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Metabolic effects of soybean oil and linoleic acid on obesity, fatty liver, and liver function.

Topics Discussed:

• Historical trends in soybean oil use: Consumption increased dramatically since the 1960s due to farming subsidies, now providing over 10% of calories for many Americans, far exceeding the 1-2% required biologically.
• Soybean oil’s effects in mice: Diets with 8-10% linoleic acid cause obesity, fatty liver, and diabetes over weeks, unlike coconut oil diets; effects persist even after diet switch unless combined with fasting.
• Role of HNF4 protein: This conserved liver transcription factor binds linoleic acid, regulating gene expression for metabolism; variants shift between carbohydrate and fat processing, with imbalances linked to fatty liver and cancer.
• Oxylipins from linoleic acid: Conversion in liver drives obesity; mice unable to produce them resist weight gain on soybean oil, suggesting these metabolites are key culprits.
• Vitamin B1 & soybean oil: Diets deplete B1 in liver and blood, contributing to obesity; supplementation with B1 analogs prevents weight gain, unlike beef tallow diets which preserve B1 levels.
• Gut & microbiome impacts: Soybean oil alters gut bacteria, potentially reducing B1 production and increasing permeability, leading to inflammation; farm animals fed soybean meal pass effects to consumers.
• Broader health implications: Reanalysis of old human studies questions linoleic acid’s heart benefits; focus on reducing processed foods and seed oils, while noting olive oil’s advantages from historical contexts.

Practical Takeaways:

• Limit processed foods and seed oils like soybean to reduce linoleic acid intake, aiming for 1-2% of calories; read labels and opt for olive oil or home-cooked meals.
• Incorporate intermittent fasting, such as 12-16 hours without eating daily, to help reverse obesity effects from high-linoleic diets, based on mouse reversibility studies.
• Choose grass-fed or naturally fed animal products to avoid indirect soybean oil exposure from feed, potentially preserving nutrient levels like vitamin B1.
• Monitor diet when traveling or changing habits, as shifts in oil types can affect medication metabolism via liver enzymes.

About the guest: Frances Sladek, PhD is a professor whose research focuses on the nuclear receptor HNF4 and the health impacts of dietary fats, particularly soybean oil.

*Not medical advice.

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How seasonal changes in light and dietary unsaturated fats affect circadian rhythms in mammals.

Topics Discussed:

• Evolutionary context of circadian rhythms: All organisms have adapted to Earth’s 24-hour day for survival, with internal clocks slightly offset and adjusted by environmental cues.
• Molecular clock mechanism: Involves a feedback loop where proteins turn on/off genes, lasting ~24 hours, regulated by phosphorylation and degradation for timing precision.
• Genetic variations in sleep: Families with mutations in clock genes like PER2 cause extreme morning lark behavior, altering protein stability and period length by hours.
• Light entrainment: Morning light shortens human clocks (average 24.2 hours) to match 24-hour days; seasonal day length changes require gradual adjustments.
• Food & metabolic links: Seasonal food scarcity/abundance affects clock via glucose and fatty acids competing for protein modifications, as shown in diabetic mouse models.
• Role of unsaturated fats: Paper finds MUFA/PUFA ratios in diet alter phosphorylation of clock proteins, speeding or slowing adaptation to winter/summer light cycles in mice.
• Modern environmental impacts: Artificial light extends “daytime” signals, while constant food access erases seasonal patterns, contributing to obesity and diabetes risks.
• Jet lag & adaptations: Sudden time shifts mimic seasonal experiments; high-sugar/fat intake may phenocopy genetic effects to aid adjustment, though not recommended for health.

Practical Takeaways:

• Expose yourself to morning natural light to help synchronize your internal clock and improve daily energy.
• Consume main meals during daylight hours and avoid late-night eating to align with natural metabolic rhythms.
• Limit evening screen time to reduce artificial blue light disrupting sleep onset.
• Consider varying diet seasonally, favoring diverse, whole foods to mimic natural availability patterns for better health.

About the guest: Louis Ptacek, MD is a neurologist and professor at the University of California, San Francisco. He researches inherited neurological diseases and sleep traits, including genetic variations causing extreme early rising.

Related Episode:

• M&M 237: Circadian Biology: Genetics, Behavior, Metabolism, Light, Oxygen & Melatonin | Joseph Takahashi

*Not medical advice.

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How ketosis and ketogenic diets work and how these tools can improve metabolic health, brain function, and even cancer management.

Topics Discussed:

• Organs have different fuel preferences: brain strongly prefers glucose, heart prefers fatty acids, skeletal muscle is flexible and likes fat/ketones.
• Humans evolved with high metabolic flexibility; regular ketosis was normal for ancestors, but today most people never experience it.
• “Keto flu” is largely glucose withdrawal plus electrolyte/sodium loss; proper salt and hydration prevent most symptoms.
• Classic medical ketogenic diet is ~90% fat (historically saturated); modern versions often use more monounsaturated fats, MCTs, and higher protein.
• Saturated fat is not inherently atherogenic in the context of weight stability or caloric deficit; excess calories from any source can dysregulate metabolism.
• Exogenous ketones (e.g. BHB) provide energy, reduce ROS, stabilize membranes, increase inhibitory tone (GABA), and have hormone-like signaling effects independent of diet.
• Cancer cells often show Warburg effect (damaged mitochondrial respiration → heavy reliance on glycolysis); lowering glucose and raising ketones can stress cancer cells.
• True keto-adaptation for athletic performance requires 6–12 weeks; after that, elite athletes can match or exceed prior high-carb performance at sub-maximal and endurance efforts.

Practical Takeaways:

• Therapeutic carbohydrate restriction (50–100 g/day for many people) plus occasional fasting or ketone supplements can restore metabolic flexibility with far fewer side effects than strict keto.
• Prioritize whole-food fats (eggs, fatty fish, beef, olive oil, butter/lard) and minimize processed keto products loaded with seed oils.
• Supplementing BHB (salts or esters) or MCT oil can ease the transition into ketosis, boost ketones without strict dieting, and may support brain and metabolic health.
• Regularly check basic blood markers (glucose, lipids, electrolytes) and consider an OmegaQuant test; optimizing metabolic health is one of the strongest preventable steps against cancer, neurodegeneration, and heart disease.

Supplemental Ketone (BHB):

• KetoCitra—Ketone body BHB with potassium, calcium & magnesium, formulated with kidney health in mind. Use code MIND20 for 20% off.

*Not medical advice.

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How dietary polyunsaturated fats, especially omega-6 from seed oils, influence inflammation & heart health.

Topics Discussed:

• Polyunsaturated fatty acids (PUFAs): Omega-6 from seed oils like safflower and corn can convert to pro-inflammatory molecules, while omega-3s produce resolving ones; imbalance biases toward chronic inflammation.
• Inflammation regulation: Acute inflammation aids healing but requires active “on” and “off” signals from lipid mediators; chronic inflammation arises from excess omega-6, delaying resolution.
• Heart health & diet: High omega-6 diets worsen post-heart attack outcomes in mice by elevating pro-inflammatory lipids.
• Evolution & historical context: PUFAs are essential but naturally balanced in pre-industrial diets; modern processing skews ratios, contributing to diseases, as shown in early rat experiments needing minimal fats for survival.
• Aging & lifestyle factors: Excess omega-6 exacerbates inflammation in older mice; sleep, exercise, and balanced fats are crucial for metabolic health and enzyme function in processing lipids.
• Cannabis & omega-6 interaction: In mice on high omega-6 diets, CBD-rich cannabis smoke reaches the heart quickly, suppresses immune response, and weakens cardiac strain, unlike in balanced-diet controls.
• Genetic models: FAT-1 mice converting omega-6 to omega-3 show better healing and neuroprotection; FAT-2 mice doing the opposite exhibit liver fibrosis and metabolic issues, highlighting omega-6 excess harms.

Practical Takeaways:

• Balance omega-6 and omega-3 intake by reducing seed oils in processed foods and increasing sources like fish or algae to support inflammation resolution and heart health.
• Monitor and adjust fat intake with age, as older individuals are more sensitive to omega-6 excess leading to immune dysregulation.
• Avoid combining high omega-6 diets with smoking, as it may impair immune and cardiac responses based on animal data.

About the guest: Ganesh Halade, PhD is a cardiovascular scientist and associate professor at the University of South Florida Morsani College of Medicine.

*Not medical advice.

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Methods & challenges of establishing causal relationships in health research, emphasizing epidemiology, randomized trials, and genetic approaches.

Topics:

• Epidemiology: Studies disease influences using observational designs like case-control and prospective cohorts, plus trials, to identify patterns and test hypotheses.
• Hierarchy of evidence critique: Rejects rigid pyramids favoring RCTs, as all studies can be biased; advocates triangulation integrating varied data types for robust conclusions.
• RCT strengths & weaknesses: Randomization balances confounders, but issues like poor blinding, attrition, or subversion can undermine results; large samples may yield spurious precision if biased.
• Confounding & reverse causation: Examples include yellow fingers and lung cancer (both from smoking) or early atherosclerosis inflating CRP-disease links; hard to fully control statistically.
• Nutrition epidemiology: Observational studies often overstate benefits (e.g., vitamin E for heart disease), leading to failed trials; incentives favor new findings over revisiting errors.
• Mendelian randomization: Uses genetic variants as proxies for exposures (e.g., ALDH2 for alcohol metabolism) to mimic randomization; reveals no heart benefits from alcohol, unlike observational data.
• Negative controls: Tests implausible outcomes (e.g., smoking and murder) or exposures (e.g., paternal smoking in pregnancy) to check for confounding artifacts.
• Evidence triangulation: Combines diverse studies with different biases (e.g., cross-cultural comparisons) for causality; applied to dismiss HDL-raising drugs despite initial promise.

Practical Takeaways:

• Scrutinize health claims by checking for negative controls or variety in evidence sources to avoid mistaking correlation for causation.
• For personal decisions like alcohol intake, consider genetic studies showing risks at all levels, and aim for moderation or abstinence based on overall evidence.
• When evaluating supplements or diets, prioritize trials over observational data, and question media hype that ignores confounding factors.

About the guest: Dr. George Davey Smith, MD, DSc is a professor of clinical epidemiology at the University of Bristol and director of the MRC Integrative Epidemiology Unit.

*Not medical advice.

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Integration of brain metabolism with neural signaling, highlighting how core metabolites regulate energy use and protect neurons.

Topics Discussed:

• Brain energy efficiency: Brains are much more energy-efficient than computers for similar processing, relying on adaptive metabolic strategies evolved under energy scarcity.
• Metabolism vs. information processing: Core metabolites like glutamate bridge basic cellular energy production and neural signaling.
• Lactate as a signal: Produced during exercise, lactate diffuses from muscles to brain, modulating neuronal excitability and providing neuroprotection.
• BHB in ketosis: During fasting or ketogenic diets, beta-hydroxybutyrate displaces glucose as fuel, enhances antioxidant defenses, and activates protective potassium channels in neurons.
• Adenosine and sleep: Accumulates from ATP breakdown during wakefulness, triggering sleep and locally inhibiting overactive neural networks for energy conservation.
• Glial cells’ role: Astrocytes and oligodendrocytes handle sophisticated metabolism, release signaling molecules like lactate, and modulate synapses, and influence diseases like Alzheimer’s.

Practical Takeaways:

• Regular exercise elevates lactate, which signals the brain to adapt metabolism and may enhance neuroprotection against stress.
• Intermittent fasting or ketogenic diets can induce ketosis with BHB, potentially boosting brain antioxidant defenses and preconditioning against metabolic stress.
• Prioritizing sleep helps clear adenosine buildup, restoring energy balance and supporting long-term neural health.

About the guest: Dr. Luis Felipe Barros, MD, PhD is a Chilean neurobiologist and professor at the Universidad de Valparaíso, where he leads a lab studying brain metabolism from glucose transport to mitochondrial function.

Related Episode:

• M&M 255 | Unlocking Energy: How Nutrition & Drugs Impact Your Mitochondria | Chris Masterjohn

*Not medical advice.

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Mitochondrial fatty acid synthesis is a little-known but essential pathway that supports energy production and metabolic health.

Summary: Dr. Sara Nowinski explains how mitochondria not only burn fuels to make ATP but also synthesize their own fatty acids inside the matrix; this conserved pathway produces lipoic acid (an essential enzyme cofactor) and longer-chain fats required for proper assembly of the electron transport chain, and disrupting it impairs respiration, glucose handling, and insulin sensitivity while enhancing it appears protective against obesity and heart injury.

About the guest: Sara Nowinski, PhD is an assistant professor in the Department of Metabolism and Nutritional Programming at Van Andel Institute in Grand Rapids, Michigan, where since 2021 she has led a lab focused on mitochondrial biology and the mitochondrial fatty acid synthesis (mitoFAS) pathway.

Topics Discussed:

• Basic mitochondrial energy production: food → pyruvate/fatty acids → acetyl-CoA → TCA cycle → electron transport chain → ATP
• Mitochondrial fatty acid synthesis (mitoFAS): a bacterial-like pathway that builds fats on an acyl carrier protein inside the matrix
• Lipoic acid: an 8-carbon fatty acid made only by mitoFAS, covalently attached to key enzymes (e.g., pyruvate dehydrogenase); cannot be rescued by supplements for cofactor use
• Longer mitoFAS products (14–16 carbons) stabilize electron transport chain assembly factors, explaining why pathway loss collapses respiration even when lipoic acid is intact
• Knocking out mitoFAS causes embryonic lethality, insulin resistance, poor glucose homeostasis, and a rare neurodegenerative disorder (MEPAN syndrome)
• Overexpressing the mitochondrial acyl carrier protein protects mice from diet-induced obesity, insulin resistance, and cardiac injury
• Muscle cell differentiation fails without mitoFAS, hinting at a role in tissue development and repair

Practical Takeaways:

• Supplemental lipoic acid can act as an antioxidant but cannot replace the lipoic acid your mitochondria must make themselves for enzyme function.
• Severe impairment of mitochondrial fatty acid synthesis is linked to insulin resistance and metabolic disruption, suggesting mitochondrial health (beyond just biogenesis) matters for glucose control.

*Not medical advice.

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How internal states like hunger and hormones shape instinctive behaviors, particularly parental care

Episode Summary: Dr. Johannes Kohl explains instinctive behaviors in mammals, emphasizing how states like hunger and hormonal cycles modulate actions such as parental care; they discuss hypothalamic circuits, hormone integration, and pregnancy-induced brain changes, highlighting the balance between motivations like feeding and nurturing offspring.

About the guest: Jonny Kohl, PhD heads the State-Dependent Neural Processing Lab at the Francis Crick Institute in London.

Discussion Points:

• Instinctive behaviors: Pre-wired actions like escaping predators or parental care enable survival without learning, yet remain modifiable by experience and internal states.
• Internal states: Defined as slowly changing conditions (minutes to weeks) like hunger or hormonal fluctuations that influence brain processing & behavior prioritization.
• Hunger regulation: Hypothalamic AGRP neurons detect caloric deficits, creating motivational discomfort relieved by food anticipation, operating on multiple timescales via neurotransmitters & peptides.
• Parental care: Virgin mice show variable pup-directed behaviors; hunger increases aggression, modulated by estrous cycle hormone ratios (estradiol/progesterone).
• Hormone-brain interactions: Steroid hormones like estradiol and progesterone diffuse into the brain, altering gene expression, neuronal excitability, and circuit plasticity over short and long timescales.
• Pregnancy adaptations: Late pregnancy rewires MPOA circuits via surging hormones, preparing robust maternal behavior before birth (anticipatory brain plasticity).

Practical Takeaways:

• Recognize hunger’s impact: Mild food deprivation can heighten irritability or aggression, which can affect social interactions.
• Consider hormonal influences: Cyclical hormone changes affect mood and motivation; tracking cycles may help predict and manage behavioral shifts.
• Prioritize self-care in parenting: Sleep and nutrition deficits mimic hunger states, potentially reducing patience; ensure rest and meals to support nurturing behaviors.
• Question chronic hormone use: Long-term interventions like birth control or testosterone can alter brain function; weigh benefits against potential side effects.

*Not medical advice.

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How mitochondria travel between cells and how this hidden communication shapes metabolism, immunity, and even potential therapies.

Episode Summary: Dr. Jon Brestoff talks about mitochondrial dynamics inside cells, their transfer between unrelated cells (distinct from inheritance during division), and its roles in adipose tissue communication, macrophage cleanup, and systemic metabolic signaling; they explore how high-fat diets disrupt this process, potential hormetic benefits, therapeutic mitochondria transplantation for diseases like Leigh syndrome and obesity, and broader immunometabolism crosstalk.

About the guest: Jon Brestoff, MD, PhD is an associate professor of pathology and immunology at Washington University School of Medicine in St. Louis, where he directs the Initiative for Immunometabolism.

Discussion Points:

• Mitochondria per cell range from ~100-5000; they move via fusion/fission, vertical inheritance (cell division), or horizontal transfer without division.
• Transfer mechanisms: free release, extracellular vesicles, or tunneling nanotubes using cytoskeleton transport.
• In healthy fat tissue, adipocytes routinely donate mitochondria to macrophages for degradation (quality control); high-fat (lard-based, long-chain FA) diets block macrophage uptake, diverting mitochondria to other organs.
• Diverted mitochondria may induce “mito-hormesis” (mild oxidative stress boosting antioxidants) or signal adipocyte metabolic status inter-organ.
• Mitochondria transplantation shows promise in animal models for ischemia-reperfusion, obesity, and mitochondrial diseases.
• Immune cells prefer glycolysis but have low mitochondrial biomass; transplanted mitochondria tilt T-cells toward anti-inflammatory regulatory phenotype.
• Circulating cell-free mitochondria rival immune cell numbers.
• Obesity inflammation stems from dying oversized adipocytes releasing lipids/mitochondria, forming crown-like structures with pro-inflammatory macrophages.
• Leigh syndrome from genetic mutations disrupting the electron transport chain.
• Transfer may be an evolutionary relic of endosymbiosis; cells may selectively use exogenous mitochondria like a “generator” during metabolic crisis.

Reference Paper:

• Study: The power and potential of mitochondria transfer

Related Episode:

• M&M 260: Energy R

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A biophysical rethink of life, health, and disease through the lens of the Energy Resistance Principle (ERP).

Episode Summary: A reframe of biology as energy flow through resistance rather than mere molecular machinery, introducing the Energy Resistance Principle (ERP): life requires a Goldilocks balance of electron flow from food to oxygen via mitochondria; too much or too little resistance drives aging, disease, and death. Explain mitochondria as energy transformers, link ERP to insulin resistance, psychiatric disorders, and healing, and explore health as a dynamic field-like state optimized by flux modulation.

About the guest: Nirosha Murugan, PhD is a biophysicist studying how physical signals pattern biology to decode and reprogram health; Martin Picard, PhD is a mitochondrial psychobiologist at Columbia University, exploring how mitochondrial energy dynamics connect to human experiences, health, and healing. They collaborate on biophotons, light emission, and multi-scale energy signaling.

Discussion Points:

• Mitochondria transform electrons from food into versatile electricity via proton gradients.
• Energy Resistance Principle: transformation needs resistance; chronic high resistance causes dissipative heat, damage, aging.
• GDF15 cytokine signals mitochondrial stress to brain, triggering energy conservation/mobilization.
• Insulin resistance: adaptive defense against electron overload, reversible by fasting/exercise.
• Psychiatric illness: excess brain energy resistance; exercise, keto, psychedelics redistribute flux.
• Health: dynamic optimization of energy resistance, not absence of disease.
• Healing: daily recovery from micro-damage via balanced resistance.
• Future: energy-based diagnostics/therapies (light, TMS) over molecule-only drugs.

*Not medical advice.

Reference Paper: The energy resistance principle

Related Episode:

• M&M 70: Mitochondria, Aging, Cellular Energy, Metabolism, Gray Hair Reversal & Brain-Body Communication | Martin Picard

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