#114 - Eileen White, Ph.D.: Autophagy, fasting, and promising new cancer therapies

Jun 8, 2020 Episode Page ↗
Overview

This episode with Dr. Eileen White, Chief Scientific Officer at Rutgers Cancer Institute, explores autophagy's role in health, neurodegeneration, and cancer. It details how autophagy protects against disease but paradoxically aids existing cancer, and discusses the critical need to understand the optimal "dose" and frequency of fasting for human health.

At a Glance
12 Insights
1h 58m Duration
17 Topics
6 Concepts

Deep Dive Analysis

Eileen White's Scientific Journey and Background

Transition from Apoptosis to Autophagy Research

Defining Apoptosis and its Role in Cancer Evasion

Serendipitous Discovery of Autophagy in Cancer Survival

Autophagy's Role in Cancer Cell Metabolism and Proliferation

Stressors Inducing Autophagy in Normal Cells

Impact of Autophagy Deficiency in Mouse Models

Tissue-Specific Autophagy Dependence and Disease Phenotypes

Targeting Autophagy for Cancer Therapy in Adult Mice

Autophagy Dependence Across Different Cancer Types

Reconciling Autophagy's Dual Role in Cancer (Paradox)

The Challenge of Dosing Fasting for Autophagy in Humans

Developing a Molecular Signature for Autophagy Induction

Pharmacological Inducers of Autophagy: Metformin and Rapamycin

The Nobel Prize for Autophagy Research

Future Research: Autophagy, Metabolism, and Immunotherapy

Autophagy's Potential in Alzheimer's Disease Prevention

Apoptosis (Programmed Cell Death)

A highly regulated process where cells self-destruct, crucial for preventing cancer by eliminating damaged cells. It involves BCL2 family proteins, BAX/BAK, and mitochondrial membrane permeabilization, often triggered by tumor suppressor P53.

Autophagy (Self-Eating)

A fundamental cellular recycling process where cells degrade and recycle their own components (proteins, organelles) to generate energy and building blocks, particularly important for survival during nutrient deprivation.

Autophagosomes

Double-membrane vesicles that form around cellular components targeted for degradation during autophagy, eventually fusing with lysosomes for breakdown and recycling.

Autophagic Flux

The dynamic process of autophagy, involving the formation of autophagosomes, their fusion with lysosomes, and the subsequent degradation of cargo. It's measured by tracking proteins like LC3-I to LC3-II conversion and degradation.

Autophagy Paradox in Cancer

The observation that while autophagy is crucial for preventing cancer by maintaining cellular health and reducing inflammation, cancer cells can also hijack and upregulate autophagy to survive and proliferate, especially under stress.

KRAS-driven Cancers

Cancers characterized by mutations in the KRAS gene, which lead to perpetual activation of cell proliferation pathways (like MAP kinase), making these cancers often highly dependent on autophagy for survival.

?
How does apoptosis work in cells?

Apoptosis is a programmed cell death pathway involving the BCL2 protein family, BAX/BAK proteins that permeabilize mitochondrial membranes, and proteases that degrade the cell, often initiated by tumor suppressors like P53.

?
What is the role of P53 in cancer prevention?

P53, a tumor suppressor, promotes apoptosis by activating proteins like PUMA and NOXA, which antagonize BCL2 and trigger cell suicide, thus preventing the progression of emerging cancer cells.

?
How do cancer cells utilize autophagy for survival?

Cancer cells can elevate autophagic flux even in a fed state and further increase it under stress, using it to recycle cellular components for building blocks and energy, thereby supporting their survival and proliferation.

?
What are some stressors that induce autophagy in normal cells?

Nutrient deprivation (sensed by mTOR, AMPK, sirtuins), organelle damage (e.g., mitochondrial dysfunction), protein misfolding, exercise, and hypoxia are potent inducers of autophagy.

?
What happens if an adult mouse's autophagy is genetically knocked out?

Adult mice with systemic autophagy knockout survive for 2-3 months before succumbing to neurodegeneration, and they die within 16 hours if fasted, highlighting autophagy's essential role in long-term health and stress response.

?
Which tissues are most dependent on autophagy?

The brain is highly autophagy-dependent due to its post-mitotic neurons needing quality control, and the liver is also very sensitive, with autophagy loss leading to steatosis and protein aggregate accumulation.

?
How can the seemingly contradictory roles of autophagy in cancer prevention and treatment be reconciled?

Autophagy is context-dependent; it preserves health by preventing chronic damage and inflammation that can lead to cancer, but once cancer is established, inhibiting autophagy can preferentially damage tumor cells.

?
Why is it difficult to "dose" fasting for optimal autophagy induction in humans?

There is currently no reliable way to quantify the degree of autophagy induced by different fasting durations or frequencies in humans, making it impossible to determine the optimal "dose" for health benefits.

?
What was the significance of the Nobel Prize for autophagy research?

Yoshinori Ohsumi received the Nobel Prize in 2016 for his profound and creative work in identifying the essential autophagy genes in yeast, which provided the foundation for understanding autophagy in mammals.

?
How might autophagy inhibition enhance immune checkpoint blockade in cancer therapy?

Inhibiting autophagy can stimulate inflammation within tumors, potentially "heating up" immunologically "cold" tumors and making them more responsive to immune checkpoint blockade therapies.

?
What is the role of autophagy in preventing Alzheimer's disease?

Autophagy is critical for clearing accumulated toxic proteins and damaged organelles in post-mitotic neurons, suggesting a vital role in preventing neurodegenerative diseases like Alzheimer's.

1. Prioritize Disease Prevention for Longevity

Understand that true longevity is achieved by delaying the onset of chronic diseases, making disease prevention the single most important tool in your health toolkit.

2. Autophagy’s Context-Dependent Role in Cancer

Stimulating autophagy can prevent cancer by delaying chronic damage and inflammation in normal tissues; however, once cancer is established, inhibiting autophagy may be beneficial as tumors often usurp it for survival.

3. Fasting to Reduce Chronic Disease Risk

Improve your metabolic health through fasting to significantly reduce the risk of major chronic diseases, including cardiovascular disease, cancer, Alzheimer’s disease, and diabetes complications.

4. Cultivate Fasting as a Health Tool

Prioritize the use of fasting as a potent and accessible method for health preservation, rather than solely seeking pharmacological agents to stimulate autophagy.

5. Exercise Potently Induces Autophagy

Engage in regular exercise, as it potently induces autophagy, which is crucial for mitigating muscle damage and supporting cellular repair processes.

6. Stimulate Autophagy for Brain Health

Focus on stimulating autophagy as a potential strategy to delay neurodegenerative diseases, given its essential role in neuronal protein and organelle quality control.

7. Autophagy Prevents Fatty Liver Disease

Autophagy is important in preventing fat accumulation and protein aggregate formation in the liver, highlighting its role in maintaining liver health and preventing conditions like steatosis.

8. Prolonged Fasting for Maximal Autophagy

To achieve a fully ‘cranked’ state of autophagy, consider a water-only fast of approximately seven days, as shorter fasts (e.g., 12 hours) are likely insufficient.

9. Three-Day Fasting for Metabolic Shifts

A three-day fast appears to be a minimum duration required to induce significant metabolic changes, such as a spike in uric acid and a bottoming out of glucose, indicating a meaningful metabolic shift.

10. Integrate Diet Quality with Fasting Practices

When implementing fasting for health, also consider the quality of your diet, as ‘what you eat’ is as crucial as ‘how many calories you eat’ or ‘how often you eat them.’

11. Rapamycin for Potential Neuroprotection

Explore rapamycin as a potential neuroprotective agent, noting pilot data suggests its benefits, likely mediated through mTOR inhibition and subsequent autophagy induction.

12. Access Deeper Longevity Content

To further enhance your understanding of longevity, consider subscribing to the podcast’s membership program for exclusive, in-depth content.

Well, you were excited about the science. And so nerds like me like to talk about science.

Eileen White

one novel function of cancer is to evade cell death.

Eileen White

just because a cell can't commit suicide doesn't explain how it can be a cancer cell can just sit in buffer and be fine.

Eileen White

when you inhibited autophagy, the survival of the cancer cells was reduced.

Eileen White

If you knock it out, it is uniformly fatal. Do not pass go, do not collect $200, you're gone.

Peter Attia

the key to living longer is delaying the onset of chronic disease.

Peter Attia

I think it's a matter of thinking of the role of autophagy in cancer as being context dependent.

Eileen White

I think that our biomedical community is mostly focused on putting out fires rather than disease prevention, although I've seen a change.

Eileen White

Longevity is about delaying the time it takes until disease comes.

Peter Attia

The problem is we didn't know how to dose it. How long would we tolerate that ignorance?

Peter Attia

sometimes scientific discoveries are so basic that you can't ever anticipate what it would ultimately lead to.

Eileen White

Proof-of-Principle Protocol for Autophagy Inhibition in Cancer Therapy

Eileen White
  1. Engineer an adult mouse model where an essential autophagy gene can be deleted throughout the entire animal.
  2. Induce cancer in this adult mouse.
  3. Once the mouse has cancer (e.g., lung cancer), delete the essential autophagy gene in the entire mouse (tumor and all normal tissues).
  4. Observe whether the tumor or the mouse dies first to determine the therapeutic window and efficacy.
approximately 50%
P53 loss of function in cancers Accounts for half of all cancers.
2 to 3 months
Survival of autophagy-deficient adult mice (fed) Before succumbing to neurodegeneration.
16 hours
Survival of autophagy-deficient adult mice (fasted) All dead within this period.
less than 1 year
Median survival extension for solid organ tumors (since 1970) Despite approximately $250 billion spent on research.
82%
Deaths attributable to chronic diseases (US, >50, excluding COPD) From cardiovascular disease, cancer, Alzheimer's, and diabetes complications.