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Why I changed course

• I spent many years in traditional cardiology, became vegan about 20 years ago after reading John Robbins's A Diet for a New America, and about 11 years ago changed my practice into a wellness practice using diet, lifestyle, and movement to reverse cardiovascular disease, diabetes, and other lifestyle diseases. [1]
• I was also a long-time marathon and ultramarathon runner, and after years of 50- and 100-mile events I began having low-glucose "bonking" episodes and mildly rising glucose; with diabetes and cardiovascular disease throughout my family, that concerned me.
• Andrew Koutnik and Tim Noakes had just published a paper on endurance fueling. I took from it that bonking and performance were tied more to maintaining blood glucose than to muscle glycogen depletion, that athletes did not need the customary amount of carbohydrate, and that the heavy-gel approach was not really based on science and may have been driven more by industry. [2]
• I tested that in a 50K by cutting carbohydrate to about 10-20 g/hour from roughly 300 calories/hour. I did not bonk, felt better than after prior races, and had no muscle soreness the next day; when I called Koutnik, he told me glucose is a toxin and creates a lot of inflammation.
• Pancakes and fruit after a run or rice, beans, and an apple at lunch had often left me exhausted. A CGM then showed large glucose spikes and made clear to me that I was prediabetic.
• I then looked more closely at long-term plant-based patients I had followed for 5-10 years. Even lean patients were developing insulin resistance and glucose intolerance, with gradually rising HbA1c and elevated insulin, and patients who consumed neither fish nor a supplement also had markedly low DHA.
• Once insulin resistance became the problem, keeping protein up while cutting carbohydrate was very difficult with whole plant foods because foods such as beans brought carbohydrate with the protein. I did not want to solve that with powders and supplements, so I moved from fish to eggs, bacon, beef, butter, and cheese; my aches and pains disappeared, my sleep became much better, and I felt very well.
• In May we told the practice that insulin resistance was too important to ignore and that we would support patients in whatever they chose. Many moved from plant-based eating toward low-carb, high-fat, keto, or carnivore diets, and I began seeing better sleep, less inflammation, and weight loss, including in people who had not been able to sustain calorie restriction when insulin was high.
• I had added fish around the beginning of the year and brought the other animal foods back starting May 1. I kept cutting my own carbohydrate from about 100 g to 50 g and then lower because I wanted to experience ketosis, and despite having loved fruit, I no longer wanted it once I felt better.

Diabetes, lipids, and cardiology

• From May to July, my total cholesterol rose from roughly 170-180 to 313 mg/dL and LDL from under 100 to 212, while HDL was 96 and triglycerides were in the high 30s. I saw myself as a lean-mass hyper-responder.
• Diabetes is the risk factor I have been running from my entire life. Looking back over my family and my cardiology patients since 1990, cholesterol did not pinpoint who had heart attacks for me, but every one of those people had glucose intolerance or diabetes, and the triglyceride-to-HDL ratio looked clear as day.
• That makes me more comfortable with particle size getting bigger and metabolic health improving even while LDL is high. Eating saturated fat was an enormous mental shift after a lifetime of low-fat eating, but I now use fat as an energy source as carbohydrate falls, and I feel good and think this is the right direction unless something changes.
• My old cardiology practice was "as low as you can go" for cholesterol, blood pressure, and glucose. Experience softened that: in an older person, a blood pressure of 110 can mean passing out, breaking a hip, or inadequate brain perfusion, so lower is not automatically better.
• We have had statins since the late 1980s and, in my view, pushing cholesterol as low as possible has not dramatically changed the problem. LDL is probably "at the scene of the crime," but inflammation, diabetes, and high triglycerides are there too; procedure-driven cardiology can also become comfortable with medications and repeat stents without spending much time on why the disease is happening.
• I changed my practice so I could see fewer people, teach nutrition and movement, and explain disease and risk well enough that patients could make their own choices. Most of the plant-based patients who trusted me through earlier success also trusted me when I said we needed to pivot.
• Some vegans were angry that I changed my mind, but my goal is preventing heart disease and diabetes, not staying tied to an intervention. I want the root cause and I am still learning; the distinction I attributed to Dr. Unwin between the art of medicine, which allows change and growth, and the science of medicine becoming dogma captures how I think about that.
• Nutrition studies are largely observational, and if two diet groups both stop eating junk food, start exercising, and quit smoking, both can improve. The harder question is what happens after those broad changes and whether we can separate the effects further.

Statins, lipid shorthand, and what I learned from patients

• A low-fat diet will tend to lower LDL, but I see a tradeoff in perhaps smaller particles and more inflammation over time. For me, statins also carry what I cited as a 4% increase in diabetes plus muscle side effects that matter because I run, so I do not want them for myself.
• Statins may still have a place after a heart attack or in someone with greater clotting risk because they may have anti-inflammatory and clotting effects. If a patient wanted one I would not refuse it; I think the decision should account for the whole person, not simply one abnormal cholesterol number.
• I agreed with the critique of the LDL-bad/HDL-good shorthand and added that drugs that lowered HDL were followed by heart attacks and were pulled, leaving HDL viewed as less protective while LDL remains the dominant target. I also said triglycerides get pushed aside and that statins do not change triglycerides at all.
• Saturated fat was similarly demonized for me: "the fat you eat, the fat you wear." A fatty brown meal with no fiber looks wrong after decades of that message, which helps explain why the change is difficult.
• The strongest pushback after our town hall often came from wives who had joined the practice to keep husbands with cardiovascular disease plant-based. Some felt I had taken away the support that was keeping their husbands safe, while some husbands who had never wanted the diet were delighted that meat was back.
• One long-term vascular patient changed how I looked at the history. He had developed disease young and I had focused on meat, but when I finally asked what he actually ate decades earlier, he told me about donuts for lunch and a major sweet tooth; I had never asked that before.
• I accept that Dr. Esselstyn had some success, but when I look at those papers I do not know how much came from the plant-based diet itself versus whether people were diabetic, stopped smoking, started exercising, or made other major lifestyle changes.
• My own Appalachian family made the same point for me. They raised pigs and ate pork and lard, but my grandfather who died at 48 smoked, worked in coal mines, and lived under major stress; another grandmother was obese, drank large amounts of Coca-Cola, and ate a lot of carbohydrate, and the family diet also had bread, mashed potatoes, pies, and cakes. I had focused on the meat.
• I agreed with the dietary-context criticism around the 2023 Harvard red-meat/type 2 diabetes study: there was never just meat on the table where I grew up; there was also a large bread, potato, rice, or other starch contribution and plenty of sweets, and even berries were saved for pies loaded with sugar and were not eaten by themselves. [3]
• I also had a major sweet tooth during my plant-based years: oatmeal needed brown sugar and dates, I later ate enormous amounts of fruit, there was maple syrup, and running gels were pure glucose with Coca-Cola as late-race fuel. I believed the fructose was going straight to my liver and was not helping me; my baseline diet was about 75-80% carbohydrate and weekends added even more simple sugar.

Running and implementing lower carbohydrate

• Three weeks before this interview I ran 100 miles at age 64 and was running again by the end of the week, with no muscle soreness and none of the prolonged fatigue I used to have after races. I believe more protein improved recovery and taking carbohydrate out reduced inflammation.
• Endurance culture had taught me to keep pushing gels and even to "train your gut" to absorb more carbohydrate. Over many hours, that amount of carbohydrate can make the gut shut down, cause bloating and sickness, and produce insulin spikes and lows; I realized my trail-race Oreos, Coca-Cola, and sandwiches were a weekend sugar binge, and Koutnik told me that while insulin stays high I cannot access my fat stores.
• In the latest 100-miler I mostly used foods such as beef jerky and had a cheeseburger around mile 70, though I added more carbohydrate late when I was struggling. High-carbohydrate chews and Coca-Cola pushed my CGM into the 200s, and after finishing around 3 p.m. my glucose did not settle until about 11 p.m.; that made me worry that high-carb endurance fueling can create diabetics who feel healthy because they can run far.
• My current day is coffee with a little MCT oil, a 5-6 mile run, more coffee with half-and-half, bacon and eggs at lunch, ketone powder or Ketone-IQ in the afternoon, and meat with a little vegetable at dinner. I am still struggling to get into marked ketosis.
• With patients, we cut carbohydrate based on their metabolic condition. For insulin-resistant, prediabetic, or diabetic patients we may move under 100 g, then 50 g, and sometimes under 20 g, and CGMs have been very useful because seeing the glucose response gets people on board. When people cut carbohydrate without adding enough saturated fat they sometimes had low energy, so we taught them that fat had to become an energy source; early changes included ankle and leg swelling disappearing and one man losing 20 lb.
• I also teach from symptoms: sleepiness after a high-carbohydrate meal, afternoon naps, and getting "hangry" can lead us to check insulin. The hardest step for many patients over 50 is accepting saturated fat after growing up in the low-fat era, but once they make the change, I find this way of eating much simpler than the chopping, combining, and planning I used to do to assemble plant-based meals.

Absolute risk, testing, and metabolic health

• If a doctor is pushing a statin, I would start with absolute risk and ask what the actual benefit is. Gary Taubes had just published a Substack article asking how much longer LDL lowering makes someone live; I cited about 1% absolute benefit, a couple of days, perhaps a month if someone is very high risk, and probably less for a woman. [4]
• I would also ask how insulin resistance and diabetes change the risk. I was guilty of not asking what people were actually eating when they had their cardiovascular event, and I now want those metabolic risk factors addressed.
• We used to stress-test asymptomatic people with diabetes because they were high risk, but even an abnormal result without symptoms did not necessarily make them live longer or better. I would focus first on diabetes and metabolic syndrome, while also respecting symptoms and functional capacity; stress testing has fallen out of favor as calcium scoring and CT angiography have become common.
• In the over-50 running community, calcium scoring or CT angiography would probably find a lot of vascular disease in people who are completely asymptomatic. I would target what keeps them asymptomatic and functional and avoid intervention solely because imaging finds disease, especially when an intervention might make things worse.
• After decades in medicine, I know I cannot predict anyone's expiration date; there are probabilities, not certainty. Improving metabolic health casts a wider net for me because diabetes raises cardiovascular and cancer risk: lowering LDL will not prevent breast cancer, while improving metabolic health might.

References

1. [00:24] Diet for a New America — https://newworldlibrary.com/product/diet-for-a-new-america-8212-br-25th-anniversary-edition
2. [02:03] Carbohydrate Ingestion on Exercise Metabolism and Physical Performance — https://doi.org/10.1210/endrev/bnaf038
3. [30:08] Red meat intake and risk of type 2 diabetes in a prospective cohort study of United States females and males — https://doi.org/10.1016/j.ajcnut.2023.08.021
4. [45:49] Lowering LDL: Surely, a "Heart-Healthy" Diet Is Worth the Effort. Isn't it? — https://uncertaintyprinciples.substack.com/p/lowering-ldl-surely-a-heart-healthy

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

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

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.

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• 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

• 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

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

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

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.