Derek Lee

PhD | Boston College, Seyfried Lab

[Thomas N. Seyfried @tnseyfried]

Our new review shows how cancer cells use evolutionarily conserved metabolic pathways to produce energy (https://t.co/Aj7o4ap41z). The end products of these pathways (lactate and succinate) can be restricted through glucose and glutamine targeting for the non-toxic metabolic management of cancer especially after the whole body is transitioned to nutritional ketosis (https://t.co/WPf2CHe1D4).

[Thomas N. Seyfried @tnseyfried]

Our new paper presents a metabolic manifesto that can help curb the current epidemic of chronic diseases and cancer. We show how mitochondrial dysfunction is the root of many chronic diseases and most major cancers (https://t.co/WPf2CHezsC). A quantitative scale of glucose ketone index (GKI) values linked to color-coded zones of health provides a cohesive readout for increasing adherence and reducing risk of chronic disease and cancer. Low GKI values can improve mitochondrial function thus reducing risk, while high GKI values can compromise mitochondrial function thus increasing risk. The GKI, used together with science-based nutrition and exercise, represents a novel therapeutic strategy for improving mitochondrial health regardless of age, gender, or genetic predisposition.

[Derek Lee @DCLee96]

@Chrest_brett @realDaveFeldman 6

[Derek Lee @DCLee96]

@Chrest_brett @realDaveFeldman All of these papers used a longer time point. As I said, time is pretty critical for these experiments.

[Derek Lee @DCLee96]

@Chrest_brett @realDaveFeldman It's about the design of the experiment. Increase dose or time, more death. Measure apoptosis instead of viability, more (implied) death. The experimental design was purposeful to not show 100% cell death.

[Derek Lee @DCLee96]

@Chrest_brett @realDaveFeldman The point of the experiment was to show that the same amount of DON at the same time point did not induce any death when glucose was present, as the rest of the figure shows. The pathways compensate for one another. I would not recommend taking the graph out of context.

[Derek Lee @DCLee96]

@Chrest_brett @tnseyfried Oxygen consumption comes from many places, not just complex IV activity - ROS, some biosynthesis pathways, etc. The dose can also play a large role in the % drop. We try to lean toward the smaller doses on inhibitors to reduce the chance of off-target effects.

[Thomas N. Seyfried @tnseyfried]

Our new study shows mitochondrial amino acid fermentation as the missing link in sustaining cancer cell energy metabolism and viability in hypoxia. (https://t.co/GtdelrVzJu).

[Derek Lee @DCLee96]

@TQTruthAnon @tomvandeusen @DolfDoofinsky @tnseyfried You're welcome and thank you for reading our work! If you have any other questions as you read more don't hesitate to reach out.

[Derek Lee @DCLee96]

@LondonCat5 @ameoate @tnseyfried Nearly all cancers are glucose dependent, including gliomas. This study is looking at the other half of the equation (glutamine). Over the long term, both glucose and glutamine are necessary for unbridled proliferation. Targeting one is good, both is better.

[Derek Lee @DCLee96]

@TQTruthAnon @tomvandeusen @DolfDoofinsky @tnseyfried We are trying to show that glutamine (which is typically considered a purely respiratory fuel through OxPhos) can be fermented - meaning energy without oxygen. This is important because we try to convey the distinct differences in ATP production between cancer and 'normal' cells.

[Derek Lee @DCLee96]

@Chrest_brett @tnseyfried Let's be careful not to disparage the extremely hard work that Pablo has done over the years to a) defy the timeline his own doctors gave him and b) beat the median survival by years.

[Derek Lee @DCLee96]

@gojox9999 @Chrest_brett @killersites @tnseyfried Gojoxx, keep in mind that this is the account of one person. The doctors at that clinic help many people; including those with very positive experiences. Unfortunately, we could could pick a single incident from any clinic and describe how horrible of an experience they had.

[Derek Lee @DCLee96]

@Chrest_brett @killersites The second study adds key markers, and I agree that cachexia is a great marker for end-stage cancer. To your original point, It's very important to distinguish healthy weight loss (KMT) vs unintentional weight loss (cachexia). Not doing so leads to misleading conclusions, is all.

[Derek Lee @DCLee96]

@Chrest_brett @killersites Obesity is a problem in many countries, not just the US. Regarding that article, do you truly believe that obesity is protective for a cancer patient? That notion is absurd at best in my opinion.

[Derek Lee @DCLee96]

@Chrest_brett @killersites I disagree, this is central to the core issue of obesity and cancer. They defined cachexia as weight loss over 5% peak weight. I admire the work that was done, but that is not a valid marker for cachexia. Many US citizens should lose at LEAST 5% body weight.

[Derek Lee @DCLee96]

@Chrest_brett @killersites We have an obesity epidemic in the US. Obesity is the #2 risk factor for cancer behind smoking. There is healthy weight loss and there is cachexia in cancer. They are measured the same, but not remotely similar physiologically.

[Derek Lee @DCLee96]

@Chrest_brett @killersites @tnseyfried An intentional intervention to a healthier diet (KMT) will improve overall health. Improved health generates more favorable outcomes when treating cancer. The Standard American Diet (SAD) promotes every imaginable risk factor for worse prognosis. Is this not true?

[Derek Lee @DCLee96]

@Chrest_brett @killersites @tnseyfried Even treatments highlighted on programs like 60 minutes ignore updates that reveal dismal outcomes. Similarly, we could go over the endless number of people disfigured and later killed from traditional treatments. It is simply a matter of cherry-picking information.

[Derek Lee @DCLee96]

@Chrest_brett @killersites @tnseyfried Half of your data is "unknown". Using a graph like this to make your point is misleading.