Fasting

Fasting →

Published 4 Days Ago  ·  All posts on Apr 8  ·  

A Six-Part Series and Getting Started

Fasting – 2026-04-08Download

This collection brings together a six-part series exploring the science of fasting alongside a practical guide to getting started with 16:8 intermittent fasting.

The series begins by questioning long-held assumptions about meal timing and examines what actually happens in the body during a fast — from the metabolic switch to fat burning, through autophagy and cellular repair, to hormonal changes, immune renewal, and the neurological effects that fasting practitioners often report as mental clarity. Each installment weighs the research honestly, distinguishing strong evidence from speculation and noting where the science is still
catching up to the claims.

The final piece shifts from understanding to doing, offering a stepped approach to building a 16-hour fasting practice, drawing on personal experience rather than theory.

I’ve been doing 16:8 intermittent fasting for years and recently started 48-hour fasts — dropping about three pounds each fast, gaining one or two back, and trending steadily downward. I wanted to understand what the research actually says about what I’m doing to myself, so I worked with Claude (Anthropic’s AI) to produce this series. I set the structure, chose the topics, pushed back on claims that felt hand-wavy, and guided the editorial tone. Claude did the writing and research synthesis. My curiosity driving Claude’s research and prose.

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Time-Restricted Eating as an Adjunct to Radiotherapy and Androgen Deprivation Therapy in Prostate Cancer →

Published 6 Days Ago  ·  All posts on Apr 6  ·  

Clinical Evidence Brief
Current state of evidence — preclinical, clinical, and investigational
Prepared March 2026

Proposed mechanisms

The biological rationale for combining dietary restriction with radiotherapy centers on the differential stress response.[1] Under conditions of nutrient deprivation, normal cells activate conserved protective pathways — reducing metabolic activity, upregulating stress resistance, and entering a quiescent state. Cancer cells, whose oncogenic mutations constitutively activate RAS, AKT, and mTOR signaling, are largely unable to make this shift; they remain metabolically active and, as a consequence, more vulnerable to radiation-induced damage. Concurrently, normal tissue is relatively protected — a divergence that forms the basis for combining fasting with radiotherapy.

The interaction between dietary restriction and androgen deprivation therapy (ADT) works through different mechanisms that depend on the class of ADT used, as described below. Separately, dietary restriction may also help counteract the metabolic side effects of ADT itself.

Time-restricted eating (TRE) — typically a 16:8 fasting-to-eating window — is among the more clinically feasible implementations of dietary restriction during active treatment, avoiding the weight loss and nutritional risk associated with sustained caloric restriction.[2] Transitioning from typical Western eating patterns to a sustained 16:8 window requires deliberate on-ramping; the author has written separately on a structured approach to this transition.[3]

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Getting started with 16-hour fasting →

Published 13 Days Ago  ·  All posts on Mar 31  ·  

This post is about ways to incrementally change when you are eating, to shift yourself from how you are eating today, to a particular time-pattern of fasting called 16:8 (pronounced “sixteen eight”.) 16:8 means every day you have a 16-hour fast (the “not eating” window,) and then an 8-hour eating window.

I’m going to start by assuming you already want to begin fasting. I’ve written more generally about fasting if you’d prefer to start with WHY you might want to try being more intentional about when you choose to eat.

Putting yourself into “intentional” mode

You SHOULD discuss your fasting with your primary care physician. Ask them what you should be aware of, or how it may affect you—they know the specifics of your body. You will discover they actually know all about fasting and diet. If you are proactively engaged in your own welfare, your physician will be happy to be a font of useful information.

For example: My primary care doctor is well aware of the beneficial effects of diet, exercise and fasting on my cholesterol markers. They are also convinced that my lifestyle changes will not be able to sufficiently improve those markers quickly enough. Thus, our discussions and my choices continue.

(And—yikes!—if your physician isn’t helpful, knowledgeable, and open to discussion, you should find a better physician.)

Fasting is about WHEN you eat

Fasting is easy to understand: It’s about WHEN you eat. Whether we use the word fasting, intermittent fasting (IF), or time restricted eating (TRE), we’re simply referring to when you eat versus when you don’t eat.

Fasting—here, and whenever I talk about it—is not about depriving yourself, nor about starvation or suffering. It is SIMPLY being intentional about WHEN you CHOOSE to eat.

I know, I know… 16 hours without eating probably sounds like a crazy-long time to not eat. But as I said at the top, I’m assuming you are motivated to try this.

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Part 6: The Brain →

Published March 4  ·  All posts on Mar 4  ·  

I’ve been doing 16:8 intermittent fasting for years and recently started 48-hour fasts — dropping about three pounds each fast, gaining one or two back, and trending steadily downward. I wanted to understand what the research actually says about what I’m doing to myself, so I worked with Claude (Anthropic’s AI) to produce this series. I set the structure, chose the topics, pushed back on claims that felt hand-wavy, and guided the editorial tone. Claude did the writing and research synthesis. My curiosity driving Claude’s research and prose.

Mental Clarity, BDNF, and Ketone Fuel

Research brief — what happens in the brain during extended fasting. The subjective experience of mental clarity is real and widely reported; the science behind it is more complicated than the popular narrative suggests.

The Clarity People Report

Many people describe a distinct shift during extended fasting — typically somewhere after the 24–36 hour mark — from brain fog to unusual mental clarity. This is one of the most consistently reported subjective experiences of fasting, across cultures and contexts. It’s real. The question is why.

Three candidate explanations, not mutually exclusive:

  1. Ketone metabolism — the brain runs efficiently on beta-hydroxybutyrate (BHB)
  2. BDNF upregulation — fasting may increase brain-derived neurotrophic factor
  3. Stable fuel supply — no more blood sugar fluctuations from meals

The first and third have strong physiological grounding. The second is where the science gets shaky.

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Part 5: Inflammation and Immune Renewal →

Published March 4  ·  All posts on Mar 4  ·  

I’ve been doing 16:8 intermittent fasting for years and recently started 48-hour fasts — dropping about three pounds each fast, gaining one or two back, and trending steadily downward. I wanted to understand what the research actually says about what I’m doing to myself, so I worked with Claude (Anthropic’s AI) to produce this series. I set the structure, chose the topics, pushed back on claims that felt hand-wavy, and guided the editorial tone. Claude did the writing and research synthesis. My curiosity driving Claude’s research and prose.

Inflammation and Immune Renewal

Research brief — how fasting reduces systemic inflammation and primes the immune system for regeneration. Two distinct but related mechanisms.

Inflammation Reduction

Jordan et al. 2019 — Stefan Jordan, Navpreet Tung, and colleagues at the Icahn School of Medicine at Mount Sinai, led by Miriam Merad. Published in Cell, 178:1102-1114. (1)

This study directly tied caloric intake to the circulating inflammatory monocyte pool — a key driver of systemic inflammation.

What they found:

  • Short-term fasting reduced monocyte metabolic and inflammatory activity and drastically reduced the number of circulating monocytes
  • The mechanism: fasting activates AMPK in hepatocytes (liver cells) and suppresses systemic CCL2 production via PPARα, which reduces monocyte mobilization from bone marrow
  • Fasting improved chronic inflammatory diseases without compromising emergency immune mobilization during acute infection — the immune system’s ability to respond to real threats remained intact
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Part 4: Hormonal Shifts →

Published March 4  ·  All posts on Mar 4  ·  

I’ve been doing 16:8 intermittent fasting for years and recently started 48-hour fasts — dropping about three pounds each fast, gaining one or two back, and trending steadily downward. I wanted to understand what the research actually says about what I’m doing to myself, so I worked with Claude (Anthropic’s AI) to produce this series. I set the structure, chose the topics, pushed back on claims that felt hand-wavy, and guided the editorial tone. Claude did the writing and research synthesis. My curiosity driving Claude’s research and prose.

Growth Hormone and Insulin Sensitivity

Research brief — the two best-evidenced hormonal responses to extended fasting, with direct human measurements.

Growth Hormone Surge

Human growth hormone (HGH) secretion increases substantially during fasting. This is among the best-measured effects of fasting in humans — researchers have drawn blood every 5 minutes over 24-hour periods to capture the pulsatile secretion patterns.

Ho et al. 1988 — Examined 24-hour GH secretion patterns in six normal adult men during fed and fasting states (day 1 and day 5 of a 5-day fast). Found that fasting enhances GH secretion through both increased pulse frequency and amplitude. (1)

Hartman et al. 1992 — The definitive study. Nine normal men, blood sampling every 5 minutes over 24 hours. Found a *-fold increase in 24-hour endogenous GH production during a two-day fast, mediated by increased secretory burst frequency and amplitude. Notably, IGF-1 concentrations were unchanged after 56 hours of fasting. (2)

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Part 3: Cellular Cleanup →

Published March 4  ·  All posts on Mar 4  ·  

I’ve been doing 16:8 intermittent fasting for years and recently started 48-hour fasts — dropping about three pounds each fast, gaining one or two back, and trending steadily downward. I wanted to understand what the research actually says about what I’m doing to myself, so I worked with Claude (Anthropic’s AI) to produce this series. I set the structure, chose the topics, pushed back on claims that felt hand-wavy, and guided the editorial tone. Claude did the writing and research synthesis. My curiosity driving Claude’s research and prose.

Autophagy

Research brief — what autophagy is, what the evidence actually shows, and where the common claims outrun the science.

What Autophagy Is

Autophagy — from Greek auto (“self”) and phagein (“to eat”) — is the process by which cells degrade and recycle damaged organelles, misfolded proteins, and dysfunctional mitochondria. Think of it as cellular housekeeping: damaged parts get broken down and the raw materials get repurposed for repair and new construction.

Yoshinori Ohsumi won the 2016 Nobel Prize in Physiology or Medicine for discovering the genetic mechanisms of autophagy. Working in baker’s yeast in the early 1990s, he identified the genes essential for the process. The mechanisms are highly conserved across species including humans. (1)

The molecular trigger is well-understood: nutrient deprivation suppresses insulin and mTOR signaling and activates AMPK — all of which are upstream regulators of autophagy. The logical chain from “fasting → reduced insulin/mTOR → autophagy activation” is mechanistically solid. Disrupted autophagy has been linked to Parkinson’s disease, type 2 diabetes, Alzheimer’s, certain cancers, and many infections. (2)

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Part 2: Getting Into Fasting →

Published March 4  ·  All posts on Mar 4  ·  

I’ve been doing 16:8 intermittent fasting for years and recently started 48-hour fasts — dropping about three pounds each fast, gaining one or two back, and trending steadily downward. I wanted to understand what the research actually says about what I’m doing to myself, so I worked with Claude (Anthropic’s AI) to produce this series. I set the structure, chose the topics, pushed back on claims that felt hand-wavy, and guided the editorial tone. Claude did the writing and research synthesis. My curiosity driving Claude’s research and prose.

Routines, Scenarios, and What to Expect

Research brief — the practical onramp. 16:8 IF as a starting point, Craig’s specific eating window, extended fasting scenarios anchored to a weekly rhythm, and what keto flu actually is.

Start With 16:8

You may want to start by getting into 16:8 intermittent fasting — an 8-hour eating window and 16-hour fast — before attempting anything longer.

Is this actually supported? Honestly, no one has studied whether practicing 16:8 first makes longer fasts easier. It’s conventional wisdom without a clinical trial behind it. But the physiological rationale is sound: regular time-restricted eating develops metabolic flexibility — the ability to switch between glucose and fat/ketone oxidation. Someone who does this daily would be expected to enter ketosis faster and with less discomfort during an extended fast. And the practical experience of managing hunger, learning your body’s signals, and knowing what electrolyte depletion feels like are real benefits of prior fasting experience, even if unstudied. (1)

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Part 1: Why Fasting Works →

Published March 4  ·  All posts on Mar 4  ·  

I’ve been doing 16:8 intermittent fasting for years and recently started 48-hour fasts — dropping about three pounds each fast, gaining one or two back, and trending steadily downward. I wanted to understand what the research actually says about what I’m doing to myself, so I worked with Claude (Anthropic’s AI) to produce this series. I set the structure, chose the topics, pushed back on claims that felt hand-wavy, and guided the editorial tone. Claude did the writing and research synthesis. My curiosity driving Claude’s research and prose.

The Big Picture

Research brief — general overview of fasting benefits. The most “hand-wavy” of the series: frameworks, history, and the broad case for why not eating is doing something useful.

The Metabolic Switch

The overarching framework for understanding fasting benefits comes from Mark Mattson’s “metabolic switch” concept, reviewed comprehensively in a landmark 2019 NEJM paper co-authored with Rafael de Cabo. (1)

The core idea: when you stop eating for long enough, the body shifts from glucose-based to ketone-based energy. This isn’t just a fuel swap — it’s a stress response that activates adaptive cellular pathways. The metabolic stress of fasting triggers increased expression of antioxidant defenses, DNA repair, protein quality control, mitochondrial biogenesis, and autophagy. These protective mechanisms outlast the fast itself — a hormetic effect where controlled stress leaves the system stronger.

This is the thread that connects the individual benefits explored in the rest of this series: better insulin sensitivity, growth hormone surges, inflammation reduction, cellular cleanup, and (possibly) neurological benefits all flow from this same metabolic switch.

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Marks were made →

Published July 23  ·  All posts on Jul 23  ·  

A friend and I recently did a 48-hour fast. (One of the low-lights was going to dinner with people on our way to a concert… everyone’s having burgers and salmon, and I’m drinking black coffee. Anyway.) Our design was to finish the fast by doing one of my usual quadrupedal movement (QM) workouts at my favorite tennis courts, and then a run (as best as possible) around 1.75 mile trail loop. Then break our fasts by eating.

By the end of the QM, I was utterly exhausted. For a cool down I worked on a sweat-angel for about 5 minutes. Left a legit puddle where my head was. And then we did the trail run. Several people joined us for the QM and run, and much fun was had by all.

There’s no real takeaway here. Just a photo and a note to myself: Sometimes I push things. Sometimes I push things too far. Where’s the edge?

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