Insulin is one of the body’s most important signals for determining whether you burn glucose or fat: when insulin rises, fat release and fat burning fall, while lower insulin allows stored fat to become available for fuel. This helps explain why reducing carbohydrates can dramatically increase fat oxidation even without changing the body’s basic ability to burn fat.

::: spoiler generated summary

Insulin and the glucose-fatty-acid cycle

• Fuel choice is not just about which substrate is available. Carbohydrates raise blood glucose and insulin; insulin suppresses fat-cell lipolysis and makes long-chain fatty-acid entry into mitochondria harder, so higher insulin shifts oxidation toward glucose and lower insulin releases stored fat for oxidation.
• The glucose fatty-acid cycle began with a 1963 paper: fat oxidation inhibits glucose oxidation at pyruvate dehydrogenase, intermediates then back up through the pathway, and glucose uptake falls. The original observations came from isolated rat muscle and heart. [1]
• Human clamp studies hold insulin and glucose at chosen levels and can use lipid emulsion to hold fatty acids constant, isolating glucose-fat competition.

Human evidence that fat oxidation suppresses glucose oxidation

• Healthy volunteers underwent two insulin clamps; one kept fatty acids elevated by lipid infusion, while the other let them fall as insulin normally makes them fall. [2]
• With insulin and fatty acids both high, leg glucose uptake fell by about one-third; glucose supplied a little over half of energy versus about three-quarters when fatty acids fell, and pyruvate dehydrogenase activity was lower. [2]
• Respiratory quotient (RQ) tracks fuel use from CO2 produced relative to O2 consumed: carbohydrate is near 1.0, fat near 0.7, and whole-body respiratory exchange ratio is the analogous whole-body measurement.
• High insulin plus high fatty acids is an artificial combination in a healthy person because insulin normally suppresses fatty-acid release; lipid infusion overrides that normal hormonal effect.

The reverse direction: glucose and insulin suppress fat oxidation

• Most people eat predominantly carbohydrate; based on a nutrient database, about 70% of calories globally come from carbohydrate.
• In healthy volunteers, a hyperinsulinemic, hyperglycemic clamp held fatty acids constant while glucose oxidation rose more than threefold and fat oxidation fell; cellular glucose availability determined fuel oxidation even without a fall in fat availability. [3]
• A companion experiment infused tagged oleate, a long-chain fat that requires the carnitine shuttle, and octanoate, a medium-chain fat that bypasses it. Under the glucose-insulin clamp with fatty acids held constant, oleate oxidation fell almost by half while octanoate oxidation did not change. [4]
• The control is at long-chain fatty-acid transport into mitochondria through the carnitine shuttle/CPT1: glucose and insulin can reduce long-chain fat oxidation while circulating fatty acids remain available. [4]
• After an ordinary carbohydrate-containing meal, glucose and insulin rise, muscle and adipose glucose uptake rises, adipose fatty-acid release falls, and long-chain fatty-acid transport into mitochondria is inhibited; the cell therefore burns more glucose. This follows the insulin signal whether total calories are in deficit or surplus.

Insulin acts at two control points

• Insulin controls fat oxidation upstream by suppressing adipose lipolysis and downstream by limiting long-chain fatty-acid entry into mitochondria.
• In a clamp controlling insulin, growth hormone, and glucagon, less than 2 µU/mL of insulin reduced fat release by half in healthy people; fasting insulin is commonly 5-10 µU/mL, so adipose lipolysis is "exquisitely sensitive to insulin." [5]
• In another study using four increasing insulin infusion rates, the insulin concentration needed to halve fatty-acid release was roughly one-third of that needed to halve fat oxidation. Insulin suppresses fat supply at lower concentrations than mitochondrial fat oxidation. [6]

Meals and exercise expose both control points

• Six active men cycled for an hour after an overnight fast, glucose, or fructose. Fructose does not increase insulin; in these trials, pre-exercise insulin averaged about 8 µU/mL fasted, 17 after fructose, and 38 after glucose. After glucose, fatty-acid release was about half the fasted value and fat oxidation fell with it. [7]
• A fourth glucose trial restored circulating fatty acids with lipid infusion: fat oxidation rose about 30% above the glucose-only trial but remained below the fasted trial, separating reduced fatty-acid supply from inhibited mitochondrial entry. [7]
• Exercise makes fuel use easier to measure, but the same mechanisms matter at rest; several carbohydrate-containing meals can keep insulin elevated through much of the waking day.
• In six endurance-trained subjects cycling for 40 minutes, a large glucose drink reduced total fat oxidation by 34%; roughly half of the reduction came from circulating fatty acids and half from intramuscular triglyceride. Because intramuscular fat was already inside muscle, its reduced oxidation points again to mitochondrial-level inhibition. [8]

Sustained carbohydrate restriction changes the fuel mix

• Five trained cyclists ate a eucaloric diet with about two-thirds of calories from carbohydrate for one week, then a calorie- and protein-matched ketogenic diet below 20 g carbohydrate/day for four weeks. RQ fell from 0.83 to 0.72, glucose oxidation fell about threefold, and muscle glycogen use fell about fourfold, while VO2max and time to exhaustion were unchanged. [9]
• Twenty matched elite ultramarathon/Ironman-distance athletes included 10 high-carbohydrate and 10 low-carbohydrate athletes; the low-carbohydrate group averaged about 10% carbohydrate and 70% fat for about 20 months. Peak fat oxidation was more than twice as high with no overlap between groups, and fat supplied 88% versus 56% of energy over a three-hour run. [10]
• Resting muscle glycogen, glycogen used during the run, and glycogen restored afterward were the same between those athlete groups, so chronic low-carbohydrate intake did not leave their muscle glycogen depleted. [10]

Insulin resistance and metabolic inflexibility

• In insulin-resistant muscle, fuel selection goes wrong in both directions: between meals and overnight it keeps burning more carbohydrate when it should shift toward fat, while a rise in insulin produces a weaker shift toward carbohydrate. This is metabolic inflexibility. [11]
• The Randle cycle is a valid physiological principle but may not explain insulin resistance in skeletal muscle; in this model, simply eating more fat is not what creates insulin resistance. [11]
• In obese subjects studied with arterial-venous leg sampling, fasting leg RQ remained near 0.85, and muscle biopsies had lower carnitine-palmitoyltransferase activity and lower activity of fat-oxidizing enzymes. [12]
• Chronic high insulin creates opposite tissue problems: insulin-resistant adipose tissue keeps releasing fatty acids despite high insulin, while muscle remains responsive to insulin's block on mitochondrial fatty-acid entry. Fatty acids are delivered but not burned and can accumulate in muscle, liver, pancreas, and other ectopic sites.

Fuel oxidation versus body-fat loss

• Which fuel is being burned at a moment is not automatically the same question as how much body fat is ultimately lost.
• In 28 overweight or obese adults, two calorie-restricted diet periods compared a ketogenic diet below 10% carbohydrate with a low-fat diet near 60% carbohydrate, allowing within-person comparison. The low-carbohydrate period had higher self-recorded intake, about 1,900 versus 1,500 kcal/day, yet produced more weight, total-fat, and trunk-fat loss. [13]
• The food was not provided and intake was self-recorded, so there is potential error; having each person act as their own control is a strength of the comparison. [13]
• A meta-analysis of 13 trials lasting at least 12 months found greater weight loss with very-low-carbohydrate ketogenic diets than low-fat diets, but the difference was modest at about 1 kg. [14]

Why calorie-restricted comparisons can wash out the insulin difference

• Every low-carbohydrate versus low-fat trial in this comparison also cut calories in both groups. The higher-carbohydrate group therefore ate fewer carbohydrates than before the study and lowered insulin too, so these trials compare lowered insulin with more-lowered insulin, not unchanged high insulin with low insulin.
• A cleaner test is caloric overfeeding in both groups, because nobody then reduces carbohydrate simply by eating less and any difference can be attributed to diet composition.

The overfeeding case and conclusion

• The only study in nutrition science that tested this overfeeding design is Sam Feltham's n-of-1 case: 5,800 kcal/day for 21 days on each of three diets, with about three months between periods to return toward baseline—low-carbohydrate at about 6% carbohydrate, low-fat, and very-low-fat plant-based vegan. [15]
• Weight gain was a little over 1 kg on low carbohydrate, over 7 kg on low fat, and about 5 kg on the very-low-fat vegan diet. It is one case in one person, but it is the only study that tested the overfeeding question this way. [15]
• Across these human data, carbohydrate restriction increases fat oxidation, produces at least as much fat loss as fat restriction and usually more, requires less of a caloric deficit, and loses relatively more visceral/abdominal fat.
• Fuel selection is not decided simply by which fuel is more abundant in blood: clamp studies held fatty acids constant and fat oxidation still fell when glucose and especially insulin rose. Insulin controls both fat release from adipose tissue and long-chain fatty-acid entry into mitochondria.
• Carbohydrate is the main dietary driver of insulin, and insulin is the main controller of which fuel is burned. Lowering carbohydrate lowers the insulin signal at both control points and lets the body burn more fat: "you burn what you eat."

References

1. [01:37] The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus — https://doi.org/10.1016/S0140-6736(63)91500-9
2. [04:25] Interaction between glucose and free fatty acid metabolism in human skeletal muscle — https://doi.org/10.1172/JCI116603
3. [09:16] Glucose and insulin-induced inhibition of fatty acid oxidation: the glucose-fatty acid cycle reversed — https://doi.org/10.1152/ajpendo.1996.270.4.E733
4. [09:58] Glucose plus insulin regulate fat oxidation by controlling the rate of fatty acid entry into the mitochondria — https://doi.org/10.1172/JCI119034
5. [14:10] Insulin regulation of lipolysis in nondiabetic and IDDM subjects — https://doi.org/10.2337/diab.38.12.1595
6. [15:18] Regulation of free fatty acid metabolism by insulin in humans: role of lipolysis and reesterification — https://doi.org/10.1152/ajpendo.2006.263.6.E1063
7. [16:01] Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise — https://doi.org/10.1152/ajpendo.1997.273.4.E768
8. [18:12] Fatty acid oxidation is directly regulated by carbohydrate metabolism during exercise — https://doi.org/10.1152/ajpendo.1997.273.2.E268
9. [19:28] The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation — https://doi.org/10.1016/0026-0495(83)90106-3
10. [20:47] Metabolic characteristics of keto-adapted ultra-endurance runners — https://doi.org/10.1016/j.metabol.2015.10.028
11. [22:26] Fuel selection in human skeletal muscle in insulin resistance: a reexamination — https://doi.org/10.2337/diabetes.49.5.677
12. [23:28] Skeletal muscle fatty acid metabolism in association with insulin resistance, obesity, and weight loss — https://doi.org/10.1152/ajpendo.1999.277.6.E1130
13. [26:02] Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women — https://doi.org/10.1186/1743-7075-1-13
14. [27:16] Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials — https://doi.org/10.1017/S0007114513000548
15. [29:30] A case study of overfeeding 3 different diets — https://doi.org/10.1097/MED.0000000000000668 :::

Learn how to make homemade bacon from pork belly with no added sugar. This easy carnivore and keto bacon recipe eliminates the unnecessary junk found in many grocery-store brands while giving you complete control over the ingredients.

::: spoiler motivation I got some new sfp modules today, and i wanted to validate them... I was feeling lazy to drag two machines together to plug in the sfp modules for a point to point link (plus many machines don't even have sfp slots), I was feeling lazy to daisy chain two switches together to use the sfp modules.....

I do have iperf3 testing already setup on a stable host server pair in my network... so :::

Setup two vlans A, B. These vlans have no dhcp, no routes, nothing - Attach a interface to each vlan, assign as static ip address on the same subnet, run iperf3 in server mode. The test comes from how you bridge the vlans: A switch with vlan A on port A, and vlan B on port B, now if you plug in SFP.A and SFP.B and bridge with a cable... iperf3 can connect.

This extends your in place network path from interface A to interface B by forcing it to go over SW.PortA->SFP.A->Test Cable->SFP.B->->SW.PortB

Host interface A
  │
  │ VLAN A
  ▼
switch.portA ── Test SFP.A
            │
            │ test-cable
            │
switch.portB ── Test SFP.B
  ▲
  │ VLAN B
  │
Host interface B

Run iperf3 in a loop, and now you can swap modules/cables and get the full benefit of a point to point cable test without having to move any machines around. This will even work with a single machine for testing, with a interface on A and B (different namespaces), you just have to double your iperf results mentally.

I realize this is fairly niche, and probably obvious to many people, but I just stumbled upon it today and thought it was pretty neat.

FWIW my SFP modules ran at 9.6gbps, so I'm happy with them!

I Finally Tried Goat Meat...

::: spoiler generated summary

Goat as a Lion-Diet Experiment

• Beef and lamb had been regular foods for years, while goat meat had never been tried, making this an experiment in whether goat is an overlooked carnivore option.
• Goat is ruminant meat, making it suitable for the lion diet of ruminant meat, salt, and water, and this was an experiment in preparation for doing lion diet.

Preparing and Braising the Goat

• The package was simply marked goat meat and contained bone-in pieces of unknown cuts, so low-and-slow cooking was used without trying to identify or separate the pieces.
• The meat was salted with kosher salt, then all the pieces were seared in tallow; for lion diet, another ruminant fat such as lamb or goat fat also works.
• The pieces included small marrow bones, skin, connective tissue, and visible fat, which looked promising for a long braise.
• After searing over medium-high heat, about 1½ cups of water went into the pot. Ruminant meat or bone broth also works while staying within lion diet.
• The goat braised at 300°F for about 3½ hours. At the two-hour mark the liquid was getting low, so about another half cup of water was added.

Finished Goat

• After 3½ hours, the goat was deeply caramelized and the meat had fallen off the bones, with a substantial amount of rendered fat remaining and very little liquid.
• There were many small bones throughout the cooked meat, so they need to be watched for and picked out while eating.
• The finished dish contained meat, bone marrow, fat, and connective tissue and had reduced far beyond the consistency normally associated with a stew.

First Taste

• Goat was expected to resemble lamb, perhaps with a stronger or gamier flavor, but it tasted neither like lamb nor like beef.
• The closest description of the flavor was a combination of beef, lamb, and chicken, and the result was delicious.
• The verdict was that goat is a carnivore gem and a great ruminant-meat choice for lion diet.

Cost and Verdict

• The goat cost about $10 per pound compared with $8.99 per pound for locally purchased one-pound packages of ground beef, making it only somewhat more expensive.
• The first experience with goat was pleasantly surprising, and it will definitely be made again; it was unexpected and well worth trying.

References None. :::

Mitochondria often struggle in insulin resistance not because they are broken, but because there are fewer of them trying to process too much incoming fuel. Exercise and improved metabolic health remain the most effective ways to build healthier mitochondria, while supplements may provide additional—but smaller—benefits.

Summary: In this mini-lecture, Ben explains why mitochondria have become one of the most talked-about topics in health while separating scientific evidence from popular hype. He begins by reviewing how mitochondria convert the energy stored in carbohydrates, fats, and ketones into ATP, the usable energy that powers virtually every function in the body. Along the way, he explains concepts such as glycolysis, the Krebs cycle, the electron transport system, coupling versus uncoupling, and the production of reactive oxygen species.

Ben then examines what happens in insulin resistance and type 2 diabetes. Rather than concluding that mitochondria are "broken," he explains that the evidence points to a different problem: people with insulin resistance generally have fewer mitochondria, more fragmented mitochondrial networks, and an excessive fuel load. As glucose and fatty acids arrive faster than the mitochondria can process them, byproducts such as lactate and acylcarnitines begin to accumulate, signaling a mismatch between fuel supply and mitochondrial capacity.

The lecture also reviews current approaches to measuring mitochondrial health, including fasting lactate, the lactate-to-pyruvate ratio, and newer biomarkers such as GDF15 and FGF21. Dr. Bikman discusses several popular mitochondrial interventions—including methylene blue, urolithin A, CoQ10, red-light therapy, and cold exposure—highlighting where human evidence is promising and where it remains limited.

The central message is that no supplement outperforms the fundamentals. Exercise consistently increases mitochondrial number and function while improving insulin sensitivity, and lowering carbohydrate intake reduces the fuel burden placed on mitochondria. Together, these strategies address the root problem more effectively than relying on supplements alone.

::: spoiler generated summary

Mitochondrial health and fuel capacity

• Mitochondria are central to cellular fuel handling and oxidative stress, so the current attention is partly warranted, but measurement is largely missing; clinical mitochondrial tests were built for rare inherited disease, not ordinary insulin resistance.
• The measurement gap is filled by methylene blue, urolithin A, red and near-infrared light, cold exposure, and other mitochondrial interventions, several of which have human evidence.
• In insulin resistance and type 2 diabetes, too much glucose and fat can arrive for the available mitochondrial capacity. Exercise builds capacity, while lower incoming fuel, insulin, and blood glucose help prevent overload.

How mitochondria process fuel

• Mitochondrion is singular and mitochondria is plural. Every human cell except the red blood cell contains mitochondria, whose main job is converting chemical energy in food or stored fat into usable cellular energy.
• Glycolysis occurs in the cytosol outside mitochondria, splitting one six-carbon glucose into two three-carbon pyruvate molecules and making a little ATP without oxygen.
• Pyruvate enters mitochondria and becomes acetyl-CoA; fats reach acetyl-CoA through beta oxidation, and the ketone beta-hydroxybutyrate can also become acetyl-CoA. These fuels converge and can compete at a common metabolic destination.
• The Krebs or citric acid cycle strips electrons from acetyl-CoA and loads NAD into NADH; NAD-focused products such as NR and NMN target this electron-carrying system.
• NADH delivers electrons to the respiratory or electron transport system in the inner mitochondrial membrane. Oxygen is the final electron acceptor and combines with hydrogen to form metabolic water, so oxygen consumption tracks electron flow.
• Energy released by electron flow is used to make ATP for contraction, nerve impulses, and other cellular work.
• Mitochondrial respiration can be coupled to ATP production or uncoupled toward heat production. Neither is inherently good or bad; brown fat deliberately uncouples mitochondria to make heat.
• Electron transport is imperfect, so some electrons leak and generate reactive oxygen species such as hydrogen peroxide. Low amounts can signal useful adaptations, while excess can damage proteins, membranes, and DNA; hydrogen peroxide relative to oxygen use is informative about oxidative stress.
• Mitochondria continually divide and fuse. The balance of fission and fusion determines mitochondrial morphology and whether the cell has a connected network or many small fragments.

What changes in insulin resistance and type 2 diabetes

• Human thigh-muscle biopsies have respiratory-system activity highest in lean insulin-sensitive people, lower in obese but still insulin-sensitive people, and lowest in type 2 diabetes; electron microscopy in the same work found mitochondria roughly one-third smaller in the obese and diabetic groups. [1]
• A separate analysis found a major loss of subsarcolemmal mitochondria, the population just beneath the muscle-cell membrane and heavily involved in fuel burning, with the diabetic group reduced to about one-seventh of the lean insulin-sensitive level. [2]
• Whole-tissue oxygen consumption can fall simply because tissue contains fewer mitochondria. When respiration is normalized to mitochondrial content, lean, obese, and diabetic groups no longer differ in respiratory capacity per mitochondrion, indicating that reduced capacity can reflect fewer mitochondria and normal individual organelles. [3]
• Network structure matters: connected mitochondria can share contents, distribute fuel, and dilute damage across a larger pool, while isolated fragments lose that buffer.
• MFN2, a protein required for mitochondrial fusion, is reduced in skeletal muscle with obesity and type 2 diabetes, inversely related to BMI, and directly related to insulin sensitivity; this fits the smaller, more fragmented mitochondrial morphology. [4]
• Ceramides accumulate in muscle with obesity and insulin resistance. [5] Ceramide exposure in the lab rapidly forced mitochondrial fission, lowered oxygen consumption, and increased hydrogen peroxide production. [6]
• The resulting problem is not necessarily broken mitochondrial machinery. A supply-capacity mismatch can consist of less mitochondrial mass, greater fragmentation, and more fuel arriving than the network can fully process.

Fuel overflow: lactate, acylcarnitines, and insulin

• When glycolysis makes pyruvate faster than mitochondria can take it in and burn it, excess pyruvate becomes lactate. Resting fasting lactate therefore carries information about mitochondrial capacity outside exercise.
• In a large community case-cohort analysis, fasting lactate rose with fasting glucose and insulin, and the highest lactate quartile had roughly twice the diabetes risk of the lowest even after adjustment for usual risk factors. [7]
• Fat has a parallel overflow signal. When fatty acids enter faster than beta oxidation can finish them, partially processed intermediates leave as acylcarnitines; people with type 2 diabetes have a pattern consistent with incomplete fat oxidation. [8]
• Insulin determines the incoming fuel mix. Hyperinsulinemia drives glucose into cells and suppresses fat oxidation [9], while insulin-resistant fat cells release excess fatty acids into blood.
• Muscle can therefore receive glucose and fatty acids simultaneously while high insulin inhibits beta oxidation. Both fuels compete for limited mitochondrial processing, leaving neither fully burned.

Measuring mitochondrial function

• Clinical mitochondrial testing was designed for rare inherited mitochondrial diseases, not ordinary insulin-resistant people, so it does not provide a validated routine measure of mitochondrial capacity in this population. [10]
• Fasting lactate is simple but imprecise because exercise, prolonged tourniquet use, medications, and impaired blood flow can raise it. [11]
• The lactate-to-pyruvate ratio reflects the NADH-to-NAD redox balance and electron traffic. A respiratory-chain block raises the ratio, while an upstream mitochondrial-entry problem can raise both lactate and pyruvate with a normal ratio; pyruvate instability also makes sample handling critical. [11]
• In children with confirmed mitochondrial disorders compared with other neuromuscular disease and healthy controls, the lactate-to-pyruvate ratio was the weakest discriminator; GDF15 and FGF21 were much stronger, with GDF15 giving the highest discrimination. [12]
• These markers were built around rare congenital disease, and there are not enough data for validated testing in ordinary metabolic dysfunction. An individual's own trajectory is more useful than comparisons across people or laboratories.

Interventions aimed at mitochondria

• Methylene blue can carry electrons past earlier respiratory complexes. In a randomized double-blind placebo-controlled study of 26 healthy adults, one low oral dose increased brain activity in attention and memory regions and produced 7% more correct memory-retrieval responses; metabolic outcomes were not measured. [13]
• Urolithin A activates mitophagy. In a four-month trial of adults aged 65 to 90, it improved muscle endurance at two months and shifted plasma biomarkers favorably, but six-minute walk distance did not differ from placebo. [14]
• A separate four-month trial in middle-aged adults found roughly 12% greater muscle strength and lower plasma acylcarnitines with urolithin A. [15]
• CoQ10 carries electrons from complexes I and II toward complex III. An umbrella review found lower fasting glucose with supplementation, while fasting insulin and HbA1c changes were statistically significant by some analyses but much more modest in real-world magnitude. [16]
• Red and near-infrared light can be absorbed by cytochrome-c oxidase, the final respiratory complex; human work using strong near-infrared stimulation found measurable activation and up-regulation of this complex. [17]
• Cold exposure raises PGC-1alpha, a master regulator of mitochondrial biogenesis. Human muscle biopsies after cold-water immersion showed about a sixfold rise three hours later, and pairing cold exposure with exercise amplified the exercise effect. [18]
• These interventions can improve electron flow, add cofactors, activate mitophagy, or increase capacity, but they do not necessarily reduce the amount of fuel arriving at mitochondria, so fuel overload can remain.

Exercise, substrate control, and ketones

• Exercise is the most reliable stimulus for increasing mitochondrial content in human skeletal muscle. In overweight older adults, calorie-restriction weight loss and exercise both improved insulin sensitivity, but only exercise increased mitochondrial content, electron-transport proteins, and fatty-acid oxidation in muscle biopsies. [19]
• Reducing dietary carbohydrate lowers glycolytic flux and pressure toward lactate accumulation; lowering insulin through carbohydrate restriction restores fat burning so glucose and fat are not both held in the queue at the same time.
• When carbohydrate and insulin fall enough, the liver makes ketones. Beta-hydroxybutyrate is more than a fuel and changes mitochondrial behavior in a tissue-dependent way.
• Beta-hydroxybutyrate increased mitochondrial respiration in fat without increasing ATP, producing uncoupling. Human adipose biopsies in ketosis used about 130% more oxygen than those from people not in ketosis. [20]
• In skeletal muscle, beta-hydroxybutyrate had the opposite coupling effect: it tightened the link between respiration and ATP production and lowered hydrogen peroxide production. [21]

The practical hierarchy

• In insulin resistance and type 2 diabetes, mitochondrial mass can fall while substrate delivery rises; lactate is the glucose-side overflow signal and acylcarnitines are the parallel fat-side signal that capacity is being reached.
• Exercise is best because it increases mitochondrial number and helps control fuel load. Methylene blue, urolithin A, red light, cold exposure, and other additions can help, but they are additions to exercise, not substitutes for it.

References

1. [13:39] Dysfunction of Mitochondria in Human Skeletal Muscle in Type 2 Diabetes — https://doi.org/10.2337/diabetes.51.10.2944
2. [14:29] Deficiency of Subsarcolemmal Mitochondria in Obesity and Type 2 Diabetes — https://doi.org/10.2337/diabetes.54.1.8
3. [15:55] Increased mitochondrial substrate sensitivity in skeletal muscle of patients with type 2 diabetes — https://doi.org/10.1007/s00125-011-2098-4
4. [17:07] Expression of Mfn2, the Charcot-Marie-Tooth neuropathy type 2A gene, in human skeletal muscle: effects of type 2 diabetes, obesity, weight loss, and the regulatory role of tumor necrosis factor alpha and interleukin-6 — https://doi.org/10.2337/diabetes.54.9.2685
5. [18:13] Ceramide content is increased in skeletal muscle from obese insulin-resistant humans — https://doi.org/10.2337/diabetes.53.1.25
6. [18:18] Mitochondrial fission mediates ceramide-induced metabolic disruption in skeletal muscle — https://doi.org/10.1042/BJ20130807
7. [20:24] Lactate and Risk of Incident Diabetes in a Case-Cohort of the Atherosclerosis Risk in Communities (ARIC) Study — https://doi.org/10.1371/journal.pone.0055113
8. [21:33] Plasma Acylcarnitine Profiles Suggest Incomplete Long-Chain Fatty Acid β-Oxidation and Altered Tricarboxylic Acid Cycle Activity in Type 2 Diabetic African-American Women — https://doi.org/10.3945/jn.108.103754
9. [22:18] Effects of insulin on skeletal muscle glucose storage, oxidation, and glycolysis in humans — https://doi.org/10.1152/ajpendo.1990.258.6.E923
10. [24:02] Diagnosis and management of mitochondrial disease: a consensus statement from the Mitochondrial Medicine Society — https://doi.org/10.1038/gim.2014.177
11. [24:34] The in-depth evaluation of suspected mitochondrial disease — https://doi.org/10.1016/j.ymgme.2007.11.018
12. [26:23] Circulating FGF21 and GDF15 as Biomarkers for Screening, Diagnosis, and Severity Assessment of Primary Mitochondrial Disorders in Children — https://doi.org/10.3389/fped.2022.851534
13. [28:52] Multimodal Randomized Functional MR Imaging of the Effects of Methylene Blue in the Human Brain — https://doi.org/10.1148/radiol.2016152893
14. [29:49] Effect of Urolithin A Supplementation on Muscle Endurance and Mitochondrial Health in Older Adults: A Randomized Clinical Trial — https://doi.org/10.1001/jamanetworkopen.2021.44279
15. [30:18] Urolithin A improves muscle strength, exercise performance, and biomarkers of mitochondrial health in a randomized trial in middle-aged adults — https://doi.org/10.1016/j.xcrm.2022.100633
16. [30:55] Effects of Coenzyme Q10 Supplementation on Glycemic Control Biomarkers: An Umbrella Review of Meta-Analyses of Randomised Controlled Trials — https://doi.org/10.1002/edm2.70182
17. [31:59] Interplay between up-regulation of cytochrome-c-oxidase and hemoglobin oxygenation induced by near-infrared laser — https://doi.org/10.1038/srep30540
18. [32:34] Passive and post-exercise cold-water immersion augments PGC-1α and VEGF expression in human skeletal muscle — https://doi.org/10.1007/s00421-016-3480-1
19. [34:53] Calorie Restriction-induced Weight Loss and Exercise Have Differential Effects on Skeletal Muscle Mitochondria Despite Similar Effects on Insulin Sensitivity — https://doi.org/10.1093/gerona/glw328
20. [36:17] Ketones Elicit Distinct Alterations in Adipose Mitochondrial Bioenergetics — https://doi.org/10.3390/ijms21176255
21. [36:57] β-Hydroxybutyrate Elicits Favorable Mitochondrial Changes in Skeletal Muscle — https://doi.org/10.3390/ijms19082247 :::

this is my 4th fast, its much easier then the first 2, a little bit better then the 3rd. Day 3 hd the most cravings around the 60-68 hour mark but that went away.

Had a touch of vertigo which didn't resolve with sodium/potassium supplements, so I broke the fast at 4 days.

Funnily enough I was super gassy after refeeding, the first time I've experienced that on carnivore.

I decided to group them by category then alphabetical by authors last name

Booklist

::: spoiler Fiction — science fiction & fantasy

• Douglas Adams

  • The Hitchhiker’s Guide to the Galaxy
  • The Restaurant at the End of the Universe
  • Life, the Universe and Everything
  • So Long, and Thanks for All the Fish
  • Mostly Harmless

• Isaac Asimov

  • Foundation
  • Foundation and Empire
  • Second Foundation
  • Foundation’s Edge
  • Foundation and Earth
  • Prelude to Foundation

• Yaroslav Barsukov

  • Sleeping Worlds Have No Memory

• Gregory Benford & Larry Niven

  • Bowl of Heaven
  • Shipstar — 2 physical copies
  • Glorious

• Matt Dinniman

  • Dungeon Crawler Carl
  • Carl’s Doomsday Scenario
  • The Dungeon Anarchist’s Cookbook
  • The Gate of the Feral Gods
  • The Butcher’s Masquerade
  • The Eye of the Bedlam Bride
  • This Inevitable Ruin
  • A Parade of Horribles
  • Operation Bounce House

• Joe Haldeman

  • The Forever War

• Frank Herbert

  • Dune
  • Dune Messiah
  • Children of Dune
  • God Emperor of Dune
  • Heretics of Dune
  • Chapterhouse: Dune

• T. Kingfisher

  • A Sorceress Comes to Call

• Katherine Kurtz

  • The Bastard Prince

• Larry Niven

  • The Integral Trees
  • The Smoke Ring

• Larry Niven & Matthew Joseph Harrington

  • The Goliath Stone

• Larry Niven & Jerry Pournelle

  • The Moat Around Murcheson’s Eye (The Gripping Hand)

• Larry Niven, Jerry Pournelle & Steven Barnes

  • The Legacy of Heorot (probable; spine partly obscured)
  • Beowulf’s Children (probable; spine partly obscured)

• Jennifer R. Pournelle

  • Outies

• Skyler Ramirez

  • The Worst Ship in the Fleet

• John Scalzi

  • The Collapsing Empire
  • The Consuming Fire
  • The Last Emperox
  • The Shattering Peace
  • The End of All Things
  • The Last Colony
  • Zoe’s Tale
  • The Ghost Brigades
  • Old Man’s War
  • The Human Division

• Neal Stephenson

  • Seveneves

• Adrian Tchaikovsky

  • Children of Time
  • Children of Ruin
  • Children of Memory

• J.R.R. Tolkien

  • The Silmarillion
  • Unfinished Tales of Númenor and Middle-earth
  • Roverandom
  • Farmer Giles of Ham
  • The Adventures of Tom Bombadil
  • Smith of Wootton Major

• J.R.R. Tolkien; edited by Christopher Tolkien

  • The Book of Lost Tales, Part One
  • The Book of Lost Tales, Part Two
  • The Lays of Beleriand
  • The Shaping of Middle-earth
  • The Lost Road and Other Writings

• Vernor Vinge

  • The Collected Stories of Vernor Vinge
  • A Fire Upon the Deep
  • A Deepness in the Sky
  • The Peace War
  • Rainbows End
  • Marooned in Realtime

• Peter Watts

  • Blindsight

• David Weber

  • Mutineers’ Moon
  • Empire from the Ashes
  • Off Armageddon Reef
  • By Schism Rent Asunder

• Andy Weir

  • Project Hail Mary
  • Artemis

• Makoto Yukimura

  • Vinland Saga, Book One

:::

::: spoiler Computing, cybersecurity & statistics

• Harold Abelson & Gerald Jay Sussman, with Julie Sussman

  • Structure and Interpretation of Computer Programs, 2nd ed.

• Ross Anderson

  • Security Engineering: A Guide to Building Dependable Distributed Systems, 3rd ed.

• Randal E. Bryant & David R. O’Hallaron

  • Computer Systems: A Programmer’s Perspective, 3rd ed.

• Daniel P. Friedman & Matthias Felleisen

  • The Little Schemer
  • The Seasoned Schemer (probable; spine partly obscured)

• Daniel P. Friedman, William E. Byrd & Oleg Kiselyov

  • The Reasoned Schemer (probable; spine partly obscured)

• Gareth James, Daniela Witten, Trevor Hastie & Robert Tibshirani

  • An Introduction to Statistical Learning: with Applications in R, 2nd ed.

• Gareth James, Daniela Witten, Trevor Hastie, Robert Tibshirani & Jonathan Taylor

  • An Introduction to Statistical Learning: with Applications in Python

• Donald E. Knuth

  • The Art of Computer Programming, Vol. 1: Fundamental Algorithms, 3rd ed.
  • The Art of Computer Programming, Vol. 2: Seminumerical Algorithms, 3rd ed.
  • The Art of Computer Programming, Vol. 3: Sorting and Searching, 2nd ed.
  • The Art of Computer Programming, Vol. 4A: Combinatorial Algorithms, Part 1
  • The Art of Computer Programming, Vol. 4B: Combinatorial Algorithms, Part 2

• Nick Rozanski & Eoin Woods

  • Software Systems Architecture: Working with Stakeholders Using Viewpoints and Perspectives, 2nd ed.

• Bruce Schneier

  • Applied Cryptography: Protocols, Algorithms, and Source Code in C, 2nd ed.

• Michael Sipser

  • Introduction to the Theory of Computation (probable; spine partly obscured)

• Adam Shostack

  • Threat Modeling: Designing for Security

• Marc Weber Tobias

  • Tobias on Locks and Insecurity Engineering: Understanding and Preventing Design Vulnerabilities in Locks, Safes, and Security Hardware

:::

::: spoiler Science, engineering, architecture & reference

• Kate Ascher

  • The Heights: Anatomy of a Skyscraper

• Frédéric Chaubin

  • CCCP: Cosmic Communist Constructions Photographed

• DK

  • Bird: The Definitive Visual Guide
  • History of the World Map by Map
  • The Universe (edition/editor unclear)

• Lawrence M. Krauss

  • The Physics of Star Trek

• Dave McOmie with Marc Goldberg

  • Safecracker: A Chronicle of the Coolest Job in the World

• Windell Oskay & Eric Schlaepfer

  • Open Circuits: The Inner Beauty of Electronic Components

:::

::: spoiler Medicine, nutrition & metabolism

• Bridgette Allan, Bernadine Douglas & Tim Noakes

  • The Banting Pocket Guide

• Richard K. Bernstein

  • Dr. Bernstein’s Diabetes Solution

• Ken D. Berry

  • Lies My Doctor Told Me

• Benjamin Bikman

  • Why We Get Sick: The Hidden Epidemic at the Root of Most Chronic Disease—and How to Fight It

• Benjamin Bikman & Diana Keuilian

  • How Not to Get Sick: A Cookbook and Guide to Prevent and Reverse Insulin Resistance, Lose Weight, and Fight Chronic Disease

• Peter Brukner

  • A Fat Lot of Good

• Jayne Buxton

  • The Great Plant-Based Con

• Judy Cho

  • Carnivore Cure

• Judy Cho & Laura Spath

  • The Complete Carnivore Diet for Beginners: Your Practical Guide to an All-Meat Lifestyle

• David Ellis, Alison Morgan & Anita Tagore

  • Why Vegans Have Smaller Brains: And How Cows Reverse Climate Change

• Jason Fung

  • The Diabetes Code

• John E. Hall & Michael E. Hall

  • Guyton and Hall Textbook of Medical Physiology, 15th ed.

• Malcolm Kendrick

  • The Clot Thickens

• Martha Clare Morris

  • Diet for the MIND: The Latest Science on What to Eat to Prevent Alzheimer’s and Cognitive Decline

• Tim Noakes & Marika Sboros

  • Lore of Nutrition
  • Real Food on Trial

• Tim Noakes, Jonno Proudfoot, Sally-Ann Creed & David Grier

  • The Real Meal Revolution

• Tim Noakes with Michael Vlismas

  • Challenging Beliefs: Memoirs of a Career

• Tim Noakes, Tamzyn Murphy, Neville Wellington, Hassina Kajee, Jayne Bullen, Sarah Rice & Candice Egnos (eds.)

  • Ketogenic: The Science of Therapeutic Carbohydrate Restriction in Human Health

• Christopher M. Palmer

  • Brain Energy: A Revolutionary Breakthrough in Understanding Mental Health—and Improving Treatment for Anxiety, Depression, OCD, PTSD, and More

• Weston A. Price

  • Nutrition and Physical Degeneration

• Thomas N. Seyfried

  • Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer

• Gary Taubes

  • Good Calories, Bad Calories
  • The Case for Keto
  • Rethinking Diabetes
  • Why We Get Fat
  • The Case Against Sugar

• Nina Teicholz

  • The Big Fat Surprise

:::

::: spoiler Neuroscience, psychology & philosophy of science

• Dave Grossman

  • On Killing: The Psychological Cost of Learning to Kill in War and Society

• Matt Johnson & Prince Ghuman

  • Blindsight: The (Mostly) Hidden Ways Marketing Reshapes Our Brains

• Thomas S. Kuhn

  • The Structure of Scientific Revolutions

• Iain McGilchrist

  • The Master and His Emissary
  • The Matter with Things, Volume I: The Ways to Truth
  • The Matter with Things, Volume II: What Then Is True?

• Gerald H. Pollack

  • The Fourth Phase of Water: Beyond Solid, Liquid, and Vapor

• Tommy Wood

  • The Stimulated Mind: Future-Proof Your Brain from Dementia and Stay Sharp at Any Age

:::

Dr. Anthony Jay talks about the carnivore diet, fat, cholesterol, and heart disease.

Anthony G. Jay, PhD, is a biochemist with a doctorate from Boston University School of Medicine, research experience at Boston University and Mayo Clinic, and publications spanning lipid metabolism, CD36, oxidized LDL, Alzheimer’s disease, and orthopedic research. The discussion covers carnivore dieting, LDL and statins, CAC versus CCTA imaging, insulin resistance, seed oils, and endocrine-disrupting chemicals. His central case is that insulin resistance and metabolic health are more informative for cardiovascular risk than LDL alone, while questioning conventional interpretations of statins and coronary-plaque imaging.

::: spoiler generated summary

Carnivore background and Mayo conflict

• A vegan attempt 10–15 years earlier felt terrible, while personal gut problems and a daughter's dairy/gluten sensitivities undermined conventional dietary advice. Paul Saladino, Shawn Baker, and feeling better with more meat moved the diet further toward carnivore.
• Boston University medical training promoted vegan-style eating, low cholesterol, and fiber, and around 1999 a book implying a vegan diet could help cure a father's cancer was passed along. That advice is bad training and propaganda.
• Heart-disease research at Boston University included plaque work around autopsies, followed later by Mayo Clinic research.
• At Mayo, a strict-carnivore telomere study was planned after a study was interpreted as fresh red meat improving telomeres while processed meat did the opposite.[1] Shawn Baker helped publicize the idea, while Mayo HR objected to the carnivore project and to a Twitter post attacking a Mayo "Eat more whole grains" poster and warned that the institution was being tarnished.
• During COVID, Mayo was left after vaccine requirements. Broad masking was also opposed, with free N95s favored for high-risk elderly people while lower-risk people built herd immunity.

Statins, CAC, and CCTA

• Standard-of-care medicine and lawsuit risk push doctors toward statins: failure to recommend them after a high cholesterol result can expose a doctor to litigation if a later heart attack occurs.
• Statins increase calcified plaque, including by more than 10% per year in the cited studies, and re-evaluation of older statin data also found increased coronary calcification.[2] The mechanism is inhibition of cholesterol synthesis along with CoQ10 and vitamin K2 production; K2 normally helps keep calcium out of arteries.
• Coronary artery calcium (CAC) scans are cheap, direct, and repeatable; a personal CAC score was zero despite supposedly high cholesterol. Repeated CAC scans give essentially the same result, while CCTA plaque readings have major scan and reader variability.
• Dave Feldman's KETO CCTA study used AI-based angiography analysis, but the imaging company knew which scans belonged to the keto group and which belonged to controls before analysis, so the AI result is not inherently unbiased.[3]
• Human repeat CCTA work has about ±18.4% interscan variability on newer machines and up to roughly 30% on different or older scanners.[4] Another study using three expert CCTA readers found very poor agreement, around 0.23, or 2.3 out of 10.[5]
• A PLOS ONE study found a strong association between longer statin use and severe coronary calcification; more than 10 years of use corresponds to about a 358% higher risk.[6]
• Relative-risk advertising can make small absolute effects look large. The same relative-risk language is used for statin-associated calcification that drug companies use for statin benefits and COVID-vaccine efficacy, and the explanation that statins merely convert dangerous soft plaque into harmless hard plaque fails because the supporting CCTA evidence is unreliable.

Cholesterol and insulin resistance

• The same institutional resistance seen with the carnivore study occurs when cardiologists and lipidologists attack carnivore because it raises cholesterol. The system makes lower cholesterol synonymous with good and higher cholesterol synonymous with bad without requiring heart-attack or plaque endpoints.
• Smoking, binge drinking, inactivity, stress, trans fats, high iron, dehydration, and sleep deprivation can all raise LDL while harming health, so older population studies can confound LDL with the behaviors producing it. Pharma, guideline pressure, and medical-association funding reinforce the cholesterol model.
• Carbohydrates drive insulin resistance, while carnivore or very-low-carbohydrate eating can drive insulin very low. If glucose stays high on carnivore, more dietary fat can help; exercise also increases glucose uptake independently of insulin. The three foundations for reversing insulin resistance are very-low-carb/carnivore eating with enough fat, exercise, and fasting.
• A newly diagnosed type 2 diabetic with an A1c of 13% can be put on metformin and insulin, then sent to a dietitian whose first lesson is how to keep eating cake while dosing insulin. The diagnosis is the moment for a major lifestyle change, not accommodation of the old diet.
• The surrounding food environment makes that change harder, but travel and convenience do not require returning to high-carbohydrate food; meat-centered options can be carried or ordered.

Fuel use and plaque reversal

• High cholesterol is contextual. On a low-carbohydrate, high-fat diet, LDL values around 280 or even 380 are not automatically high-risk if triglycerides and the metabolic context are good. LDL is a transporter carrying energy-related cargo, not intrinsically a toxin.
• Mike McKnight's 118-mile/189-km event in 24 hours with zero calories after years of low-carb eating is an example of deep fat adaptation and why calorie-centric assumptions about endurance can fail.
• The heart preferentially burns fatty acids, with the figure put near 95% even in people who eat substantial carbohydrate. Decades of high-carbohydrate eating can make the heart poor at burning fat, then insulin resistance limits glucose use, leaving a "starving heart" that scavenges fatty fuels and contributes to plaque. Carnosine and carnitine are additional fuels, and vegans are low in carnosine.
• In a study of 28,024 women, early-onset coronary risk is linked most strongly to lipoprotein insulin resistance at a hazard ratio around 6.4, hypertension about 2.2, triglycerides about 2.1, and LDL about 1.38.[7] That gap makes insulin resistance the central cardiovascular risk signal.
• ApoB and Lp(a) associations in other studies are usually around 1.6–1.8, still far below 6.4 for insulin resistance.
• Patrick Theut and Dr. Ford Brewer are public examples of lowering CAC after going very low-carb/keto. A private Florida client had CAC fall from about 400 to zero within a year and remain zero on repeat scanning. Because plaque contains lipid, teaching cells to burn fat is the biological route to reversing it; changes can begin in roughly six weeks, while full fat adaptation can take years.

CAC tiers, microplastics, and lipid markers

• CAC severity bands are zero plaque for tier 1; roughly 300–1000 for tier 2, which deserves serious reversal work; and above 1000 for tier 3, where exercise and hypertension require more caution because intense effort could dislodge plaque. Stress itself worsens insulin resistance and plaque risk.
• A microplastics study found plastic particles inside carotid plaque and a large increase in cardiovascular events, with 353% higher heart attacks in people with microplastics in their arteries.[8] This links plaque instability with earlier work on plastics and hormones.
• LDL is not cholesterol itself. Cholesterol is valuable material for steroid hormones and the brain, and the brain is rich in cholesterol and DHA; calling LDL "bad cholesterol" obscures that distinction.
• Ancel Keys helped entrench the cholesterol story. The Seven Countries Study[9] cherry-picked seven countries from a larger set of 22, and the CDC later canonized Keys.
• Thomas Dayspring calling Lp(a) a genetic disorder fits the same pattern: a normal molecule becomes a disease target as new Lp(a)-lowering drugs arrive, after the narrative moves from total cholesterol to LDL, ApoB, particle measures, and Lp(a).
• Recovered Minnesota Coronary Experiment data compared a linoleic-acid/seed-oil diet with a saturated-fat control in a double-blind trial; the reanalysis shows worse heart-disease outcomes in the seed-oil group despite cholesterol lowering.[10]

Medical institutions and endocrine disruptors

• Brown and Goldstein were held up as heroes in medical training for familial hypercholesterolemia and statins. FH moved from an extremely rare disorder to about 1 in 250 as definitions and LDL-receptor variants expanded, allowing a rare-disease model to be generalized to much of the population.
• Doctors often believe they are saving lives because training, licensing, guidelines, and professional associations all reinforce the same model. That institutional behavior is a cult or religion, not open science.
• Earlier plastics and hormone work grew out of laboratory experience, including the Robert Ferrante cyanide-murder case across the hall and the contrast between easy access to toxic chemicals and heavy restrictions on tiny amounts of testosterone for research.
• BPA, parabens, phthalates, atrazine, fragrances, and related chemicals can mimic estrogen, with aggregate exposure linked to low testosterone, male feminization, depression, and other hormone problems. That plastics work later fed into the microplastics concern in the heart-disease book.

Insulin resistance, seed oils, and soy

• Gil Carvalho's advice favoring oats, soy, canola oil, more fiber, and statins, and Muhammad Alo's statement that insulin resistance affects under 10% of people, embody the dietary and cardiology consensus. That consensus is wrong.
• An NHANES analysis found insulin resistance in roughly 44% of U.S. adults under about age 40 by the cited medical criteria.[11] Another national cardiometabolic-health study used by Ben Azadi puts metabolic dysfunction closer to 93%.[12] Either way, carbohydrate-heavy advice is inappropriate for a population with widespread insulin resistance.
• Fat cells turn over slowly: bomb-pulse carbon-14 work puts average adipocyte age near 10 years.[13] A six-week seed-oil intervention cannot erase years of stored fatty acids or adequately test long-latency cardiovascular outcomes.
• Modern seed-oil studies rarely measure heart attacks, strokes, or plaque over the decades needed. Omega-6 fats are highly oxidizable without the resolvin/protectin pathway associated with omega-3s, so saturated fat is better than high omega-6 intake.
• Soy is estrogenic through isoflavones such as genistein and daidzein. Short U.S. soy trials can show little difference because background endocrine-disruptor exposure is already high, while a European randomized crossover study in men found six weeks of soy-flour supplementation lowered serum testosterone.[14] Soy therefore adds another estrogenic exposure.

References

1. [03:20] Processed Meat, but Not Unprocessed Red Meat, Is Inversely Associated with Leukocyte Telomere Length in the Strong Heart Family Study — https://doi.org/10.3945/jn.116.234922
2. [07:31] High dose and long-term statin therapy accelerate coronary artery calcification — https://doi.org/10.1016/j.ijcard.2015.02.072
3. [11:44] Carbohydrate Restriction-Induced Elevations in LDL-Cholesterol and Atherosclerosis: The KETO Trial — https://doi.org/10.1016/j.jacadv.2024.101109
4. [13:17] Coronary CT Angiography: Variability of CT Scanners and Readers in Measurement of Plaque Volume — https://doi.org/10.1148/radiol.2016161670
5. [14:15] Interobserver variability among expert readers quantifying plaque volume and plaque characteristics on coronary CT angiography: a CLARIFY trial sub-study — https://doi.org/10.1016/j.clinimag.2022.08.005
6. [16:53] Long-term statin therapy is associated with severe coronary artery calcification — https://doi.org/10.1371/journal.pone.0289111
7. [34:13] Association of Lipid, Inflammatory, and Metabolic Biomarkers With Age at Onset for Incident Coronary Heart Disease in Women — https://doi.org/10.1001/jamacardio.2020.7073
8. [43:05] Microplastics and Nanoplastics in Atheromas and Cardiovascular Events — https://doi.org/10.1056/NEJMoa2309822
9. [45:51] Seven Countries Study — https://www.sevencountriesstudy.com/about-the-study/
10. [47:21] Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73) — https://doi.org/10.1136/bmj.i1246
11. [58:10] Insulin Resistance and Cardiometabolic Risk Profile Among Nondiabetic American Young Adults: Insights From NHANES — https://doi.org/10.1210/clinem/dgab645
12. [58:39] Trends and Disparities in Cardiometabolic Health Among U.S. Adults, 1999-2018 — https://doi.org/10.1016/j.jacc.2022.04.046
13. [59:26] Dynamics of fat cell turnover in humans — https://doi.org/10.1038/nature06902
14. [62:25] Dietary supplements of soya flour lower serum testosterone concentrations and improve markers of oxidative stress in men — https://doi.org/10.1038/sj.ejcn.1601495 :::

Ketogenic and low-carbohydrate diets often focus on a specific carbohydrate target: keep your net carbs under 30 grams. But as registered dietitian and certified diabetes educator Franziska Spritzler demonstrates in this presentation from Metabolic Health Summit, a carbohydrate target is not a therapy. Effective implementation means a full assessment of medical history, medications, labs, food preferences, lifestyle, and the motivation that will carry a patient through year one and beyond.

Spritzler specializes in low-carbohydrate and ketogenic nutrition and has extensive experience helping people use these approaches to improve metabolic health. she walks through the practical decisions clinicians face: when a ketogenic diet is warranted versus a more flexible low-carbohydrate approach, why she recommends 1.2 to 1.8 grams of protein per kilogram rather than the RDA's 0.8, how to manage medication adjustments for patients at risk of hypoglycemia or hypotension, and how to handle electrolytes, carbohydrate counting, sweeteners, and plant-based variations without losing the patient along the way.

Questions Answered in This Episode:

• What actually separates a ketogenic diet from a low-carbohydrate diet, and when does the difference matter? • Why is the protein RDA too low for long-term metabolic health, and what range does Spritzler recommend instead? • Who should avoid ketogenic diets entirely, and why are most contraindications manageable with closer supervision? • How should medications be monitored and adjusted when a patient begins carbohydrate restriction? • Should patients count net carbs or total carbs, and why are packaged "net carb" labels unreliable? • Can a ketogenic diet be done as a vegetarian or vegan?

A practice-tested blueprint for turning carbohydrate restriction from a prescription into a therapy patients can sustain.

::: spoiler generated summary

Defining ketogenic and low-carbohydrate therapy

• A ketogenic diet is high in fat, moderate in protein, and very low in carbohydrate, with the purpose of reaching nutritional ketosis beginning at about 0.5 mmol/L beta-hydroxybutyrate; for most people this means less than about 30 g net carbohydrate per day.
• Net carbohydrate here means total carbohydrate minus fiber naturally occurring in foods. A ketogenic diet can include meat, fish, eggs, cheese, non-starchy vegetables, smaller amounts of berries, nuts and seeds, and minimally processed fats and oils.
• A low-carbohydrate diet is more flexible in fat and protein and generally provides about 30-100 g net carbohydrate per day, with beta-hydroxybutyrate below 0.5 mmol/L. It can include everything in a ketogenic diet plus more starchy vegetables, medium-sugar fruits, beans, legumes, and sometimes grains, but it may not be as effective for some conditions.

Assessment before changing the diet

• A full assessment before dietary intervention includes current and past medical problems, family history, medications and supplements, diet and weight history, previous keto or low-carb experience, food preferences, allergies or sensitivities, and a three-day food record.
• The assessment also includes lifestyle factors such as eating out, travel, cooking, physical activity, family and social support, short- and long-term goals, and especially the underlying "why" that can maintain commitment when motivation falls.
• Baseline labs usually include a comprehensive metabolic panel, complete blood count, HbA1c, standard lipid panel, sometimes advanced lipoprotein markers, vitamin D, and fasting insulin for most people who are not taking insulin.

Protein and carbohydrate targets

• The protein RDA of 0.8 g/kg/day may prevent outright deficiency, but it is not enough for optimal long-term metabolic health. Plant and animal protein are not equivalent in essential-amino-acid content and bioavailability, so more plant protein is needed to reach the same protein quality.
• Protein needs become more important with aging because muscle becomes less efficient at incorporating essential amino acids, and inadequate protein during weight loss or low activity can increase lean-mass loss. Preserving muscle supports metabolic health, strength, function, and quality of life.
• A practical protein range is 1.2-1.8 g/kg of actual or ideal body weight, especially using ideal weight when BMI is over 30, with about 1.5 g/kg often in the middle of the useful range. For a 145-pound or 66-kg target weight, that is roughly 79-119 g protein per day, with about 100 g in the middle.
• The carbohydrate RDA of 130 g/day is based on the brain's glucose requirement under conditions where the brain runs exclusively on glucose. The brain can use ketones for part of its energy, and the liver can make the glucose still needed by the brain and other tissues even when dietary carbohydrate is very low.
• A low-carbohydrate diet up to about 100 g/day can improve weight, blood sugar, blood pressure, and other metabolic outcomes. For epilepsy, Parkinson's disease, certain cancers, some mental-health disorders, and some insulin-resistant conditions, a ketogenic or very-low-carbohydrate level may be more useful or necessary.
• There are no head-to-head trials of 20 g versus 60 g carbohydrate, while clinical experience, patient experience, and the larger body of variable-carbohydrate research support lower carbohydrate intake as more effective for reversing type 2 diabetes, prediabetes, and other insulin-resistant conditions.

Nutritional ketosis and keto-adaptation

• Phinney and Volek defined nutritional ketosis as beta-hydroxybutyrate beginning around 0.5 mmol/L and reaching about 3 mmol/L, sometimes higher after exercise. The useful level is individual: some people have appetite, craving, mental, or physical benefits at the low end, while others need 1-2 mmol/L or higher.
• Ketosis can begin within a few days, but keto-adaptation is slower. Full adaptation to using ketones and fatty acids as major fuel sources can take several months or longer.

Contraindications and starting the diet

• Most people can safely follow a ketogenic diet, but people with inborn errors of fatty-acid metabolism cannot, and acute intermittent porphyria in genetically susceptible adults can be triggered by very-low-carbohydrate intake because it interferes with heme synthesis.
• Many other potential contraindications can still be managed with dietary adjustment, closer clinical supervision, medication titration, and coordination with specialists.
• Anorexia nervosa was traditionally viewed as a contraindication, but a pilot study combining a ketogenic diet with ketamine under psychiatric supervision found improvements in women's relationship with body image and food; more research is needed before routine implementation. [1]
• The person and clinician work as a team because this is the person's journey. Some people want to enter ketosis rapidly, while someone coming from a very high-carbohydrate, processed-food diet may do better reducing carbohydrate gradually to limit keto-flu symptoms.
• Low-carb and ketogenic diets can be sustained for years, with long-term use allowing for bumps, life changes, and periods when the diet needs adjustment without being abandoned.

Type 2 diabetes

• Type 2 diabetes involves hyperinsulinemia, insulin resistance, elevated glucose and fatty acids, and progressive beta-cell dysfunction. Diabetes can be diagnosed with HbA1c at least 6.5%, fasting glucose at least 126 mg/dL, or random glucose at least 200 mg/dL with symptoms; prediabetes includes HbA1c 5.7-6.4% or fasting glucose 100-125 mg/dL.
• There is substantial evidence for ketogenic and low-carbohydrate diets in type 2 diabetes. Recent randomized-trial meta-analysis shows a dose-response in which lower carbohydrate intake produces greater improvements in glycemic control and weight. [2]
• Virta Health's two-year study had 74% retention at that point, more than half of participants had reversed their type 2 diabetes, and about three-quarters of the ketogenic group had lost at least 5% of body weight. [3]
• For someone seeking reversal of type 2 diabetes, a very-low-carbohydrate intake around 20-30 g/day is recommended. Anyone taking glucose-lowering or blood-pressure medication that can produce hypoglycemia or hypotension needs home monitoring and prompt medication adjustment with the prescribing clinician; routine labs are typically repeated every three to six months.
• The 2015 case was a man in his late 50s who thought he had prediabetes and hypertension, but his HbA1c was 6.7%, his fasting glucose was above 120 mg/dL, and triglycerides were elevated. He was taking an antihypertensive plus diuretic, had started low carb on his own, wanted to lose about 20 pounds, and was tired with muscle cramps.
• His carbohydrate stayed below 30 g/day, protein was aimed at the moderate-to-high end of the range, and fat was used to satiety without a fixed fat target. Because his medication retained potassium and he was also restricting salt, potassium-heavy salt products were avoided, modest sodium was used, blood pressure was monitored closely, and magnesium glycinate was added for cramps.
• By February 2016 his HbA1c had fallen to 5.7%, triglycerides were normal, muscle cramps were gone, he had lost 20 pounds, hunger was low, and he felt mentally stronger and calmer while enjoying the diet.
• His HbA1c stayed about 5.6-5.8% through December 2019, then later rose into roughly the 6.0-6.7% range after major family stress, job loss, and a less strict low-carb diet with more snacking, dark chocolate, and extra carbohydrate. He kept the 20-pound weight loss and became motivated to tighten the diet again before starting metformin.

Type 1 diabetes

• Type 1 diabetes is an autoimmune disease that destroys pancreatic beta cells, and people with type 1 diabetes still require insulin regardless of diet unless a cure becomes available. Diagnostic glucose criteria are the same as type 2 diabetes, with pancreatic autoantibodies helping identify type 1 disease.
• The research base is smaller because type 1 diabetes is much less common, but the higher-quality research supports carbohydrate reduction for better glycemic control and other improvements, including weight loss when needed.
• The TypeOneGrit survey of roughly 300 adults and children following Dr. Richard Bernstein's very-low-carbohydrate approach at about 30 g/day found an average HbA1c just under 5.7% and a glucose standard deviation around 28 mg/dL, with very narrow glucose variability in this community. [4]
• Fewer carbohydrates make insulin dosing more predictable. If a bowl of rice estimated at 45 g carbohydrate is wrong by 20%, the insulin mismatch can be large; if cauliflower rice contains about 5 g carbohydrate, the same percentage error is only about 1 g and is much less likely to change the insulin dose.
• People eating fewer carbohydrates use less mealtime insulin and may also need less basal insulin. Clinician support is important for insulin adjustment, although many people with type 1 diabetes have had to learn to adjust doses themselves because their clinicians do not support very-low-carbohydrate diets.
• Home monitoring means frequent glucose checks, especially when the diet is changing, CGM to see trends and head off highs or lows, ketone monitoring when using ketogenic therapy, and the same routine laboratory follow-up as type 2 diabetes except fasting insulin.
• The 2014 case was a man in his mid-40s who had recently started insulin and a ketogenic diet after a type 1 diabetes diagnosis. His HbA1c fell from 12.5% to 5.5%, his home glucose was mostly in the 80s to low 100s, and he needed only very small basal insulin doses during the honeymoon phase.
• The honeymoon can last up to about a year in many people, and case studies indicate that very-low-carbohydrate diets may prolong it. This client tracked food, macronutrients, insulin, and glucose in detail; his successful diet remained unchanged, glucose and ketones were monitored closely, and he carried rapid-acting glucose for hypoglycemia even on tiny basal doses.
• His LDL-C later rose from 137 to 224 mg/dL and ApoB reached 150 mg/dL, a pattern now recognized as classic lean-mass hyper-responder physiology. Because he wanted to stay ketogenic without a statin, keto-compatible fiber from avocado, berries, nuts, and seeds was increased and some butter and cream were reduced, followed by periodic lab checks.
• About seven years later he was still doing well, eating somewhat more carbohydrate because he is very active and finds it easier to sustain, using small bolus doses after a honeymoon that lasted about two years, and rotating similar meals to make insulin responses predictable. His LDL-C and ApoB remained somewhat high but acceptable to him and his doctor, and his CGM time in range was about 98%.

Polycystic ovary syndrome

• PCOS is an endocrine disorder in reproductive-age women involving genes, chronic low-grade inflammation, androgen excess, impaired reproductive-hormone balance, and in most women hyperinsulinemia and insulin resistance. Effects can include excess facial or body hair, scalp hair loss, deeper voice, acne, ovulatory dysfunction, irregular periods, infertility, and often central obesity.
• PCOS is commonly managed with metformin for insulin sensitivity, spironolactone for androgen effects, and birth-control pills for menstrual regulation. Diagnosis requires two of three findings after other disorders are excluded: clinical or biochemical hyperandrogenism, ovulatory dysfunction, or polycystic ovaries on ultrasound.
• Women with PCOS often have higher testosterone and luteinizing hormone and lower progesterone and sex-hormone-binding globulin. The keto and low-carb studies are small, but meta-analyses of randomized trials support improvements in weight and hormonal balance, including insulin.
• A study followed 12 women with PCOS and overweight or obesity after none became pregnant in an IVF cycle. They then used a ketogenic diet for about 14 weeks before another IVF cycle, after which two-thirds became pregnant and carried to term and all improved their weight and hormonal balance. [5]
• Either ketogenic or low carbohydrate can be used, and the transition can be fast or slow. Monitoring focuses on symptoms such as ovulation, hunger, energy, and mental well-being, with metabolic and reproductive labs repeated about every three to six months.
• The 2015 case was a 33-year-old woman with lean PCOS, years of irregular periods and infertility, a prior successful IVF pregnancy, and a recent failed second IVF cycle. She was taking 500 mg metformin daily, eating a very high-carbohydrate diet with frequent sweets, sometimes eating frozen yogurt for dinner, and wanted to conceive naturally without more IVF.
• The plan started slowly below 100 g carbohydrate per day, kept protein up, allowed fat to appetite, included both starchy and non-starchy vegetables, encouraged fatty fish and some red meat, kept healthy snacks available, and minimized sweets; she also changed her sweetened coffee creamer.
• Her period returned by April, she conceived naturally by June, and she carried a healthy baby to term while continuing the diet. Lower carbohydrate or ketosis may be needed by some women with PCOS, but under 100 g/day was enough for her.

Practical resources and ketone monitoring

• Individualized recommendations can be paired with simple resources for what a healthy plate looks like, the best protein, fat, and carbohydrate sources, how to use leftovers, and how to eat out.
• Food tracking is especially useful at the beginning because people often underestimate or overestimate carbohydrate, protein, and fat. Cronometer can also track micronutrients, while KetoDiet and Carb Manager are other low-carb-focused options; long-term tracking is optional unless the person finds it useful.
• Ketone monitoring can confirm ketosis and help identify the beta-hydroxybutyrate level at which a person feels best. Blood beta-hydroxybutyrate is the gold-standard method; breath meters and urine strips are other options but have weaker evidence behind them.

Electrolytes and keto-flu symptoms

• When insulin falls on a ketogenic diet, people lose fluid and electrolytes, which can contribute to dizziness, fatigue, muscle cramps, and the general keto-flu feeling. Hydration and mineral intake continue to matter after the initial transition.
• Roughly 3-7 g sodium per day from food plus added sodium or salty foods is used when appropriate. Congestive heart failure, uncontrolled hypertension, and chronic kidney disease require individualized sodium guidance from the medical provider.
• Potassium is widely available in keto-friendly animal and plant foods such as meat, fatty fish, greens, avocado, nuts, and seeds, so many people can meet their needs from food.
• Magnesium is harder to obtain in large amounts from food; the target is roughly 320-400 mg/day, with supplementation such as magnesium glycinate or Slow-Mag when needed.

Net carbohydrate and packaged keto foods

• The classic ketogenic definition of net carbohydrate is total carbohydrate minus fiber naturally occurring in food, because that fiber is not digested and absorbed into the bloodstream in the same way as digestible carbohydrate.
• Packaged keto products often subtract added processed fibers and sugar alcohols from total carbohydrate, but some of these ingredients can be partly digested, absorbed, and raise blood glucose. An avocado's natural fiber subtraction is not equivalent to assuming every added fiber or sugar alcohol in a packaged bar has no glycemic effect.
• Whole foods are the main focus, with naturally occurring fiber subtracted. For processed foods with added fiber and sugar alcohols, at least half of those carbohydrates are generally counted, with erythritol as an exception.
• Newer fiber formulations may behave differently, and some people do not see a glucose rise, but anyone who needs a very strict ketogenic therapy should test their own glucose because individual responses can differ.

Sweeteners

• Sweetener use depends on the person and the sweetener. The listed sweeteners generally have minimal effects on blood glucose, insulin, and by extension ketones in studies, but results vary across studies and individuals.
• Allulose is a preferred sweetener because many randomized trials have found increased incretin hormones and lower glucose, including in type 2 diabetes, but a randomized controlled trial in people with type 2 diabetes did not find those glucose or incretin benefits. [6]
• Research on sweeteners and the gut microbiome is mixed: some studies find adverse microbiome or glucose-regulation effects and other randomized trials do not find that relationship.
• Some people do best avoiding some or all sweeteners because they trigger cravings, hunger, or other side effects. Others can use small amounts regularly without problems, and that flexibility may help sustain nutritional ketosis.

Vegetarian and vegan ketogenic diets

• A vegetarian or vegan ketogenic diet is possible, but it is harder than an omnivorous ketogenic diet because adequate protein has to be reached while carbohydrate remains low. Lacto-ovo vegetarian keto is easier because eggs and cheese provide protein without much carbohydrate, whereas whole plant protein sources also bring digestible carbohydrate.
• A vegan ketogenic diet may require more coconut oil or MCT oil to maintain ketosis, and micronutrient supplementation is essential on a fully plant-based diet. With careful planning, both vegetarian and vegan ketogenic meal patterns can be constructed.

Empowerment and long-term self-efficacy

• The final goal is not only teaching someone how to follow the diet but helping them feel capable of doing it after the clinical work ends. People need different levels of reassurance, accountability, contact, and independence, so support should match the person.
• The client or patient has to remain an active participant because they will make the long-term decisions about food and how to handle real-life situations. Guidance remains available without making the person dependent on the clinician.
• Motivation is usually high at the beginning when hunger falls, glucose improves, and weight is coming down, but enthusiasm can fade. Returning to the original "why" reconnects the diet to the health outcome that mattered enough to begin.
• Perfect glucose or a perfectly predictable rate of weight loss are unrealistic expectations. The useful focus is on controllable actions: food and beverage choices, movement, stress management, mindset, and attitude.
• Everyone slips sometimes. Failures become learning opportunities by reviewing what happened as a team and building a strategy for the next time a similar situation occurs.

References

1. [18:23] Ketogenic diet and ketamine infusion treatment to target chronic persistent eating disorder psychopathology in anorexia nervosa: a pilot study — https://doi.org/10.1007/s40519-022-01455-x
2. [21:05] Dose-dependent effect of carbohydrate restriction for type 2 diabetes management: a systematic review and dose-response meta-analysis of randomized controlled trials — https://doi.org/10.1093/ajcn/nqac066
3. [21:16] Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-randomized Clinical Trial — https://doi.org/10.3389/fendo.2019.00348
4. [27:50] Management of Type 1 Diabetes With a Very Low-Carbohydrate Diet — https://doi.org/10.1542/peds.2017-3349
5. [38:45] Adding a ketogenic dietary intervention to IVF treatment in patients with polycystic ovary syndrome improves implantation and pregnancy — https://doi.org/10.1016/j.reprotox.2023.108420
6. [49:04] Short-term effects of allulose consumption on glucose homeostasis, metabolic parameters, incretin levels, and inflammatory markers in patients with type 2 diabetes: a double-blind, randomized, controlled crossover clinical trial — https://doi.org/10.1007/s00394-023-03205-w :::

No cream was harmed in the production of this ice.... cream....

::: spoiler generated summary

Why I Tried It

• I'm doing a dairy-free August challenge. Coconut milk and nut milk do a number on my gut, but I still want carnivore or protein ice cream.
• Joanne told me she makes ice cream with protein powder and water. I expected it to fail, but trying it left me speechless when it worked.

Ingredients

• I use Equip beef-isolate protein powder because whey protein is dairy. Other beef-isolate protein powders can be used.
• I add one scoop of collagen powder. Plain unflavored collagen also works, and water is the only other required ingredient.
• Extra fat is optional for more mouthfeel. Melted butter or egg yolks are carnivore options; MCT oil or olive oil can also work.
• Two scoops of protein powder give the whole pint 40 g of protein, and I normally eat half a pint.

How I Make It

• Start with about an inch of water, whisk in two scoops of protein powder and one scoop of collagen, immersion-blend until smooth, fill with water to the line, and freeze for 24 hours.
• I don't think this will work in a regular ice-cream maker. The Ninja Creami's very fast shaving action is what turns the frozen mixture creamy.
• For ice creams without added sugar, use the light ice cream setting. A spin takes about four minutes.

Texture and Result

• A first spin can come out powdery and need a re-spin. I've added a tablespoon of MCT oil before a re-spin; a little water might also smooth it out, although I haven't tried that.
• This chocolate batch came out perfectly on the first spin. It was unbelievably silky, smooth, and creamy with only water, protein powder, and collagen.

References None. :::

but he did manage to make a realistic face eventually

I asked on X what the weirdest thing a carnivore diet helped you with was, and the responses were incredible.

From stubborn skin issues to autoimmune symptoms and other surprising improvements, here are some of the weirdest things carnivore has helped people with and why.

::: spoiler generated summary

Overview

• Thousands of people were asked about unexpected bodily changes after going carnivore, with answers ranging from humorous minor changes to improvements that raise questions about what people accept as normal.
• The recurring pattern is that many day-to-day problems can change substantially with diet, including secretions, pain, skin, dental health, and digestion.

Bodily secretions

• Many people have less earwax buildup, less eye gunk, and less body odor after going carnivore.
• The exact reason diet changes earwax or these other secretions is uncertain, while having less of them is generally a positive change.

Pain

• A lot of people have less overall pain, including less joint pain, nerve pain, neuropathy, musculoskeletal pain, and tendon pain.
• Achy joints at age 50 or 60 may not simply be normal aging; diet may play a major role, and scientific literature supports dietary effects here, particularly around hypoglycemia.

Skin

• Itching, dry skin, psoriasis, eczema, dandruff, acne, and general rashes often improve substantially on carnivore.
• What enters the gut can show up through the skin, and skin problems are clearly connected in many cases with gut function or gut dysfunction.

Dental health

• Teeth are built to last a lifetime, so widespread cavities, gum disease, tooth loss, bridges, implants, and partials point to a diet humans are not suited for.
• Carnivore commonly improves gum and dental health, including less gum swelling and tooth sensitivity, and some people have tooth remineralization; dental health became very solid on keto and then carnivore.

Digestion

• Digestive health is one of the biggest improvements: reflux, IBS, bloating, gas, and hiccups can diminish, and many people essentially stop farting.
• Hiccups can disappear; gut distension from high-fiber foods or sugary foods may contribute to hiccups, although the exact cause is hard to know.
• Digestion should be silent, painless, comfortable, and smooth. Persistent pain, discomfort, bloating, gas, and foul smells are signs that digestion is not working as it should.

:::

Many people think a carnivore diet is only possible if you're buying grass-finished ribeyes, premium bacon, and expensive specialty foods. That's simply not true.

If you're on a tight budget, you can still build a nutrient-dense carnivore diet with everyday foods like eggs, ground beef, chicken, pork, organ meats, canned seafood, butter, and even a few inexpensive processed meats when necessary. It isn't about perfection. It's about making better choices with the budget you have.

Remember to always ask yourself: Compared to what?

::: spoiler generated summary

Core budget approach

• The goal is the best health people can afford through the best-quality meat they can afford, not premium grass-finished ribeye.
• A carnivore diet can still work with very little beef when money is tight, and cheap animal foods are far better than the boxed junk foods they displace.
• Larger packs, discount supermarkets, basic home cutting and preparation, and judging every food by "compared to what?" reduce costs.

Lowest-cost staples

• Ground beef is the best option when affordable; the store example is $8.97 per pound, and larger five- or ten-pound packs reduce the unit price.
• Bone-in, skin-on chicken thighs cost $1.17 per pound, while a ten-pound bag of leg quarters costs $7.84; the bones can also make broth.
• Sixty ordinary eggs cost $7.13, about 12 cents each, and premium omega-3 or darker-yolk marketing makes only a slight practical difference.
• Family packs of pork chops cost $3.38 per pound, while pork shoulder steaks cost $1.95 and provide a steak-like daily meal at a small fraction of ribeye prices.

Organ meats and collagen-rich foods

• Chicken liver costs about $1.50-$1.60 per pound and is a superfood supplying concentrated vitamins and minerals.
• Chicken gizzards cost $1.36 for 20 ounces and supply abundant protein and collagen, while chicken skin supplies excellent collagen building blocks.
• Preparations that make liver and gizzards enjoyable keep taste and texture from excluding them.

Processed budget meats

• Five-pound bologna costs $1.93 per pound, 24 hot dogs cost $4.46, and store-brand luncheon meat costs $1.84 per can; these foods are mostly meat even though their ingredients are not perfect.
• These foods can fill the remaining appetite when eggs and liver provide the vitamins and minerals, and they are better choices than cereal and boxed snack foods.
• Luncheon meat does not cause cancer and is not bad food; it is simply less good than expensive grass-finished ribeye.
• Food quality is relative: an item can be inferior to premium beef while still functioning as health food compared with ultra-processed carbohydrate foods.

Canned fish and added fat

• Canned fish is the main useful food in the center aisles, and inexpensive cans priced around 19 cents per ounce are often placed below eye level.
• Tuna or other fish packed in water avoids cheap packaged olive oil that is likely adulterated with soybean or canola oil.
• Drained fish with mustard gains missing fat from egg yolks, saved pork grease, butter, or lard.
• Hydrogenated lard is not equivalent to hydrogenated vegetable oil and remains a suitable cooking fat at about 14 cents per ounce.

Butter, snacks, and products to avoid

• Plain store-brand butter at about 39 cents per ounce is preferable to premium butter at roughly 58-60 cents, because the nutritional difference is very small.
• Spreads combining butter with canola oil, margarine, vegetable-seed-oil products sold as plant butter, and other imitation butter products are avoided.
• Pork rinds cost about 73 cents per ounce and can add occasional crunch to tuna or other meals while staying within carnivore eating.
• Protein chips and protein popcorn are expensive junk foods with added whey, not meaningful substitutes for meat, eggs, or canned fish.

Practical conclusion

• Meat, eggs, fish, organ meats, and animal fats fit within a household budget.
• Cheap supermarket animal foods are health foods compared with the junk foods they replace.
• Food quality improves when finances allow, but the best possible use of available money still makes cheap carnivore beneficial for health.

References None. :::

Australasian Metabolic Health Society's Grand Round July 2026 Chaired by Dr Gary Fettke

Dr David Unwin FRCGP works at the Norwood NHS Surgery in Southport near Liverpool, UK where he has helped care for a practice of 9700 people since 1986 as a family doctor. To date 157 of his patients with T2 diabetes have achieved drug-free remission. This gives a remission rate of 50% at 30 months duration of those choosing a lower carb diet. This equates to a remission rate of over 20% of the diabetic population of the entire practice. One of the best results for any clinic in the world.

For the past few years, he has been a UK Royal College of General Practitioners expert clinical advisor on diabetes. David was also elected to fellowship of the college for his work in the training of trainee general practitioners. As a result of his interests in both better communication with patients and Type 2 diabetes he was made Royal College of General Practice National Champion for Collaborative Care and Support Planning in Obesity & Diabetes in 2015.

In 2016 he was the proud UK National winner of the NHS Innovator Of The Year Award for published research into lifestyle changes; working with patients’ personal health goals as an alternative to drug therapy in type 2 diabetes –so that his GP practice has saved £370,000 on drugs for diabetes since 2018. As part of this he has also published over 30 research papers into improving blood pressure, lipid profiles, renal function and liver function by improving diet by reducing carbohydrate, especially sugar while increasing protein and healthy fats. His teaspoon of sugar infographics have now been translated into thirty five languages and have been downloaded millions of times. In 2021 one of his papers published in BMJ Nutrition(1) was voted as ‘paper of the year’ by the International Academy of nutrition educators. His 2023 BMJ Nutrition paper on the low carb diet in T2 diabetes(2) is the most popular paper ever published by that journal.

With his psychologist wife Dr Jen Unwin he has presented to large audiences all over the world (Florida, Minnesota, California, Denver, New Zealand, Poland, Zurich, London, Glasgow and Edinburgh)

::: spoiler generated summary

The epidemic and the practice

• Roughly the same 10,000 people were cared for over 40 years, while type 2 diabetes increased about tenfold and began affecting people in their twenties as well as older adults.
• Since low-carbohydrate groups began in 2013, the team has reached 159 cases of drug-free type 2 diabetes remission; about half of the patients choose this approach, while the others receive approaches suited to them.
• David Unwin is a scientific adviser to Abbott on continuous glucose-monitor education and access, not on promoting drugs, and CGM is central to helping people understand their own food responses.
• Andrew began with an HbA1c of 81 mmol/mol, reached 51 with low-carbohydrate eating and CGM, and drifted more than once; he then achieved remission over about four years with 16% weight loss, while his cholesterol-to-HDL ratio fell from 15.

Why glycaemic control matters

• Each year with HbA1c above 58 mmol/mol costs about 100 days of life, so average control can mean losing roughly a third of life expectancy, with especially serious consequences when type 2 diabetes begins young. [1]
• Diabetes increases cardiovascular and stroke risk and is associated with eight forms of cancer; insulin resistance and hyperinsulinaemia connect diabetes with those cancers, making prevention important.
• Retinopathy, nephropathy, neuropathy, and microalbuminuria all rise as HbA1c worsens, and a 10% HbA1c improvement such as 65 to 54 is associated with a 45% lower risk of microvascular complications. [2]
• Remission matters because the goal is normal blood glucose without medication; average control is inadequate when better control can prevent cumulative damage.

Prevention and early remission

• In the 2020 prediabetes evaluation, none of 71 people choosing a low-carbohydrate approach developed type 2 diabetes over about 22 months, and 93% reached normal HbA1c. [3]
• Drug-free remission occurred in 77% of people who began within the first year of type 2 diabetes, compared with 51% after five years, so delay makes remission harder. [4]
• Chronological age is not the decisive issue: the oldest remission patient was about 92, and resolving poorly controlled diabetes relieved polyuria and made daily life at home easier.
• Metabolic age matters, and prevention or early action is easier, faster, and more practical than waiting for prolonged hyperglycaemia to damage metabolic function.

How type 2 diabetes develops

• HbA1c measures average blood sugar over about three months, but high glucose can damage the endothelial glycocalyx within hours, so glucose spikes and time in range matter as well as the average. [5]
• Insulin lowers blood glucose by moving glucose into cells; when excess carbohydrate is not used for energy, it becomes triglyceride and fat, particularly in the abdomen and liver.
• Liver fat drives insulin resistance and hyperinsulinaemia, while pancreatic fat reduces insulin production; this twin process can progress for years before glucose control finally breaks down. [6]
• Reducing carbohydrate and weight can improve insulin sensitivity and pancreatic function, but remission is the right word because old habits can bring diabetes back; bariatric surgery, GLP-1 drugs, and low-carbohydrate eating reduce intake by different routes.

Making carbohydrate visible

• Productive consultations turn a problem into a puzzle: the food causing the glucose rise is identified without blame or negativity, and collaborative work keeps patients engaged in finding their own solution.
• Starch is sugar in metabolic terms, so bread, rice, potatoes, pasta, cereal, fruit juice, and other starchy or sugary foods belong in explanations of glycaemic consequences.
• A 150 g serving of boiled rice has approximately the glycaemic effect of just over 10 teaspoons of sugar; brown rice improves it by about one third, while salad, courgettes, meat, fish, eggs, and full-fat dairy barely raise CGM glucose. [7]
• The entire five-litre bloodstream contains only about one teaspoon of glucose, while a banana can supply five or six teaspoons, making CGM feedback and teaspoon-of-sugar infographics immediately understandable.

Practice outcomes and cardiovascular risk

• In the 186-patient low-carbohydrate cohort followed for nearly three years, average weight fell 12%, HbA1c improved, triglycerides fell 35%, total cholesterol fell 12%, and the cholesterol-to-HDL ratio improved by 2%. [4]
• Blood pressure also improved despite substantial deprescribing of antihypertensive drugs, so the visible result understates the physiological improvement. [8]
• Every cardiovascular marker routinely measured in the British health service improved despite higher intake of eggs, butter, cheese, red meat, protein, and fats within the low-carbohydrate approach.
• OpenPrescribing data have kept Norwood Avenue the lowest-cost local practice for diabetes drugs, with an estimated cumulative saving of £373,000 against the local average, although the practice receives none of it to fund the service.

CGM, relapse, and maintenance

• A latte doubled David Unwin's glucose to 11 mmol/L and impaired his thinking; cereal with banana and raisins doubled it and then produced an insulin-driven low with hunger and agitation, while a low-carbohydrate meal left it flat.
• CGM should be used earlier, before people become ill enough to need insulin, because it rapidly reveals problem foods; the average time to drug-free remission is about eight weeks and is planned for a forthcoming paper.
• Dan has maintained remission for years after identifying bread, rice, and potatoes with one CGM; another patient achieved remission three times over ten years, and a patient whose HbA1c reached 120 brought it down after identifying biscuits.
• Relapse usually means the person has left the diet and needs help returning, not that the diet has failed; unexpected HbA1c and weight patterns can signal insulin deficiency, pancreatic cancer, or misclassified type 1 diabetes; monthly group consultations for 30 or more people provide affordable long-term support.

Ultra-processed food addiction

• Repeated regain was once called "carb creep," but ultra-processed food can be seriously addictive for many people, like alcohol or nicotine, and ignoring addiction allows long-term results to deteriorate.
• Moderation does not work for everyone with carbohydrate addiction: one biscuit becomes ten, and intelligent people continue eating foods they know damage their health.
• Yale Food Addiction Scale data show a strong association between food addiction and type 2 diabetes, with affected people 6.7 times more likely to have type 2 diabetes. [9]
• Food addiction is a promising target for preventing type 2 diabetes in younger people, and Jen's CRAVED tool offers a way to screen for it.

References

1. [13:04] Estimating life years lost to diabetes: outcomes from analysis of National Diabetes Audit and Office of National Statistics data — https://doi.org/10.1097/XCE.0000000000000210
2. [17:37] The relationship of glycemic exposure (HbA1c) to the risk of development and progression of retinopathy in the Diabetes Control and Complications Trial — https://doi.org/10.2337/diab.44.8.968
3. [18:05] Insights from a general practice service evaluation supporting a lower carbohydrate diet in patients with type 2 diabetes mellitus and prediabetes: a secondary analysis of routine clinic data including HbA1c, weight and prescribing over 6 years — https://doi.org/10.1136/bmjnph-2020-000072
4. [19:30] What predicts drug-free type 2 diabetes remission? Insights from an 8-year general practice service evaluation of a lower carbohydrate diet with weight loss — https://doi.org/10.1136/bmjnph-2022-000544
5. [21:31] Loss of endothelial glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo — https://doi.org/10.2337/diabetes.55.02.06.db05-1103
6. [23:55] Type 2 diabetes: etiology and reversibility — https://doi.org/10.2337/dc12-1805
7. [29:18] It is the glycaemic response to, not the carbohydrate content of food that matters in diabetes and obesity: The glycaemic index revisited — https://doi.org/10.4102/jir.v1i1.8
8. [37:55] Substantial and Sustained Improvements in Blood Pressure, Weight and Lipid Profiles from a Carbohydrate Restricted Diet: An Observational Study of Insulin Resistant Patients in Primary Care — https://doi.org/10.3390/ijerph16152680
9. [49:16] Food addiction is strongly associated with type 2 diabetes — https://doi.org/10.1016/j.clnu.2023.03.014 :::

I'm omad normally; just hit 30 hours thinking about food a bit but not hungry.

+water+electrolytes+coffee

I've been considering adding regular fasting into my schedule, maybe weekend fasts?

The longest fast I've done is 5 days before, but that was back when i was doing crappy keto, and now i've been strict zero carb for awhile.

I like multiple factors. I played with a bunch of different hardware security tokens over time. Fingerprint reading on the token is pretty good, I don't like the idea of typing in a PIN to an untrusted computer to talk to the token. I played with the only key, and it's interesting, but it's been pretty much abandoned by its original developers. So I think it's in dead end. But it did have a physical input keypad on the key. So the PIN didn't have to trust the computer that's nice

What do you use? What is your strategy? Any fun anecdotes?

Background/Objectives: Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), particularly semaglutide, have demonstrated efficacy for weight loss in obesity; however, up to 40% of weight lost may derive from lean body mass. The ketogenic diet independently improves insulin sensitivity and promotes fat oxidation while preserving lean tissue. This study aimed to describe changes in body composition, insulin sensitivity, and cardiometabolic markers in patients who followed a personalized ketogenic dietary protocol while receiving low-dose semaglutide over a 6-month insulin resistance reversal program. Methods: Seven analyzed adults (six female, one male) with overweight or obesity (baseline BMI 25.6–47.2 kg/m2) participated in a clinician-supervised 6-month program combining a whole-food ketogenic diet with semaglutide (≤1.0 mg/week). Body composition and fasting metabolic markers were assessed at 1, 3, and 6 months. Results: Mean total weight loss was 21.9 kg, of which a mean of 92% was attributable to BIA-estimated fat mass. Skeletal muscle mass was largely preserved as measured by BIA (mean loss 1.2 kg), and one patient gained lean tissue. Fasting insulin declined by a mean of 15.6 µIU/mL. Visceral fat decreased by a mean of 37.0%. Six of seven patients showed reductions in high-sensitivity C-reactive protein. Triglycerides decreased in six of seven patients, and HDL cholesterol increased in all seven. LDL cholesterol responses were heterogeneous. Conclusions: In this small, uncontrolled case series, combining a ketogenic diet with low-dose semaglutide was associated with substantial fat loss, apparent preservation of lean mass as measured by BIA, and improvements in insulin sensitivity and cardiometabolic markers. Because the semaglutide dose and dietary protocol were individualized to each patient’s response, the program illustrates a personalized approach to insulin resistance. These preliminary findings are hypothesis-generating and warrant confirmation in controlled prospective studies.

Full Paper - https://doi.org/10.3390/jpm16060313

i just found out that firefox finally made profiles easy to use - a first class feature like chrome.

I found out from this techlore video https://youtu.be/dwFSytu_JUw

and even better then chrome, in macos dock bar, each active profile has its own icon

Chrome has had profiles for a long long time, easy to segment accounts/jobs for better isolation (extensions, etc).

Firefox has always had profiles hidden, they were just a super pain in the butt to the point where it wasn't really usable.

Better isolation is great!

This is a fun way to kill a few days learning nixos and setting up a home media stack.

I have done a tremendous amount of bikeshedding playing with this project. great fun

Finally justifying my home network over-building - all I had to do was try to move around 100gib objects constantly!

this module wraps a VPN namespace around (Seerr, Prowlarr, Sonarr/Radarr, (torrent/nzb), jellyfin), it's pretty declarative, there are some things that still manually need to be setup by hand (not the fault of nixos).

For extra complexity - My nixos is a thin os backed by NFS over 10g fibre, on a isolated vlan that can only egress the network to known wireguard ports.

I spent so much time trying to optimize bandwidth I ran out of things to download!

Dementia is a metabolic disease, not a genetic one. Here's what's really destroying your brain, and how to reverse it. Dr. Anthony Chaffee MD.

::: spoiler generated summary

Brain evolution and fuel

• Human cranial-capacity analyses found a reduction of about 10-17% from the Mesolithic to modern times, while domesticated pigs had brains about 18% smaller than wild boars.[1][2]
• Dementia and neurodegeneration are largely preventable consequences of chronic shortages of ketones, cholesterol, and animal nutrients together with exposure to sugar and seed oils.
• Human fasting studies found that rising ketone availability lowers cerebral glucose use and supplies a major share of brain energy.[3][4]
• The neonatal period depends heavily on ketone metabolism; germline loss of ketone oxidation causes fatal postnatal metabolic failure in mice.[5]
• Pregnancy accelerates fasting ketosis, and breast-fed infants generate more ketones than formula-fed infants.[6][7]

Animal nutrients and brain maintenance

• Cholesterol, saturated fat, B12, D3, vitamin A, choline, creatine, carnitine, and DHA supply structural and metabolic materials for myelin, synapses, membranes, and mitochondria.
• An 18-person Alzheimer pilot found cognition improved after six weeks off statins and declined after six weeks back on them.[8]
• Severe infant B12 deficiency causes developmental regression and MRI-visible cerebral atrophy.[9]
• Lower B12 markers within conventional ranges predict faster brain-volume loss over five years.[10]
• Low maternal B12 intake during pregnancy predicts poorer speech and mathematical performance through childhood.[11]
• Adolescents raised on macrobiotic diets can retain marginal B12 status and cognitive deficits after changing to omnivorous diets.[12]

Aging and dietary injury

• MRI comparisons found age-related cerebral shrinkage in humans but not across 99 chimpanzees.[13]
• Long-lived whales and wild animals on natural diets do not show the same age-related brain shrinkage, making chronic malnutrition a better explanation than normal aging.
• Fructose, excess linoleic acid, brain insulin resistance, glycation, vitamin D deficiency, and inadequate DHA, EPA, creatine, carnitine, and vitamin A converge on mitochondrial dysfunction and neuroinflammation.
• Porphyromonas gingivalis antigens were detected in most examined Alzheimer brains and in a high proportion of glioblastoma tissue cores.[14][15]

Ketogenic interventions

• A randomized childhood epilepsy trial found substantial seizure reduction with a ketogenic diet.[16]
• Alzheimer brains retain acetoacetate metabolism despite reduced glucose uptake, and a randomized ketogenic-diet trial found improvement in clinical outcomes.[17][18]
• Randomized ketogenic and Mediterranean diet studies both improved Parkinson symptoms, with greater nonmotor improvement in the ketogenic trial.[19][20]
• Early autism data and a Huntington case study link ketogenic diets with functional improvement.[21][22]
• A multiple-sclerosis case series with symptom improvement and MRI lesion shrinkage is being prepared for publication.

Genetic risk and prevention

• In a 15-year cohort of 2,157 older adults, high meat intake was associated with slower cognitive decline and lower dementia risk among APOE epsilon-4 carriers.[23]
• Genes modify susceptibility, but correcting brain fuel and nutrient supply can prevent or reduce the metabolic conditions that drive neurodegeneration.

References

1. [00:09] Decrease of Human Skull Size in the Holocene — https://digitalcommons.wayne.edu/humbiol/vol60/iss3/5
2. [00:21] How domestication, feralization and experience-dependent plasticity affect brain size variation in Sus scrofa — https://doi.org/10.1098/rsos.240951
3. [01:07] Generalized decrease in brain glucose metabolism during fasting in humans studied by PET — https://doi.org/10.1152/ajpendo.1989.256.6.E805
4. [01:24] Brain Metabolism during Fasting — https://doi.org/10.1172/JCI105650
5. [01:49] Obligate Role for Ketone Body Oxidation in Neonatal Metabolic Homeostasis — https://doi.org/10.1074/jbc.M110.192369
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GPT-5.6 Thinking - high :::