diets. Out of 57 studies, he found 29 ties, Low Carb won 28, Low Fat won 0.

Champ mentioned that hospital vending machines are a big problem. Lots of people talked about this at the conference-- it isn't something that was on my radar previously. But hearing from these doctors dealing with patients in the real world. . . that is be a huge problem!!

Eugene Fine, MD: Ketogenic Diet and Cancer Treatment

Dr. Eugene Fine was presenting to talk about glucose-avid metastases.

He talked about a 10-patient study he was part of called RECHARGE, where all ten patients had advanced PET+ cancer, and they treated those patients with a very low carbohydrate ketogenic diet (VLCKD), where carbs make up <= 5% of total energy intake. In that study, the patients whose cancers stabilized had 3x higher ketosis. (I have a photo of the chart and the Y-axis shows Dietary BHB / Baseline BHB. I don't have a full understanding, so I am going off of the description of said chart: "Ketosis is 3-fold higher among stabilizers"). Links to information about this study are here, here, and here. The ten patients in this study completed without adverse side effects (note: the patients were specifically chosen because they had glucose-dependent tumors).

For new work, he is working on a 65-patient human randomized controlled trial on patients with breast cancer. A previous study showed that the drug Metformin dropped Ki-67 protein (a prognostic marker for breast cancer, marker of cellular proliferation) in three weeks. The ketogenic diet is usually better than Metformin at controlling glucose and insulin levels, so with that knowledge and the RECHARGE trial vouching for its potential, the keto diet was cleared to be attempted in this 65-patient trial.

They only have data back from their first patient.The patient's Ki-67 (and therefore the patient's health) got worse. That patient was randomized to. . . the ketogenic diet. So the keto diet did not stop this patient's cancer from progressing. Dr. Fine was straightforward about this, and admitted that he was surprised. This was unexpected. He did say that from looking at the patient's tracked BHB levels, the patient was not in nutritional ketosis (BHB too low). He said he, the other researchers, and the doctors take the blame for that. It was interesting. And though obviously sad and painful for the anonymous patient, it was refreshing to see Dr. Fine own up to being surprised by the results. He did not try to sugar-coat things.

Fine went on to talk about how researchers in mouse imaging now think they can trace BHB circulating in the body. He also mentioned ongoing research of rapamycin as a potential anti-cancer drug, as it down-regulates mTOR (but does it cause counter-regulatory effects?).

Angela Poff, PhD: Non-Toxic Methods of Exploiting Cancer Metabolism

Dr. Poff is a PhD working out of the University of South Florida. She mentioned that in many cancers, there is a direct correlation between blood glucose and tumor growth. She showed a chart from this study (study led by Thomas Seyfriend, author of Cancer as a Metabolic Disease) to show this correlation.

Poff said ketones may have an anti-cancer effect in some cancers. Goes back to work done by Magee in 1979.

The idea is that ketones lead to better oxidative metabolism, lower inflammation, lower HDAC, lower blood glucose.

She said exogenous ketones can inhibit some tumor growth.

Cancer cells have increased free radicals.

Hyperbaric chambers can restore oxygen to tumors. In an animal study, animals with cancer did best with a combination of ketogenic diet, ketone esters, and hyperbaric oxygen chamber treatment.

She then discussed press-pulse metabolic therapy. Where press = a chronic environmental stressor and pulse = an acute event with high mortality. She hypothesized that ketosis could be a press stressor for cancer, while hyperbaric oxygen could be a pulse (acute) distressor for cancer. So I think of it like: jab the cancer with sustained ketosis to keep it on the ropes, then go for the knockout punch with the hyperbaric oxygen chamber.

She also talked briefly about the danger of cancer cachexia (loss of skeletal muscle) and how there is no current standard of care to treat cachexia.

From slide: "Cancer will likely require a multifaceted approach", "Effects will be cell, cancer, and model-type dependent", and "Metabolic therapies often work best as adjuvant and investigated as such, including with standard of care". Poff used very cautious language, but she clearly sees lots of potential for ketosis in certain cancer treatments.

Adrienne Scheck, PhD: Tumor Metabolism and the Ketogenic Diet

In vitro, BCNU (a cancer drug) + ketones are effective against cancer.

A 2017 study by Scheck and others showed glowing tumors in mice. I wasn't sure what the takeaway was here honestly, but I'm also kind of dense sometimes :)

She mentioned an increase in survival for mice fed KetoCal vs. standard diet. Study abstract here-- 9 of 11 mice treated with radiation and fed KetoCal were cured

Ketogenic diet reduces Reactive Oxygen Species

Scheck initially thought the ketogenic diet was snake oil; no longer believes so. (Does she think it's extra-virgin olive oil now?)

In vitro, ketones have great effects separate from glucose restriction. BHB increases histone acetylation, increases DNA damage following radiation, is an inhibitor of HDAC, and BHB + radiation leads to enhanced treatment of glioma cells.

Promising keto/cancer research.

Parker Hyde, PhD candidate: Nutritional Ketosis and Advanced Stage Breast Cancer

While all the speakers were excellent, Parker really stood out. He made all of this research hit home as he told the story of his mother being diagnosed (on her 40th birthday) with breast cancer. He made all the high-level scientific discussion reach a personal level. He has spent the last 20 years trying to figure out how to cure breast cancer. (1/6 or 1/8 women will get breast cancer diagnosis in their life. And median survival for metastatic breast cancer [AKA stage 4 breast cancer] is just 26.9 months)

90-95% of occurrence of metastatic breast cancer (MBC) is due to non-heritable traits.

Over 40% of metastases have PIK3CA mutations, and there are reasons to believe ketosis can help against such mutations.

Hyde took care to say not all breast cancers are the same.

Women with post-menopausal obesity have twofold increase in being diagnosed with breast cancer.

Insulin resistance and obesity are correlated (with one another, and with breast cancer diagnoses, if I recall correctly)

Hyde referenced work by Phinney and Volek, and he stated the hypothesis that nutritional ketosis could help breast cancer outcomes. Because metabolism is important, it would decrease inflammation, mTOR would be inhibited, sleep quality would be improved, and emotional functioning would be improved.

He mentioned ketosis being a hammer and everything else being nails.

Then he dug into his work-- the KETO-CARE study (Keto & Chemo for Breast Cancer). 6 months, non-randomized controlled study. Standard care (20 patients, AKA n=20), keto (n=20). For the first three months, the study would feed the patients everything to tightly control what they ate (test biological effect). Then the next three months would be free living (test feasibility-- can the patients maintain the diet on their own?).

Hyde had some very interesting imaging; it showed that the heart even begins using ketones! 

It also showed improvements for the patients who were getting the ketosis treatment.

(Blurry photo below, sorry for poor cell phone image quality. Still interesting. I forget what the imaging specifically highlights, but it was certainly a good thing that less of it was showing up in the 3-month image than the baseline image. The patient was treated with the ketogenic diet.)

Powerfully, here is one of the KETO-CARE ketosis-treated patient's quotes. Important to remember this impacts real people. A real person:

"I am so glad I participated in this clinical trial. The study team have taught me a new way of eating that is healthier for me in many ways aside from any effects it may have on my cancer treatment. My most recent scans showed that my liver mets have regressed and are almost undetectable! I have lost 20 pounds without trying and am off sugar without any cravings. I never thought that would happen!"

Q&A Session, Cancer Speakers

A nutritionist from Costa Rica asked about something he'd seen: advisees who got hyperglycemia after taking Vitamin C injections. Dr. Poff responded that many blood glucose meters actually measure Vitamin C on accident, so their hyperglycemia may not be real; it may just be a defect showing hyperglycemia when the true cause of the meter's spike is Vitamin C.

Is cancer a metabolic disease? Answered: Yes, and a genetic disease, and an epigenetic disease.

A Virta doctor asked if there are concerns about chronically inhibited HDAC from ketosis. Champ's answer included something about ketones potentially protecting against radiation. Poff answered that inhibited HDAC could actually increase the antioxidant response.

An infectious disease doctor asked about wound care. He speculated that carbohydrates are exacerbating wound problems but that administrative restrictions (e.g. national dietary guidelines as standard of care) keep him from being able to prescribe low carb as a treatment. He asked if micro-RNA could play a role in wound care. They responded that it would make a good clinical trial. Poff cited some work done by Lisa Gould, Shannon Lynn Kesl in a mouse model where exogenous ketones quickened wound healing. She said it is not published yet, but told the doctor he could email Poff for more research. (Here is Poff's Facebook page if you are interested)

Someone from Vancouver asked a question about T-cells, B-cells, immune cells that require glucose, and essentially asked if it is a concern that ketosis could inhibit the work of these glucose-dependent cells. Dr Scheck said she was not convinced glucose would go too low. Champ said glucose lowering does not across-the-board help on its own.

An area physician asked about treating patients with insulin to treat cachexia (to lower blood glucose). Champ cited work from the 1960s and/or 1970s: case reports of two patients whose tumors were reported to have gone away using such a strategy. However, he said after that a clinic opened in Mexico for that kind of treatment and it did not go well.

How do ketogenic diets affect PET scan imaging? Do the ketones affect the imaging itself and that's why colors stop showing up after adopting keto? Champ said the scans are trustworthy. Hyde added in measured language about how the Warburg effect (e.g. starve cancer by starving cancer cells of glucose) is complex.

A researcher from the NIH asked about efficacy of treatment vs. toxicity of treatment and asked about lean body mass of patients. Hyde said they are tracking lean body mass with DEXA scans. Mentioned that gaining weight is typically a contraindication for health. He said they are collecting health information on toxicity. Dr. Fine said most patients lost weight, which was positive since most were overweight (so the weight loss was indication of health improvement). Champ said weight loss is not encouraged by the mainstream (due to conflation with cachexia), so that is a barrier in a lot of people's treatment. (General idea: fat loss = good, skeletal muscle loss [cachexia] or lean body mass loss = bad). Champ says we now see heavier patients doing worse. Dr. Maryam Lustberg (panel moderator) jumped in and said social lives complicate nutritional ketosis adherence. Hyde brought it back to the personal again and said patients face discrimination. Several patients, upon cancer diagnoses, end up losing jobs. Then they drop out of studies (which shows in the dropout rate as if they could not do the ketogenic diet).

An OSU nurse asked about how the panel's dream for how their work could be applied to real time. Hyde said they need more funding so they could get more data. Dr. Fine said cancer is more complex than many people originally thought. Keto diet doesn't always work on its own. Also, the reverse Warburg effect exists (some cancer cells are actually fueled by ketones). Scheck said patients think of diet as "just food". Said dieticians need keto training and cancer training. She also said funding is tough because most comes from pharmaceutical companies (so keto makes no $$ for them). Scheck also talked about the need for biomarkers and the need to find out which cancers keto helps vs. the ones that keto makes worse. Finally, practically, all clinicians would need to be fully bought-in to support patients in this approach (think, hospital food, etc).

An oncologist from Uruguay asked about the importance of keeping the glucose/ketone index (G/Ki) between 0.7 and 1.0 (based on Seyfried's animal study recommendations. Hyde said they have seen promising results with relatively low ketones (0.5-0.6 BHB levels). Said you can get that low of a glucose/ketone index in vitro or in mice but not in reality. Dr. Fine said you can't extrapolate from mouse models for the G/Ki. Scheck talked about one patient she know of with a G/Ki =/= 1 who is doing well. She talked about the concern of telling a patient to "hit this number" which can in turn increase stress and cortisol levels, which is counterproductive. She said they don't even know the ideal G/Ki for epilepsy treatment which has used ketosis for decades.

Someone from a medical college in Georgia asked about ketosis for blood-based cancers. No one knew anything about keto for blood-based cancers.

Dr. Kushner asked what it is going to take to help ketosis become accepted by the mainstream. He said something about there being little communication between scientists and SROs (scientific research organizations??). 

Someone referenced Cantley's article in Nature. I'm not sure for what, but here's a page showing Nature's results for Lewis Cantley Panelists talked about increasing dialogue with NCI, talked about RFAs. Scheck said they need nutrition to be one of the three legs of the stool of cancer care. Champ talked about the difficulty fighting with institutional review boards (IRBs). Scheck said she got into ketosis studying via a high school student group (but I didn't get the name written down, unfortunately). Grassroots. Hyde said they haven't sought traditional grant money-- they need more collaboration. Dr. Fine talked up experiment.com (like kickstarter but for science)-- raised $75K from it, and then 2 weeks after campaign, an anonymous donor gave big $$ to fund their research.

The Uruguay nutritionist asked about BCAA supplementation for cancer patients on the ketogenic diet. Poff said a mouse study did not show a benefit (anything would be speculation at this point)

Someone from Penn who specializes in microbiome asked what the pivotal studies are that need done. Poff said mechanism is important for traditional funding (perfect for drug companies). The ketogenic diet has too many mechanisms so it makes traditional funding hard to come by. Scheck said that whatever study you are doing, you need to collect as much data as you can, whether you know what you need it for or not. The questioner said we need to collaborate and break down silos. Lustberg biopsies taken over time will lead to greater acceptance.

And with that, those are my notes from the first part of Day 2 of the keto conference. . . this doesn't even get us to Day 2 lunch yet! So I'm ending this post for now. More about Day 2 later-- Day 2 would go on to look at the research of ketosis in relation to neurology and performance (with a keynote speech by Gary Taubes in the middle).