Best Tools for Gut Health & Weight Loss | Dr. Chris Thompson

Episode Overview

• Dr. Andrew Huberman (Professor of Neurobiology and Ophthalmology at Stanford School of Medicine) interviews Dr. Chris Thompson (Professor of Medicine at Harvard Medical School and Chief of Interventional Gastroenterology at Mass General Brigham in Boston) on how the gastrointestinal system functions as a mechanical, digestive, and endocrine organ ("second brain").
• The conversation explores the anatomy of the digestive tract—from the esophagus and stomach to the small bowel and colon—highlighting how dietary fiber, resistant starch, and fermented foods feed the microbiome to maintain gut barrier integrity and prevent metabolic disease.
• They examine the history, mechanisms, and limitations of bariatric surgeries and modern GLP-1 agonists, addressing widespread drug discontinuation, muscle loss (sarcopenia) from weight cycling, and metabolic adaptation ("set point theory").
• Finally, Dr. Thompson outlines the five stages of metabolic dysregulation, how to detect insulin resistance 10 to 15 years before a Type 2 diabetes diagnosis, and cutting-edge minimally invasive endoscopic procedures, AI-guided surgery, and pancreatic GLP-1 gene therapies.

Key Concepts

• Speaker Disclosures and Affiliations: Dr. Huberman notes the podcast is separate from his Stanford teaching and research roles, explicitly states he has no affiliation with Prenovo, and discloses episode sponsors Element (LMNT), Lingo, AG1 (AG1 Pro with 5g creatine monohydrate, calcium HMB, and zinc carnosine), Function, and Our Place. Dr. Thompson explicitly states he does not own stock in any continuous glucose monitor (CGM) company, and discloses that he founded a medical device company for an endoscopic ultrasound (EUS) biopsy needle, is involved in the healthcare platform Everself, developed the Endoscopic Sleeve Gastroplasty (ESG) procedure in 2012, developed nitinol-encased magnetic anastomosis rings in his lab (noting he is conflicted and cannot perform that part of combined procedures), and was involved in early work for a company developing a viral vector GLP-1 gene therapy.
• GI Tract Anatomy and Pathologies: The gut is a digestive organ, an endocrine organ, and is often called the "second brain."
• Esophagus & Swallowing: Moves food to the stomach. Chronic reflux can cause fibrotic scarring (a stricture) or Barrett's esophagus (a precancerous condition). In achalasia (where the bottom of the esophagus fails to relax, causing food/fluid to get stuck or regurgitate), doctors can tunnel between esophageal layers (only a few millimeters thick) to cut the muscle and relieve obstruction. Food going up the nose when eating (nasopharyngeal regurgitation) can result from an oropharyngeal transfer problem (treatable with speech pathology/biofeedback), high tension in the upper esophageal sphincter, or Zenker's diverticula (a herniation of mucosa through muscle creating a food-trapping pocket), which can be fixed via a tiny incision through the mouth to take down the septum and prevent food aspiration and lung scarring.
• Stomach: Normally shaped like a tube, the stomach stretches and relaxes into a bag-like shape just from the smell or sight of food (alongside a cephalic-phase insulin spike); failure to relax causes nausea. Thompson admits he does not know if researchers have figured out the exact mechanism by which smelling or seeing food triggers this cephalic-phase process, noting some of it may be learned. The fundus (top) holds food and secretes ghrelin (the hunger hormone); the body grinds food mechanically and secretes acid; the antrum (bottom) pushes food slowly into the duodenum. Gastroparesis (delayed stomach emptying causing nausea/vomiting) can be post-viral, diabetic, or neurohormonal.
• Small Bowel: Receives pancreatic and biliary secretions for early digestion and primarily absorbs calories. Its lining is only one cell thick (columnar epithelium/enterocytes) with the surface area of a pickleball court, protected by mucin-producing goblet cells, tight junctions, and immune cells.
• Colon: Absorbs water and houses the microbiome, which ferments fiber into short-chain fatty acids (especially butyrate) and produces GLP-1 for satiety signaling.
• The Microbiome, Mucin Degradation, and Butyrate: Gut microbes eat dietary fiber; a World Health Organization (WHO) paper in The Lancet ("fiber synthesis") found the vast majority of Western populations do not get enough fiber. If deprived of fiber, microbes eat the protective intestinal mucus layer, halting butyrate production and destroying tight junctions. Oral butyrate supplements do not make it to the colon where needed; instead, primary bacteria break down fiber into acetate and lactate, which cross-feed secondary bacteria to produce butyrate in the colon. Butyrate feeds colonocytes, maintains tight junctions, triggers GLP-1/satiety pathways, and keeps the bowel acidic to prevent pathologic aerobic organisms from taking root. While fasting may cause microbes to temporarily eat the mucin layer (followed by a rebound), Thompson hedges that he does not see it as a major issue and believes the benefits of intermittent fasting (giving the pancreas time to relax and letting insulin drop) probably outweigh that risk.
• Ulcers and H. pylori: In Australia, Barry Marshall won the Nobel Prize for proving Helicobacter pylori causes gastric ulcers by consuming the bacteria himself to induce ulcers. H. pylori was also found in the stomach of Ötzi the Iceman, a 5,000-year-old frozen human found in the Italian Alps whose microbiome showed that industrialization has caused a massive loss of genetic diversity in human gut bacteria. However, based on Thompson's studies of gastric bypass patients, ulcers are also caused by microvascular ischemia (from Type 2 diabetes or smoking), stress-induced acid production, and excess acid in a large gastric bypass pouch hitting the jejunum (which lacks pancreatic bicarbonate to neutralize acid).
• Gut Hormones and the Discovery of Incretins:
• Hormonal Cascade: Ghrelin (from the gastric fundus) rises before meals and drops after eating. CCK (from the duodenum) causes the gallbladder to dump bile and signals satiety. GIP (from K-cells in the proximal small bowel) acts like "Robin" to GLP-1's "Batman," aiding insulin sensitivity and reducing nausea at higher GLP-1 doses. GLP-1 (triggered strongly by glucose) and PYY (triggered by proteins and fats to keep you full longer) are secreted by L-cells in the distal small bowel and colon. Leptin is secreted by fat cells in proportion to fat mass as a long-term thermostat, though obesity causes hypothalamic leptin resistance due to low-grade inflammation.
• Next-Generation Agonists: Retatrutide (a triple agonist targeting GLP-1, GIP, and glucagon) showed a 30% reduction in body weight in Eli Lilly clinical trials; glucagon tells the body to burn fat and dump liver glycogen, potentially providing a muscle-sparing effect.
• History of GLP-1: In the 1930s in London, researchers injected emulsified animal duodenums IV into animals, lowering blood glucose and coining the term "incretin." Sheila Sherlock's lab in London proved the "incretin effect" by showing oral glucose produced much more insulin than equal IV glucose. Dr. Bell at Eli Lilly cloned preproglucagon (identifying GLP-1 and GLP-2), and Dr. Bloom in London proved GLP-1 rose with glucose and lowered blood sugar, though natural GLP-1 is rapidly degraded at its N-terminus by the enzyme DPP-4. In the 1990s in the Bronx, Dr. John Eng discovered exendin-4 in Gila monster venom—a molecule nearly identical to GLP-1 with a single amino acid substitution at the second position from the N-terminus that resists DPP-4 degradation, forming the basis for modern GLP-1 drugs.
• GLP-1 Pharmacology, Non-Adherence, and Sarcopenia: Huberman mentions hearing that up to 20% of US adults (18+) have taken a GLP-1 drug, hedging that he does not know if the exact number is true. However, over 1 million people per month come off GLP-1s (~30% stop in the first month and ~50% by the end of the first year, similar to blood pressure and cholesterol drug non-adherence), and over 85% of patients in Thompson's endoscopic practice have already struggled on or stopped a GLP-1. GLP-1 drugs deliver a super-physiologic dose (ramping levels up 1,000-fold over normal physiological levels and bathing the brain's area postrema rather than pulsing with meals); Thompson hedges that long-term multi-decade ramifications are unknown. Furthermore, about one-third (1/3) of weight lost on first-generation GLP-1s like semaglutide is lean mass (muscle/bone). Cycling on and off GLP-1s is dangerous because regained weight is fat rather than muscle, progressively worsening body composition and potentially inducing sarcopenia. Additionally, Huberman notes GLP-1 drugs can cause blindness in a very rare subset of individuals with a specific structural optic nerve head ischemic vulnerability (which can be screened for).
• The 5 Stages of Metabolic Dysregulation: Citing the UNC NHANES study, only 12% of the total US population—and less than one-third (1/3) of lean people—are metabolically healthy. The Whitehall II study of British civil servants showed elevated fasting insulin predicts Type 2 diabetes 10 to 15 years before diagnosis. Metabolic dysregulation progresses through five stages before Hemoglobin A1C rises:
• Calorie/Glucose Excess: Post-meal glucose spikes (e.g., to 200 mg/dL), which glycate proteins.
• Hyperinsulinemia: Eating every few hours keeps insulin chronically elevated because insulin takes a few hours to come down after clearing glucose.
• Ectopic Fat Deposition: Once subcutaneous, visceral (omentum/mesentery), and organ-associated fat depots are full, fat is stored in cells not meant to hold fat, such as liver, muscle, and pancreas cells (like Wagyu beef).
• Insulin Resistance: Quantified via HOMA-IR (multiplying fasting blood glucose by fasting insulin and dividing by a constant; a score > 2 indicates insulin resistance).
• Metabolic Inflexibility: The body fails to switch between burning fat while fasting and burning carbs when fed, leading to beta-cell apoptosis and obesity (measured via Respiratory Exchange Ratio [RER] breath studies of $CO_2$ divided by $O_2$, where 0.7 is pure fat burning and 1.0 is pure carb burning).
• History of Bariatric Surgery and Foregut Exclusion: Bariatric surgery began in the 1950s at the University of Minnesota with the jejunoileal (JI) bypass, which caused bacterial overgrowth in the long blind limb and renal failure (malabsorbed fat bound calcium in the gut, leaving free oxalate to be absorbed into the blood and bind calcium in the kidneys). In the mid-to-late 1960s, Dr. Mason invented the gastric bypass, followed later by lap bands, VBG, and sleeve gastrectomy. Contrary to early beliefs that surgery worked purely via mechanical restriction and malabsorption, hormone signaling drives the benefits:
• Fistula Closure: In 2003, Thompson closed a small gastro-gastric fistula endoscopically in a bypass patient, immediately resolving their diabetes; a follow-up study showed 60% of patients with closed fistulas had diabetes resolution vs. 0% left open.
• Foregut Exclusion & The "Sick" Duodenum: Rubino's studies in non-obese diabetic GK rats showed excluding the duodenum/proximal jejunum resolved diabetes (suggesting the duodenum produces an "anti-incretin"). Overfeeding in mice and humans causes the small bowel to become longer and heavier with elongated villi, an 8-fold increase in natural killer (NK) cells, a 1.5-fold increase in macrophages, and disorganized tight junctions (zonula occludens).
• Endoscopic Duodenal & Ileal Therapies: Endoscopic duodenal liners/sleeves yield a 1-point drop in A1C and ~7% total weight loss. Surgical ileal interposition (moving L-cell-rich distal ileum up to the duodenum in lean Type 2 diabetics in Brazil) cured diabetes without weight loss. Duodenal mucosal ablation/resurfacing (burning the sick duodenal lining with steam or hot water so stem cells regenerate a healthy lining) drops A1C by over 1 point and prevents weight regain after stopping GLP-1s.
• Increased Gut Permeability ("Leaky Gut") and Nutrition Debates: While Thompson hedges on using the lay term "leaky gut" because he does not want to blame it for everything, he states increased gut permeability is 100% real. A recent study growing 3D organoids from small bowel biopsies of patients with obesity and MASH (metabolic dysfunction-associated steatohepatitis) showed disorganized tight junctions and downregulated tight junction RNA; another study showed the tracer 51Cr-EDTA zipped directly into the bloodstream of MASH patients compared to healthy controls or treated celiac patients. When lipopolysaccharide (LPS) from Gram-negative bacteria leaks through tight junctions into the portal vein, it binds Toll-like receptor 4 (TLR4) in the liver and triggers NF-kappa B inflammation; a Duke study injecting LPS directly into healthy humans proved via clamp studies that it caused massive inflammatory spikes and immediate insulin resistance. Regarding nutrition:
• Ultra-Processed Foods: An NIH crossover study in Bethesda (~20 subjects) found people ate ~500 calories more per day ad libitum on an ultra-processed diet compared to whole foods.
• Fructose & Sweeteners: Liquid high-fructose corn syrup should be treated like alcohol because it rapidly overwhelms the liver, whereas whole fruit is fine due to its fiber matrix. Artificial sweeteners are better than high-fructose corn syrup, though they usually come in ultra-processed foods.
• Fats & Seed Oils: Polyunsaturated seed oils reduce LDL and have health benefits if not oxidized in sun-exposed containers or repeatedly deep-fried into trans fats, though olive oil and small amounts of butter are ideal (Huberman cites a UC Davis study finding many commercial avocado oils contained zero avocado oil).
• Set Point Theory, Endoscopic Procedures, AI, and Gene Therapy:
• Set Point Theory: During crash dieting, GLP-1, PYY, and CCK drop, ghrelin surges, muscles become ~25% more fuel-efficient (burning 25% less fuel for the same task), and basal metabolic rate drops. An NIH study of The Biggest Loser contestants found they burned 500 fewer calories/day at rest after weight loss, and the Look AHEAD trial (intensive diet and exercise) achieved only ~6% weight loss at 10 years with no heart disease improvement.
• ESG, Ghrelin Ablation, & Magnets: Thompson's Endoscopic Sleeve Gastroplasty (ESG) folds and stitches the stomach via the mouth to trigger vagal stretch receptors (nodose ganglia, NTS, hypothalamus) and delay emptying, yielding ~18% weight loss; adding argon plasma coagulation to ablate fundus ghrelin cells yields 20–25% weight loss. His lab also published a study ~10 years ago in the Czech Republic using nitinol-encased ring magnets to connect the jejunum to the ileum for hindgut GLP-1 spikes, which can be combined with endoscopic suturing to replicate a gastric bypass without incisions.
• Diagnostics, AI, & Robotics: Standard fine needle aspiration (FNA) needles had only a 50/50 chance of diagnosing pancreatic cancer because they split tissue like an IV needle; Thompson's team engineered a new bevel design to capture core tissue for immunostaining and drug testing. In endoscopy, AI heads-up displays highlight blood vessels, count stitches, and grade surgeon performance, while robotics shortened the trainee learning curve for complex tumor resections from 2–3 years down to a couple of weeks. Groups (including in London) are also using hyperspectral imaging (narrow-band LEDs and CMOS chips) to fingerprint tumor margins without dyes. When asked if 20-minute whole-body tube scans will detect all tumors in 10 years, Thompson hedges, "I don't know if we'll get there. I'm hoping."
• GLP-1 Gene Therapy: A viral vector carrying the GLP-1 gene linked to the beta-cell insulin promoter is injected via EUS into the tail of the pancreas as episomal DNA (not integrating into host DNA), causing terminally differentiated beta cells to co-secrete GLP-1 and insulin naturally in response to nutrients. In rodent models, mice maintained their new weight settling point after stopping semaglutide. Human trials just began in the Netherlands, though Thompson hedges it is very early and might be more useful for diabetes than weight loss.

Quotes

• At 0:00:05 - "Feed your microbes, you know, they need to be fed, and what they eat is fiber, okay? That's what you want them eating, you want them eating fiber. And if you're not feeding them fiber, they'll eat your mucus layer, okay?" - Dr. Chris Thompson explaining how fiber deprivation causes gut bacteria to consume the protective intestinal mucin lining.
• At 0:00:20 - "They're not producing the butyrate you need, and the butyrate's needed to maintain the tight junctions, right? So there's layers to this, it's like a snowball effect that if you're not feeding those microbes, that microbiome, keeping it healthy, you're going to run into all sorts of, all sorts of trouble." - Dr. Chris Thompson detailing the cascade from low fiber intake to loss of butyrate and breakdown of the gut barrier.
• At 0:06:50 - "It's very thin, it's one cell thick, has about the surface area of like a pickleball court." - Dr. Chris Thompson describing the delicate columnar epithelium of the small intestine responsible for calorie absorption and barrier defense.
• At 0:17:09 - "The rule of thumb is, you know, you don't want to have more than three a day, and you don't want to go longer than three days without having a bowel movement. So that's kind of the general rule." - Dr. Chris Thompson providing the clinical baseline for normal bowel movement frequency.
• At 0:25:33 - "You can't just take butyrate and then—it's not going to make it to the colon, right? It needs to be in the colon to have its, to have its effect." - Dr. Chris Thompson explaining why oral butyrate supplements fail compared to bacterial cross-feeding of dietary fiber in the colon.
• At 0:28:20 - "Barry Marshall was phenomenal in Australia, and he found H. pylori could cause gastric ulcers, right? And he had to consume—no one believed him—he had to consume them himself, consume it, and then he got gastric ulcers." - Dr. Chris Thompson recounting the Nobel Prize-winning discovery of bacterial gastric ulcers.
• At 0:31:25 - "There's a number, over a million people a month are coming off GLP-1s, right? And that's for a variety of reasons. About 30% come off GLP-1s in the first month, and then 50% or so by the end of the year, right?" - Dr. Chris Thompson highlighting the massive real-world discontinuation rates of GLP-1 receptor agonists.
• At 0:32:52 - "In my practice, where we do endoscopic therapies, over 85% of people have already been on a GLP-1, and either they're struggling on it or they've come off." - Dr. Chris Thompson illustrating why minimally invasive endoscopic procedures are increasingly sought after pharmacological therapy.
• At 0:36:01 - "When you lose weight, about a third of the weight you lose would be lean mass, right? So mostly muscle, right, maybe some bone, et cetera. And the problem is when you cycle on and off, right, so say you come off of it and you put your weight back on, you're not putting the lean mass back on, okay? You're putting the fat back on." - Dr. Chris Thompson warning how weight cycling on GLP-1 drugs progressively degrades body composition and leads to sarcopenia.
• At 0:48:47 - "Before you swallow any food, right, you already have insulin coming up a little, your stomach's already starting to stretch to accommodate the meal." - Dr. Chris Thompson describing the cephalic phase of digestion triggered merely by seeing or smelling food.
• At 0:53:13 - "And the people that were eating the processed foods—they could eat at will—they were eating like 500 calories more a day." - Dr. Chris Thompson citing the NIH crossover study in Bethesda demonstrating how ultra-processed foods bypass natural satiety signaling.
• At 1:09:24 - "And what they found was that less than a third of people that are lean are metabolically healthy. That's crazy. 12% of the whole population, less than a third of lean people are metabolically healthy based on their parameters." - Dr. Chris Thompson citing the UNC NHANES study to show that normal body weight does not guarantee metabolic health.
• At 1:10:20 - "It's sticky. Glucose is sticky, it glycates things, it causes problems, so the insulin's got to get it out of the bloodstream." - Dr. Chris Thompson explaining why the pancreas secretes high levels of insulin in response to frequent dietary glucose spikes.
• At 1:11:51 - "Then the last bucket is ectopic fat. And ectopic fat is where you have fat in cells that it's not their job to store fat, right? Like liver cells, or muscle cells, or pancreas cells. And that becomes, that becomes a problem." - Dr. Chris Thompson explaining the third stage of metabolic dysregulation when normal fat depots overflow into vital organs.
• At 1:28:33 - "It democratized the field. It took mediocre surgeons and it made them excellent. And the excellent surgeons were still excellent, right? But it really helped the ones that were struggling." - Dr. Chris Thompson discussing randomized trials showing how surgical robotics dramatically flatten the learning curve for complex endoscopic tumor resections.
• At 1:41:12 - "They're ramping things up thousandfold over what they would be in even the healthiest person. Most people don't know that, by the way. They think that like the GLPs are bumping things up like two or fourfold. It's like never before in human history, at least to my knowledge, have people walked around with this level of GLP-1 circulating in their blood." - Dr. Andrew Huberman emphasizing the super-physiologic nature of pharmacological GLP-1 dosing.
• At 1:50:33 - "You just ablate the duodenum, okay, and what happens is your A1C drops by over a point." - Dr. Chris Thompson explaining how duodenal mucosal resurfacing regenerates healthy intestinal tissue and reverses diabetic markers.
• At 1:54:07 - "Well, increased gut permeability is 100% real." - Dr. Chris Thompson validating the scientific reality of compromised intestinal tight junctions in obesity and MASH.
• At 1:57:54 - "This was done at Duke. They actually took LPS and they injected it into healthy people, and they found that their inflammatory markers went through the roof, and they found all sorts of other problems out, including—they did clamp studies in these patients—they found it induced insulin resistance." - Dr. Chris Thompson citing direct human evidence linking bacterial endotoxins from a permeable gut to systemic insulin resistance.
• At 2:07:39 - "Your muscles become more efficient—I think they become 25% more efficient in doing a similar task, they're going to burn less fuel to do the same task, it's amazing, right?" - Dr. Chris Thompson explaining the biological mechanisms of metabolic adaptation that cause weight regain after crash dieting.

Takeaways

• Meet Daily Fiber Targets: Consume roughly 35 grams of fiber per day for adult men and 25 grams per day for adult women (or supplement with powdered psyllium husk, which Huberman notes "hyper-normalized" his digestion without causing bloating) to feed colonic microbes and prevent them from eating your intestinal mucin layer.
• Supplement with Resistant Starch Type 2 (RS2): Consider adding RS2 (such as raw powdered potato starch) to your diet; clinical studies supplementing 40 grams of RS2 demonstrated significant improvements in fatty liver disease and insulin sensitivity even while patients remained weight-stable.
• Incorporate Low-Sugar Fermented Foods Daily: Eat fermented foods like kefir, kimchi, sauerkraut, plain yogurt, or low-sugar kombucha, which act as both prebiotics and probiotics (Bifidobacteria, Lactobacillus) and were shown by Justin Sonnenburg and colleagues to increase microbiome diversity and lower inflammatory markers more effectively than fiber alone.
• Practice Time-Restricted Eating: Give your pancreas time to rest and allow insulin levels to drop by spacing out meals or practicing intermittent fasting; while newer studies suggest eating earlier in the day and fasting in the afternoon might be metabolically better, Thompson notes that doing any form of time-restricted eating is better than not doing it (and both he and Huberman personally skip breakfast).
• Monitor Stool Quality and Frequency: Use the "3-to-3" rule of thumb (no more than 3 bowel movements per day, and no longer than 3 days without one); note that tiny, pebble-like "scybala" stools indicate a lack of dietary fiber, while dark, tarry, shiny stools indicate gastrointestinal bleeding requiring medical evaluation.
• Follow Updated Colon Cancer Screening Guidelines: Begin colon cancer screening at age 45 (via a colonoscopy every 10 years if normal, genetic stool tests like Cologuard every few years, or CT colonography), or start at age 40—or 10 years younger than a relative's diagnosis—if you have a family history of colon cancer; catching precancers/cancers early allows for same-day, organ-sparing endoscopic removal.
• Test Early for Metabolic Dysregulation (Before A1C Rises): Do not rely solely on Hemoglobin A1C or BMI; instead, use a continuous glucose monitor (CGM) for 1 to 2 months to identify foods that spike your glucose, check your fasting insulin and calculate your HOMA-IR score (aiming to stay at or below 2), and monitor liver enzyme ALT, waist-to-height ratio, or DEXA scans to catch ectopic fat deposition 10 to 15 years before diabetes develops.
• Protect Lean Mass and Avoid Weight Cycling on GLP-1s: If taking a GLP-1 drug, avoid cycling on and off the medication, get a baseline DEXA scan, and perform regular resistance training to signal your body to preserve muscle mass during caloric restriction (though Thompson hedges he is not familiar with a study where resistance training on GLP-1s was the primary outcome).
• Discuss GLP-1 Microdosing and Optic Screening with Your Physician: Because approved drug dosages are a byproduct of regulatory trials rather than personalized medicine, patients struggling with side effects or cost can discuss microdosing (using a sterile vial and insulin syringe) with their doctor to maintain weight loss without nausea, and consider screening for structural optic nerve head ischemic vulnerability.
• Combine Three Exercise Modalities for Weight Loss: Pair resistance training (to preserve lean muscle) with Zone 2 cardio (for baseline fat oxidation) and High-Intensity Interval Training (HIIT), which triggers acute stress responses that specifically mobilize visceral fat via beta-adrenergic and gonadotropic hormone receptors.
• Eliminate Liquid Fructose and Ultra-Processed Foods: Treat high-fructose corn syrup like alcohol by removing sodas and liquid sugars that overwhelm the liver (whole fruit is fine due to its fiber matrix), and avoid ultra-processed foods that drive ~500 calories/day of passive overeating.
• Meet Baseline Omega-3 Thresholds and Choose Quality Cooking Fats: Prioritize olive oil and small amounts of butter, avoid seed oils that have been oxidized in sun-exposed containers or repeatedly deep-fried, and hit a basic threshold of Omega-3 fatty acids by eating fatty fish twice a week or taking algae supplements (though Thompson notes universal Omega-3 supplementation data for cardiovascular/metabolic health is mixed and probably better for early Alzheimer's).