You named the community a 4 letter very charged word
Recorded at the Public Health Collaboration annual conference in London, UK, on 11th May 2019.
generated summary
What fibre is and whether we need it
- Carbohydrates include glucose, fructose and galactose as monosaccharides; sucrose, lactose and maltose as disaccharides; and starch and glycogen as digestible polysaccharides.
- Fibre is the indigestible polysaccharide fraction, with water-soluble forms in foods such as oats and beans and insoluble forms such as bran. Its passage through the bowel does not itself establish a health benefit.
- The 2005 macronutrient panel gives zero as the lower limit of dietary carbohydrate when fat and protein are adequate; dietary carbohydrate is not strictly necessary for survival. [1]
- The 2015–2020 American dietary guidelines classify fibre as nonessential. Nonessential status does not establish whether fibre has beneficial effects. [2]
How the fibre belief arose
- Sylvester Graham linked meat to lust and masturbation and promoted plant foods; Ellen G. White of the Seventh-day Adventists connected animal foods with moral corruption.
- John Harvey Kellogg, who typeset White's writings as a child, adopted objections to meat and masturbation and a belief that fibre cleansed the body; Graham crackers and cornflakes emerged from this milieu.
- Surgeon Denis Burkitt associated higher-fibre populations with lower frequencies of diabetes, obesity, heart disease and cancer and popularised the connection between small stools and large hospitals.
- Belinda Fettke traced opposition to Gary Fettke's low-carbohydrate advice through Australian dietitians and cereal manufacturer Sanitarium to Seventh-day Adventist influence.
- An Adventist-authored 2018 paper documents the church's global influence on plant-based eating; this history connects the movement with later fibre and plant-food promotion. [3]
Guidelines, targets and the cost of reaching them
- The 1977 McGovern dietary goals encouraged vegetables and whole grains alongside less fat, without a numerical fibre target. [4]
- Fibre received repeated attention in the 2000 US guidelines; by 2005 the target was 14 g per 1,000 calories, including for young children and reaching roughly 34 g for young men. [5][6]
- British guidance also uses 30 g for adults; the fibre targets and the earlier five-a-day message lacked supporting evidence predating their introduction. [7]
- The January 2019 Reynolds review postdates the earlier fibre target and cannot supply evidence that existed before the target was established. [8]
- The Guardian linked the review to criticism of low-carbohydrate diets; the illustrative 30 g fibre menu contained about 175 g carbohydrate, 44 g sugar and nearly half a woman's daily calories. [9]
- This distinction concerns sugar molecules and the food source and disputes excluding fruit and milk sugars when comparing sugar intake.
- High-fibre bran cereals have high fibre density but may also contain added sugar; pursuing a fixed fibre target can direct food choices toward processed cereal products.
What the intervention and observational evidence shows
- The 1997 Bristol stool scale identifies types 3 and 4 as desirable stool forms. [10]
- The DART randomised trial followed 2,033 men after heart attacks for two years and tested fish, fat and advice to eat about 18 g fibre daily. Mortality outcomes were numerically higher with fibre advice but not statistically significant. [11]
- Three Cochrane reviews cover fibre and cardiovascular disease, whole-grain cereals and cardiovascular disease, and whole grains and type 2 diabetes; each identifies a need for stronger long-term intervention evidence. [12][13][14]
- Observational evidence dominates the field. A 2018 umbrella review assessed 21 outcomes and classified evidence as convincing for three: all-cause mortality, cardiovascular mortality and pancreatic cancer. [15]
- Reynolds found roughly 15% lower relative all-cause mortality with about 30 g versus 5 g daily fibre; the result is an observational association and cannot by itself establish causality. [8]
- Bradford Hill's causation criteria involve an approximate twofold relative-risk threshold for examining causality. [16]
- Yang's 2015 analysis gives an approximately 16% relative difference; the numerical contrast of 63 and 73 illustrates the smaller absolute gap. [17]
- One cohort in the Reynolds evidence had lower-fibre participants with about twice the alcohol use and roughly 1.5 times the obesity, inactivity and low education; adjustment for measured variables leaves potential lifestyle confounding.
- The central distinction is between fibre as a cause of better health and fibre intake as an indicator of healthier overall behaviour.
The carbohydrate–fibre matrix
- The four-box matrix separates low-carbohydrate/low-fibre foods (C: meat, fish, eggs, dairy); low-carbohydrate/high-fibre foods (A: non-starchy vegetables, lower-sugar fruit, nuts and seeds); high-carbohydrate/high-fibre foods (B: legumes, starchier vegetables, sweeter fruit and whole grains); and high-carbohydrate/low-fibre foods (D: refined grains and junk).
- High- versus low-fibre epidemiological comparisons mostly contrast Box B with Box D, with few comparisons involving meat-based Box C diets.
- Many older cohorts began around 1968, when low-fibre consumption is linked to poorer-quality diets, distinct from modern low-carbohydrate patterns.
- Box B includes higher income, education and activity and less smoking or drinking; Box D includes fewer socioeconomic advantages. An increase to 30 g fibre would not itself remove those differences.
Proposed benefits and their mechanisms
- Fibre can slow carbohydrate absorption, while reduced intake of digestible carbohydrate also lowers the incoming glucose load; whole foods and refined carbohydrate differ in their effects.
- Fibre-rich foods and some plant oils contain plant sterols that compete with intestinal cholesterol absorption and lower circulating cholesterol. Plant-sterol-associated cholesterol lowering is linked to adverse heart-disease and cancer outcomes. [18]
- Weight-loss and energy-intake mechanisms draw on reviews including Aune's 2016 analysis; an apples-versus-apple-juice comparison does not isolate the effect of fibre from other food differences. [19]
- A synthesis of seven clinical studies examined fibre, weight loss and C-reactive protein: food-based dietary changes coincided with lower C-reactive protein, while the psyllium-husk supplementation study did not show a reduction. [20]
- Faster bowel transit can limit contact with potentially carcinogenic substances; avoiding their consumption is the corresponding dietary approach.
- Fibre-related changes in transit can affect absorption of magnesium, copper, calcium, iron, potassium and sodium; longer transit allows more time for nutrient extraction.
- An empty bowel alone is insufficient as a disease-prevention mechanism; fasting would also empty the bowel.
The microbiome does not depend on fibre alone
- Gut flora is influenced by parental health, vaginal birth and breastfeeding before later dietary choices.
- Antibiotics and antacids can damage the microbiome; real foods, herbs and spices support it, and junk food can harm it.
- Raw milk, unpasteurised cheese, live yoghurt and kefir contain microorganisms without dietary fibre; beans on toast is unlikely to determine microbiome quality by itself.
- A 1991 experiment measured intestinal gas in ten volunteers consuming 200 g baked beans daily, including methane production in some participants. [21]
When fibre causes problems
- In a constipation study, participants had bloating, bleeding, pain and straining on habitual diets; continued high-fibre intake showed little improvement, lower fibre improved symptoms, and zero fibre had the greatest improvement. [22]
- Fibre does not have uniform effects in digestive disorders; a one- to two-week fibre reduction can serve as a symptom trial for people with IBS or related difficulties.
- Adding a swelling fibre gel during constipation is compared to putting more material into a blocked sink; a universal 30 g target is rejected.
What is really driving the advice, and the low-carb solution
- With protein at about 15% of energy and fat capped at 30%, carbohydrate supplies about 55%, matching the high-carbohydrate direction of the 1977 goals. [4]
- Fibre promotion supports high-carbohydrate Box B over refined-junk Box D, while low-carbohydrate Box C receives criticism; cereal manufacturers, vegan advocates and Adventist groups reinforce this approach.
- Box A combines low carbohydrate with high fibre through flax and alfalfa seeds, blackberries with full-fat yoghurt, asparagus and salmon, Jerusalem artichokes, cabbage and cauliflower; such meals can approach 30 g fibre.
- The lower-carbohydrate 30 g-fibre example is calculated at roughly one-third the calories, one-quarter the carbohydrate and one-fifth the sugar of the Guardian example.
- Harvard's benchmark of at least 1 g fibre per 10 g carbohydrate can be met more easily with Box A foods than Box B foods; low carbohydrate intake need not mean low fibre intake. [23]
- Fibre is nonessential; universal intake targets lack convincing long-term trial support; the proposed mechanisms do not resolve the question; fibre can aggravate bowel symptoms; and low-carbohydrate diets can contain substantial fibre.
References
- [03:42] Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids — https://doi.org/10.17226/10490
- [04:21] Dietary Guidelines for Americans, 2015–2020 — https://www.dietaryguidelines.gov/about-dietary-guidelines/previous-editions/2015-dietary-guidelines
- [08:12] The Global Influence of the Seventh-Day Adventist Church on Diet — https://doi.org/10.3390/rel9090251
- [08:41] Dietary Goals for the United States (1977) — https://www.govinfo.gov/app/details/CPRT-95SPRT23395O
- [08:58] Dietary Guidelines for Americans, 2000 — https://www.dietaryguidelines.gov/about-dietary-guidelines/previous-editions/2000-dietary-guidelines-americans
- [09:12] Dietary Guidelines for Americans, 2005 — https://www.dietaryguidelines.gov/about-dietary-guidelines/previous-editions/2005-dietary-guidelines-americans
- [09:28] SACN Carbohydrates and Health Report (2015) — https://www.gov.uk/government/publications/sacn-carbohydrates-and-health-report
- [10:41] Carbohydrate quality and human health: a series of systematic reviews and meta-analyses — https://doi.org/10.1016/S0140-6736(18)31809-9
- [11:03] Blow to low carb diet as landmark study finds high fibre cuts heart disease risk — https://www.theguardian.com/lifeandstyle/2019/jan/10/high-fibre-diets-cut-heart-disease-risk-landmark-study-finds
- [12:35] Stool form scale as a useful guide to intestinal transit time — https://doi.org/10.3109/00365529709011203
- [13:18] Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: DART — https://doi.org/10.1016/S0140-6736(89)90828-3
- [14:15] Dietary fibre for the primary prevention of cardiovascular disease — https://doi.org/10.1002/14651858.CD011472.pub2
- [14:23] Whole grain cereals for the primary or secondary prevention of cardiovascular disease — https://doi.org/10.1002/14651858.CD005051.pub3
- [14:29] Whole grain foods for the prevention of type 2 diabetes mellitus — https://doi.org/10.1002/14651858.CD006061.pub2
- [15:02] Dietary fiber and health outcomes: an umbrella review of systematic reviews and meta-analyses — https://doi.org/10.1093/ajcn/nqx082
- [16:22] The Environment and Disease: Association or Causation? — https://doi.org/10.1177/003591576505800503
- [16:55] Association between dietary fiber and lower risk of all-cause mortality: a meta-analysis of cohort studies — https://doi.org/10.1093/aje/kwu257
- [22:49] Plant sterols lower cholesterol, but increase risk for coronary heart disease — https://doi.org/10.3844/ojbsci.2014.167.169
- [23:37] Whole grain consumption and risk of cardiovascular disease, cancer, and all cause and cause specific mortality: systematic review and dose-response meta-analysis of prospective studies — https://doi.org/10.1136/bmj.i2716
- [24:26] The effects of dietary fibre on C-reactive protein, an inflammation marker predicting cardiovascular disease — https://doi.org/10.1038/ejcn.2009.8
- [27:57] Investigation of normal flatus production in healthy volunteers — https://doi.org/10.1136/gut.32.6.665
- [28:46] Stopping or reducing dietary fiber intake reduces constipation and its associated symptoms — https://doi.org/10.3748/wjg.v18.i33.4593
- [33:48] Identifying whole grain foods: a comparison of different approaches for selecting more healthful whole grain products — https://doi.org/10.1017/S1368980012005447
Recorded at the Public Health Collaboration annual conference in Manchester, UK, on 20th June 2017.
zoeharcombe.com/2017/06/dietary-fat-guidelines
::: spoiler generated summary
Food composition and dietary-fat arithmetic
- Nearly all natural foods supply protein; pure sugar and pure fats are the exceptions, while butter still has some protein.
- Natural foods largely separate carbohydrate-and-protein foods—fruit, vegetables, grains and pulses—from fat-and-protein foods—meat, fish, eggs and dairy; nuts, seeds and avocado are uncommon mixed examples.
- Meat and fish are generally carbohydrate-free, eggs have traces, and fluid dairy can contain 5–10 g carbohydrate per 100 g; processed foods combine fat and carbohydrate in highly palatable products.
- With real-food protein typically around 15% of calories, a 30% fat ceiling leaves about 55% for carbohydrate; a 25% fat target leaves 60%, while low-carbohydrate eating requires more fat.
- Every fat-containing food includes saturated, monounsaturated and polyunsaturated fats; among ordinary food groups, dairy has more saturated than unsaturated fat.
- USDA food data put a typical sirloin steak at about 2% saturated fat, while oily fish has twice its total fat and 1.5 times its saturated fat; olive oil has 14 times the total fat and seven times the saturated fat of that steak. [1]
- One tablespoon of olive oil contains more saturated fat than a 100 g pork chop, and lard is predominantly monounsaturated; simplified warnings about meat, eggs and saturated fat do not match these food-composition comparisons.
How the guidelines emerged
- The 1977 US McGovern committee introduced dietary-fat goals, incorporated into the 1980 Dietary Guidelines for Americans; Britain followed with NACNE proposals in 1983 and the COMA cardiovascular document in 1984. [2][3][4]
- Earlier medical advice identified floury, vegetable and sugary foods as fattening, illustrated by an 1869 Tanner quotation reproduced in Gary Taubes's Good Calories, Bad Calories. [5]
- The new recommendations shifted the dietary focus to ceilings of 30% of calories from total fat and 10% from saturated fat; those limits necessarily raised the carbohydrate share without evidence establishing that level as healthy or safe.
- Coronary heart disease motivated the policy. In the US in 1950, annual all-cause mortality was about 1.45%, and about 589 people per 100,000 died from heart disease: roughly 0.59% of the population but about 40% of deaths.
- Those measures convey different risks; heart disease accounting for 40% of deaths does not mean 40% of living people die from it each year.
- Early Russian pathologists fed cholesterol-rich animal material to rabbits and observed arterial damage, although rabbits do not naturally eat animal foods; this model differs substantially from human diets.
- Ancel Keys tested dietary cholesterol in people in the early 1950s; in a 1954 symposium he concluded that dietary cholesterol did not affect human blood cholesterol or atherosclerosis. These findings clear animal foods of raising blood cholesterol or causing atherosclerosis, while fat remained the focus. [6]
First review: randomized trials available when policy began
- The February 2015 analysis included six historical randomized trials involving 2,467 men, nearly all already ill; none tested both the 30% total-fat and 10% saturated-fat targets. [7]
- Headlines vindicating butter or crediting fat with longer life went beyond the review: it tested evidence for the guidelines, not butter or fat's effects on lifespan.
- They included the Rose Corn Oil trial, LA Veterans trial, Oslo Diet-Heart Study and Sydney Diet-Heart Study; one trial was released after the 1977 committee met. [8][9][10][11]
- Pooled all-cause deaths were 370 versus 369, with no significant difference; coronary-heart-disease mortality likewise did not improve, and the forest-plot estimates lay on the line of no effect.
- The Sydney intervention reached the 10% saturated-fat target alone, but had significantly more deaths in its intervention arm; its original authors also warned about possible toxicity of the vegetable oil.
- Blood cholesterol fell in both trial arms and more in the diet-intervention arms, yet this did not coincide with fewer heart deaths; cholesterol reduction alone did not establish improved mortality in these trials.
- Plant sterols in vegetable oils can compete with cholesterol absorption and lower blood cholesterol without improving heart-disease outcomes; a 2014 paper identified a possible adverse coronary effect, leading to advice against large vegetable-oil intakes. [12]
- The 1965 Research Committee trial concluded that a low-fat diet had no role after myocardial infarction, and the Rose Corn Oil trial cautioned that corn oil might cause harm. [13][8]
- Dietary advice was nevertheless applied to about 276 million Britons and Americans on the basis of trials involving fewer than 2,500 mostly ill men; that population offered no direct evidence for healthy people or women.
Second review: observational evidence before the guidelines
- The review of six prospective cohorts available before the UK recommendations included only men, mostly healthy, followed for roughly four to 20 years. [14]
- The Western Electric, London Banks and Busmen, F. Heart, Honolulu and Seven Countries cohorts found no association between total fat and coronary-heart-disease deaths. [15][16][17][18]
- Only the Seven Countries Study linked saturated fat and heart-disease deaths, through a between-country correlation, not a within-population relationship; other cohorts identified smoking and paternal age.
- Some cohorts found inverse associations between alcohol and heart disease, potentially reflecting affluence and its benefits, not a benefit from drinking; Keys found no association with smoking, activity or body weight in his study.
- The Seven Countries Study enrolled about 13,000 men aged 40–59 from 1956 and linked saturated fat to cholesterol and cholesterol to coronary disease; its original conclusions concerned associations, not demonstrated causation. [18]
- In a 25-year follow-up, Menotti and Keys obtained a cholesterol–heart-disease correlation of 0.72 (R²≈0.52); a reanalysis yielded a stronger latitude correlation of 0.96 (R²≈0.92), with sunlight/vitamin D as a possible explanation across 16 cohorts. [19]
- The stronger latitude relationship points toward sunlight and vitamin D, with lower exposure in Finland and higher exposure nearer the equator; country comparisons also differ in climate, history and wealth.
- Across the historical cohorts, all-cause mortality was just under 5% and coronary mortality around 1%; in Seven Countries, five-year coronary mortality was 21% with pre-existing coronary disease versus 1% without it.
- Neither the six observational cohorts nor the randomized evidence supported those population-wide fat limits.
Third and fourth reviews: more recent trials and cohorts
- Updating the randomized evidence to ten trials and about 62,000 participants added women, healthy people, and studies lasting one to eight years, including Minnesota, DART and the Women's Health Initiative. [20][21][22][23]
- The pooled results remained null for all-cause and coronary-heart-disease mortality despite larger cholesterol reductions in nine of the ten intervention comparisons.
- Only the Minnesota Coronary Survey included healthy men and women together, but they were institutionalized psychiatric patients who might have been taking cardiovascularly relevant medication, limiting applicability to the general population.
- Even these later trials never directly tested both official fat limits; STARS came closest at 27% total fat and 8–10% saturated fat, but it enrolled only 55 people and its initial positive result lost significance with Fisher's exact test. [24]
- The updated prospective-cohort review identified seven cohorts, six usable in meta-analysis, with the Kushi cohort excluded; its pooled results again found no significant association between total or saturated fat and coronary deaths. [25]
- Four isolated positive cohort findings failed Bradford Hill causal criteria, and the combined results of these four reviews gave no support for the fat guidelines.
Other research and the Cochrane controversy
- A 20-year vegetarian history preceded the research; its findings favored animal foods despite an initial inclination away from meat.
- Skeaff and Miller's 2009 review combined 28 studies and about 280,000 people without a significant effect; Siri-Tarino's 2010 analysis of about 350,000 people likewise found no saturated-fat association with coronary disease. [26][27]
- Mozaffarian's 2010 review found a benefit when saturated fat was exchanged for polyunsaturated fat, while Hooper's 2011 Cochrane review contained one positive result amid eleven nonsignificant results. [28][29]
- Chowdhury's 2014 review found a significant association for trans fats but not saturated, monounsaturated or polyunsaturated fats; Schwingshackl and Hoffmann's review also found no significant effects. [30][31]
- Hooper's 2015 saturated-fat Cochrane update was a 150-page review with a single significant signal: cardiovascular events after lowering saturated fat; seven other outcomes, including all-cause, cardiovascular and coronary mortality, heart attacks and strokes, were nonsignificant. [32]
- Ravnskov and colleagues criticized the Mozaffarian analysis for excluding the Rose Corn Oil and Sydney trials while including a Finnish Mental Hospital study that was neither randomized nor adequately controlled. [33][8][11]
- The Cochrane cardiovascular-event estimate pooled eleven trials although only one documented an actual exchange of saturated for polyunsaturated fat; the others intended dietary changes without verifying them.
- The positive signal depended on adding unpublished heart-event data from four studies originally about skin cancer, high cholesterol, insulin resistance or diabetes, involving only 646 additional people.
- Those extra data were not peer reviewed; study heterogeneity was high (I²=65%), and the positive cardiovascular-event signal lost statistical significance in sensitivity analysis.
- No trial contributing to that Cochrane result studied healthy men and women together, limiting its applicability to the general population.
- Malhotra, Redberg and Meier's 2017 editorial challenged the saturated-fat artery-clogging theory, while the Hooper 2015 cardiovascular-event result remained central to criticism of that view. [34]
After the guidelines: obesity and the sources of dietary fat
- Mark Hegsted and legislators acknowledged in 1977 that the evidence lacked proof and scientific consensus, yet the committee asserted that the recommended dietary changes could cause no physical or mental harm. [2]
- UK obesity rose from about 2.7% in 1972 to 25% by the end of the century; US obesity accelerated around the 1976–1980 guideline transition. The timing raises a question about a possible connection.
- The 2015 US dietary-guideline charts attribute much saturated fat intake to pizza, desserts, candy, chips, tortillas, sauces, mixed ready meals and processed meat, before reaching cheese, milk, butter, nuts and seeds. [35]
- The UK Family Food figures likewise place pastries, cakes, biscuits and sweets prominently among fat sources; real meat, fish and eggs account for only 7%, with substantial intake also coming from dairy, added fats and processed products. [36]
- Processed food, not saturated fat itself, is the main dietary target; the central public-health guidance is to eat real food.
References
- [06:13] USDA FoodData Central — https://fdc.nal.usda.gov/
- [07:44] Dietary Goals for the United States (1977) — https://www.govinfo.gov/app/details/CPRT-95SPRT23395O
- [07:50] Nutrition and Your Health: Dietary Guidelines for Americans (1980) — https://www.dietaryguidelines.gov/about-dietary-guidelines/previous-editions/1980-dietary-guidelines-americans
- [08:07] Diet and Cardiovascular Disease: COMA Report (1984) — https://assets.publishing.service.gov.uk/media/5bab9af640f0b60633988006/Diet_and_Cardiovascular_Disease__1984_.pdf
- [08:20] Good Calories, Bad Calories — Gary Taubes — https://www.penguinrandomhouse.com/books/176680/good-calories-bad-calories-by-gary-taubes/9781400033461/
- [13:04] Symposium on Atherosclerosis (1954), including Ancel Keys — https://doi.org/10.17226/20269
- [14:11] Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983 — Harcombe et al. (2015) — https://doi.org/10.1136/openhrt-2014-000196
- [15:42] Corn Oil in Treatment of Ischaemic Heart Disease — Rose et al. (1965) — https://doi.org/10.1136/bmj.1.5449.1531
- [15:43] A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis — Dayton et al. (1968) — https://doi.org/10.1016/S0140-6736(68)91531-6
- [15:44] Effect of Diet on Five-Year Mortality in the Oslo Diet-Heart Study (1970) — https://doi.org/10.1161/01.cir.42.5.935
- [15:47] Dietary Prevention of Coronary Heart Disease: The Sydney Diet Heart Study — Woodhill et al. (1978) — https://doi.org/10.1007/978-1-4684-0967-3_18
- [18:35] Plant sterols lower cholesterol, but increase risk for coronary heart disease — Harcombe and Baker (2014) — https://doi.org/10.3844/ojbsci.2014.167.169
- [19:51] Low-fat Diet in Myocardial Infarction: A Controlled Trial — Research Committee (1965) — https://doi.org/10.1016/S0140-6736(65)91469-8
- [20:19] Evidence from prospective cohort studies did not support the introduction of dietary fat guidelines in 1977 and 1983 — Harcombe et al. (2016) — https://doi.org/10.1136/bjsports-2016-096409
- [20:50] Diet and Coronary Death: The Western Electric Study — Shekelle et al. (1981) — https://doi.org/10.1056/NEJM198101083040201
- [20:52] Diet and Heart: A Postscript — Morris et al. (1977), London banks and busmen — https://doi.org/10.1136/bmj.2.6098.1307
- [20:54] Framingham Heart Study — Official research milestones — https://www.framinghamheartstudy.org/fhs-about/research-milestones/
- [20:56] Seven Countries Study — Official publications archive — https://www.sevencountriesstudy.com/study-findings/publications/
- [23:41] Inter-cohort Differences in Coronary Heart Disease Mortality in the 25-Year Follow-up of the Seven Countries Study — Menotti et al. (1993) — https://doi.org/10.1007/BF00209531
- [27:15] Evidence from Randomised Controlled Trials Does Not Support Current Dietary Fat Guidelines — Harcombe et al. (2016) — https://doi.org/10.1136/openhrt-2016-000409
- [27:54] The Minnesota Coronary Survey (1989) — https://doi.org/10.1161/01.atv.9.1.129
- [27:57] Diet and Reinfarction Trial (DART) (1989) — https://doi.org/10.1016/S0140-6736(89)90828-3
- [27:59] Low-Fat Dietary Pattern and Risk of Cardiovascular Disease: Women’s Health Initiative (2006) — https://doi.org/10.1001/jama.295.6.655
- [29:48] St Thomas’ Atherosclerosis Regression Study (STARS) (1992) — https://doi.org/10.1016/0140-6736(92)90863-x
- [30:35] Evidence from Prospective Cohort Studies Does Not Support Current Dietary Fat Guidelines — Harcombe et al. (2016) — https://doi.org/10.1136/bjsports-2016-096550
- [32:18] Dietary Fat and Coronary Heart Disease: Summary of Evidence from Prospective Cohort and Randomised Controlled Trials — Skeaff and Miller (2009) — https://doi.org/10.1159/000229002
- [32:41] Meta-analysis of Prospective Cohort Studies Evaluating the Association of Saturated Fat with Cardiovascular Disease — Siri-Tarino et al. (2010) — https://doi.org/10.3945/ajcn.2009.27725
- [32:56] Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat — Mozaffarian et al. (2010) — https://doi.org/10.1371/journal.pmed.1000252
- [32:59] Reduced or Modified Dietary Fat for Preventing Cardiovascular Disease — Hooper et al., Cochrane (2011) — https://doi.org/10.1002/14651858.CD002137.pub2
- [33:11] Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk — Chowdhury et al. (2014) — https://doi.org/10.7326/M13-1788
- [33:24] Dietary Fat Intake and Risk of Cardiovascular Disease and All-Cause Mortality — Schwingshackl and Hoffmann (2014) — https://doi.org/10.1136/bmjopen-2013-004487
- [33:44] Reduction in Saturated Fat Intake for Cardiovascular Disease — Hooper et al., Cochrane (2015) — https://doi.org/10.1002/14651858.CD011737
- [34:07] The Questionable Benefits of Exchanging Saturated Fat with Polyunsaturated Fat — Ravnskov et al. (2014) — https://doi.org/10.1016/j.mayocp.2013.11.006
- [37:30] Saturated Fat Does Not Clog the Arteries: Coronary Heart Disease Is a Chronic Inflammatory Condition — Malhotra, Redberg and Meier (2017) — https://doi.org/10.1136/bjsports-2016-097285
- [39:20] Dietary Guidelines for Americans, 2015–2020 — https://www.dietaryguidelines.gov/about-dietary-guidelines/previous-editions/2015-dietary-guidelines
- [40:08] Family Food Statistics — UK Government — https://www.gov.uk/government/collections/family-food-statistics
:::
I would absolutely expect a doctor to have a reasonable understanding of nutrition. It’s the source of many illnesses.
That is a reasonable expectation, however the training doesn't cover it (see my article referenced earlier, or just ask your own doctor how my hours of nutritional training they have).
Figure 11d - These findings suggest that microbiota depletion substantially attenuates KD efficacy.... i.e. they used antibiotics to reduce KD effectiveness. Very interesting.
Cancer progression is frequently accompanied by systemic inflammation and host-wide disturbances, including neuroinflammation-associated cognitive impairment, yet interventions that simultaneously target tumor growth and host dysfunction remain limited. Here we show that a ketogenic diet suppresses tumor growth while improving emotional and cognitive deficits in tumor-bearing mice. The diet elevates circulating and intratumoral uridine and enriches Flavonifractor plautii, a gut bacterium that contributes to host uridine availability. In tumor cells and patient-derived organoids, uridine cooperates with β-hydroxybutyrate to promote cytosolic DNA accumulation and activate cGAS–Sting signaling, consistent with enhanced antitumor immune activity. In parallel, ketogenic diet, uridine supplementation and F. plautii transplantation reduce systemic and hippocampal inflammatory readouts and improve neurobehavioral phenotypes. These findings identify a diet–microbiota–metabolite axis that links ketogenic metabolism to tumor immune signaling and reduced peripheral-to-brain inflammation in preclinical cancer models.
Full Paper - https://doi.org/10.1038/s41467-026-78868-0
in mice
today's inspiration - https://faseb.onlinelibrary.wiley.com/doi/epdf/10.1096/fj.202603664RR
asking my browser to enforce your policy is a bold choice.
I used to play, but it's been a minute. Have you tried Vietnam?
People make games not companies, if your sitting on such a huge gaming endowment hire good people and make original games.
Buying a studio is just a name, especially a older studio with many years since it's last success, people turn over, move around...
Unmoderated communities become defacto moderated by admins
a natural scientist claiming “All X is Y” with full confidence and without using a ton of qualifiers, then don’t talk to them.
Great, I agree, common ground.
reading individual scientific papers isn’t very useful. Talk to a doctor for nutrition advice.
Most medical doctors don't actually get nutritional training outside of tube-feeding techniques. So they will need to either read the literature themselves, or give you their best approximation of a healthy diet based on their biases. https://discuss.online/post/40032579
- Power off compromised device
the anti-scientific carnivore community on here and while your take is technically correct, it just sounds like it leads into their horseshit.
Hello! You summoned us! What papers would you like us to read? I find the people on that community are highly literate and willing to read any evidence for or against. Science means sometimes your beliefs get challenged, and possibly changed.
If we were to compress all of human existence into a year - farming existed only in the last day, sugar was introduce in the last 40 minutes, and seed oils in the last 15 minutes.
We are still adapting to these profound changes to our food environment.
It's ok to fundamentally disagree with someone and still be civil and polite when speaking with them.
It's ok not to win a discussion, just participate until it doesn't bring you joy, then stop.
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What's the difference between a mechanical engineer and a civil engineer?
answer
A Mechanical engineer builds weapons, a civil engineer builds targets.
what happens when a midlife dietary change collides with decades of diagnosis, stigma, and trial-and-error? Guest Robyn Dobbins (lived-experience advocate, podcast host, health coach, and community coordinator at the nonprofit Metabolic Collective) makes the case for why personal narratives matter in metabolic mental-health advocacy—covering early symptoms, postpartum struggles, routines and relationships, low-carb/keto tradeoffs, community building, and how cholesterol conversations show up along the way.
generated summary
Early signs, secrecy, and early adulthood
- As a high-school freshman, Robyn experienced isolation, low self-worth, and persistent suicidal thoughts without acting on them. Her older sister knew and helped her; concern about stigma kept her symptoms hidden from others.
- School clubs, leadership roles, and lettering in football coincided with severe distress when Robyn was alone. Maintaining different outward and internal experiences was exhausting, and the outward activity concealed her symptoms.
- During college, suicidal thoughts became less prominent while anger, jealousy, unfavorable social comparisons, academic struggles, and severe anxiety increased. A routine request to choose chips for friends led to a panic episode.
- Robyn completed a degree in environmental education, served with Maryland's conservation corps, and worked in outdoor education and at a residential school for boys, where she taught math and met Matt. She rarely shared her emotional difficulties.
- The conversation includes direct questions about suicidal thoughts, their frequency, and another person's safety. External activity and apparent social functioning can coexist with severe internal distress.
Motherhood, psychiatric diagnoses, and the cost of sedation
- After the birth of Robyn's first child in 2005, isolation, financial pressure, and disrupted routines coincided with an acute crisis. She wrote about wanting to die, struggled to speak, and acknowledged thoughts of harming herself or her baby without intent to act.
- Matt took Robyn to the hospital for urgent assessment. She was observed without admission, diagnosed with postpartum depression, given antidepressants, and discharged without a substantive counseling session or specialist referral.
- Her first period on antidepressants coincided with improvement, with no clear attribution to the medication. During her second pregnancy she stopped the drug without a gradual taper after consulting a clinician, then deteriorated amid relocation and Matt's frequent absence for work.
- Robyn experienced intense anger while caring for young children, including avoiding play, holding a bedroom door closed during an overwhelmed episode, and frequent yelling. She later felt enduring guilt about how this affected them.
- Robyn resumed medication during pregnancy because symptoms became unmanageable. A marriage counselor subsequently urged hospital evaluation after an angry episode. Following a move, she stopped medication without informing her new clinicians and struggled for several years.
- Personal accounts of bipolar disorder matched Robyn's anger, periods of reduced sleep, compulsive organizing and cleaning, and disproportionate emotional reactions. A general practitioner prescribed an antipsychotic and referred her to psychiatric care.
- Her psychiatric visits involved questionnaires, repeated medication and dose changes, long travel, high costs, and little sustained exploration of her personal history. She experienced financial guilt and expected medication to remain necessary throughout her life.
- A general practitioner eventually maintained a fixed regimen. Robyn experienced profound sedation, relied on alarms for her children's school routine, slept for much of the day, and had only two or three functional waking hours, sometimes with continuing anger.
- In an Easter photograph, Robyn sat on a couch while her children hunted eggs. She had difficulty joining family activities, while Matt performed much of the household work alongside his employment and travel.
- Robyn remained active in scouting but needed significant rest around major events. During an overnight leadership camp, her evening medication caused severe impairment in speech and mobility, and other volunteers helped her with personal care and getting to bed.
- Her usual food included convenient processed meals, cereal, and nightly ice cream. Dietary changes were not raised during psychiatric care, and she initially had no awareness of nutrition as a possible influence on mental well-being.
The dietary change that began as an effort to avoid a statin
- At age 40, elevated cholesterol prompted a proposed statin, and Robyn wanted to avoid adding another medication. Her general practitioner agreed to six months of dietary change. She began Vinnie Tortorich's no-sugar, no-grains (NSNG) approach on August 6, 2017.[1]
- Robyn eliminated sugars and grains, later avoided seed oils, and initially shifted from nightly ice cream to yogurt. Matt joined her. Their approach generally avoided low-carb imitations of bread and other foods.
- After about six months, Robyn had lost approximately 25 pounds, had changes in cholesterol measurements her doctor welcomed, and had more energy for walking. She continued the same prescribed psychiatric doses and initially viewed these as separate issues.
- NSNG permits different degrees of carbohydrate restriction and does not necessarily produce therapeutic ketosis. Robyn progressed to a heavily meat-based diet, was fully carnivore for a period, and later sometimes included berries or a sweet potato.
- Robyn has never measured ketones. Her belief that she may have been in ketosis was based on her eating pattern and subjective sensations, and the timing of her mental-health improvement was not established by measurement.
Recognizing improvement and tapering psychiatric medication
- After Matt's job loss, the family moved from South Carolina to Texas. During the household transition and after the move, Robyn experienced energy, curiosity, and enjoyment of ordinary activities such as watching sunsets, without initially linking these changes to nutrition.
- A podcast conversation with Dr. Georgia Ede about ketogenic nutrition and mental health prompted Robyn to connect her changed functioning with her diet. She and Matt involved their children in monitoring any deterioration during a possible medication reduction.
- With a general practitioner's oversight, Robyn gradually reduced her antipsychotic and antidepressant around 2018–2019. Missing doses had previously caused severe disturbances, so she used a planned taper and accepted the possibility that medication might become necessary again.
- Robyn has not resumed those psychiatric drugs since tapering. She became active in walking, yoga, and strength training and experienced greater awareness of her surroundings and participation in family life.
- The medication taper followed an established dietary change, involved family monitoring, and was supervised by a medical prescriber. Unsupervised psychiatric medication discontinuation carries potential rebound effects, which Robyn specifically cautioned against.
High LDL, Hashimoto's, and the sweet-potato experiment
- Robyn initially had improved cholesterol measurements during weight loss but later experienced a sharp LDL increase while lean. The lean mass hyper-responder pattern combines high LDL, high HDL, and low triglycerides after carbohydrate restriction; the lipid energy model seeks to explain this response.[2][3]
- Several physicians recommended statins, which Robyn declined amid uncertainty about her individual cardiovascular risk. She also pursued thyroid symptoms and markedly elevated thyroid antibodies, with both parents having undergone thyroid removal.
- An earlier clinician declined to pursue Robyn's thyroid antibodies until a nodule developed. Dr. Tro Kalayjian subsequently identified Hashimoto's and addressed the high LDL with both conventional statin risk factors and uncertainty about carbohydrate-restriction-associated lipid elevations.
- David Feldman's 2018 white-bread-and-processed-meat self-experiment reduced LDL to 83 mg/dL over roughly seven days; Nick Norwitz later conducted an Oreo-based carbohydrate self-experiment. These interventions examined short-term LDL responsiveness, not long-term cardiovascular outcomes.[4][5]
- Dr. Kalayjian offered a daily choice of rice, oatmeal, or sweet potato to test LDL reduction with carbohydrate reintroduction. Robyn ate a palm-sized sweet potato at her first meal without added fat for about three months, and her LDL decreased.
- Robyn experienced renewed sugar cravings after adding sweet potato. She stopped yoga and, after approximately two further months at half a potato daily, experienced declining exercise, a wish to return to bed on waking, and depressive symptoms.
- Reducing to one-quarter of a sweet potato daily did not resolve Robyn's symptoms. Anger and daytime sleep increased, and during COVID illness she still maintained the food intervention until Matt urged her to stop.
- Robyn stopped the sweet-potato intervention, resumed carnivore eating, and did not restart psychiatric medication. Returning to her earlier level of comfort took approximately four months of sustained effort, renewed exercise and yoga, and outside support.
- Robyn prioritizes daily mental functioning and family relationships over lowering LDL through a dietary change she associated with psychiatric deterioration. She acknowledges unresolved cardiovascular risk and has declined statin therapy without establishing that high LDL is harmless.
The KETO-CTA research and its disputes
- The KETO-CTA prospective study enrolled 100 lean mass hyper-responders and near-hyper-responders for coronary calcium and CT angiography at baseline and one year. All 100 participants completed follow-up, producing 200 scans for examining coronary plaque progression.[6]
- The April 7, 2025 KETO-CTA publication used the initial Cleerly coronary-plaque analysis. Public criticism followed while additional quantitative analyses of the same scans were pending.[7]
- HeartFlow and QAngio analyses of the same scans yielded broadly consistent findings that differed from Cleerly. Median plaque progression was low, and some participants had plaque regression while LDL remained high. Longer-term cardiovascular outcomes remain unknown.[8]
- The team repeatedly requested and offered to fund Cleerly quality-control checks or a new analysis, without obtaining the requested re-analysis. The disagreement involved legal consultation and delayed the research process while data validation continued.
- A five-year follow-up was under planning, with some original participants willing to return. The proposed work included tighter contracts, blinding procedures, quality control, and data collection safeguards.
- Cardiovascular risk evidence frequently comes from metabolically unhealthy populations and is applied to otherwise metabolically healthy individuals. This raises questions about the ability of statistical adjustments to capture differences between these populations.
- The lipid energy model and the lipid hypothesis each require evaluation across their predictions and exceptions. Prospective population-specific data, transparent methods, and reproducibility are central to testing the competing explanations.
- The documentary and research center on people using carbohydrate restriction for substantial health concerns, beyond weight loss alone. The focus is on the relationship between LDL measurements and cardiovascular outcomes in the recruited population.
- Drug studies have finite observation periods, possible run-in phases, and differences in adverse-event monitoring. GLP-1 medicines can have benefits while longer-term outcomes and adverse effects require continued study.
- Clinical communication about incomplete evidence includes known effects, uncertainties, and patient choices. Robyn's carbohydrate-reintroduction trial with Dr. Kalayjian involved this kind of shared decision-making.
Advocacy, food behavior, and maintaining change
- Robyn became active in Vinnie Tortorich's online community and launched the Ketobiography interview podcast to share everyday experiences of low-carb and ketogenic living, including less dramatic examples.[9]
- Robyn associates higher carbohydrate intake with rapid deterioration and therefore maintains strict dietary habits. She also explores how people without immediate symptom changes sustain adherence, since simple dietary rules do not eliminate cravings or behavioral difficulties.
- Robyn's father maintained NSNG during cancer care and experienced a strong therapeutic response alongside substantial side effects. She attributes part of his resilience to his dietary habits but does not regard low-carb eating as protection from every illness.
- Dave Feldman sometimes uses informal 30-day low-carb trials with family and friends, comparing bloodwork before and after, and estimates a success rate around 50%. Energy changes vary, as do individual reasons for carbohydrate restriction.
- Weight loss can fluctuate over time without following a straight downward slope, as in Amy Berger's illustration. Comparing individual progress with unusually rapid transformations can create unrealistic expectations, and experiences may differ between women and men.
- Dietary consistency involves individual food triggers, persistent habits, and resuming routines after setbacks. Certain low-carbohydrate snacks can still prompt overeating, and short-term outcomes may not capture longer-term changes.
Long-term adaptation, movement, and changing health needs
- Dave uses poker as an analogy for outcome variability: the example of roughly 2,000 hours of play illustrates how short observation periods can mislead. Short-term fluctuations can also complicate interpretation of diet outcomes.
- In a 2018 self-experiment, Dave gained 19 pounds over approximately six weeks while tracking lipids, body composition, and respiratory exchange ratio. His later usual body weight remained about six to seven pounds above his earlier baseline.[10]
- Robyn maintained her dietary pattern while the unexpected death of her mother and other stresses disrupted her exercise over approximately two to three years. She experienced sustained grief with some similarities to depression but distinguished it from her earlier psychiatric illness.
- A trainer helped Robyn resume strength training, which was followed by more walking, outdoor activity, and improved subjective well-being. She maintains nutrition as a foundation while also valuing movement, sleep, sunlight, and routines.
- Robyn investigated possible indoor environmental factors, including mold, purchased air-cleaning equipment, and experienced better sleep and breathing. She did not establish a causal explanation through testing.
- Metabolic Mind's THINK+SMART program helped Robyn identify missing elements of her former routine, particularly exercise, and resume those practices.[11]
- At age 48, Robyn is focusing on perimenopause, hormonal changes, and maintaining thyroid function while living with Hashimoto's and a family history of thyroid surgery. She has read Amy Alkon's Going Menopostal and consults her clinician about options.[12]
Making metabolic mental-health support accessible
- Robyn participated in The Cholesterol Code documentary about LDL changes and coronary research after carbohydrate restriction. Her psychiatric history and dietary experience are part of the context for her medical decisions.
- Metabolic Mind brings together research, clinicians, and personal experiences; the Coalition for Metabolic Health connects people with experts; and Metabolic Collective is an independent grassroots organization organized around peers and families.
- Metabolic Collective developed through community focus groups and volunteers and supports community-led projects, including storytelling training, connections between podcast hosts and advocates, and the MAMAS family-support initiative drawing on an Al-Anon model.
- The organization's work centers on access to information, lived experience, peer support, and individualized decisions about metabolic strategies alongside clinical care, without a single required dietary pattern or assured outcome.
References
- [01:13] Vinnie Tortorich, What Is NSNG? — https://vinnietortorich.com/what-is-nsng/
- [01:34] Are You a Lean Mass Hyper-responder? — https://cholesterolcode.com/are-you-a-lean-mass-hyper-responder/
- [01:35] The Lipid Energy Model: Reimagining Lipoprotein Function in the Context of Carbohydrate-Restricted Diets — https://doi.org/10.3390/metabo12050460
- [01:44] White Bread and Processed Meat Experiment — https://cholesterolcode.com/the-tandem-drop-experiment-part-2-carbs/
- [01:44] Oreo Cookie Treatment Lowers LDL Cholesterol More Than High-Intensity Statin Therapy in a Lean Mass Hyper-Responder on a Ketogenic Diet: A Curious Crossover Experiment — https://doi.org/10.3390/metabo14010073
- [01:54] The Impact of Carbohydrate Restriction-Induced Elevations in Low-Density Lipoprotein Cholesterol on Progression of Coronary Atherosclerosis: The Ketogenic Diet Trial Study Design — https://doi.org/10.1097/MCA.0000000000001395
- [02:00] Longitudinal Data From the KETO-CTA Study: Plaque Predicts Plaque, ApoB Does Not (retracted in 2026) — https://doi.org/10.1016/j.jacadv.2025.101686
- [02:06] The Impact of Sustained LDL-C Elevation on Plaque Changes: Primary Coronary Plaque Progression Results From the Keto CTA Study (2026 preprint, not peer-reviewed) — https://doi.org/10.64898/2026.01.15.26343955
- [02:27] Ketobiography — https://shows.acast.com/less-of-me-success-stories/about
- [02:45] Weight Gain Experiment (2018), Experiment List — https://cholesterolcode.com/experiment-list/
- [03:18] Metabolic Mind, What Is THINK+SMART? — https://www.metabolicmind.org/thinksmart/what-is-think-smart/
- [03:19] Amy Alkon, Going Menopostal — https://www.amyalkon.net/
Type 2 diabetes is often treated as a chronic, progressive disease, but Dr. David Unwin has spent years showing that, for many patients, remission is possible through low-carb nutrition and a different approach to care.
In this episode, Dr. Bret Scher speaks with Dr. Unwin about how his work as an NHS primary care physician changed after he began focusing on insulin resistance, carbohydrate intake, and the underlying drivers of type 2 diabetes rather than blood sugar alone.
Dr. Unwin shares how his approach to care evolved and discusses published real-world findings on type 2 diabetes remission among patients who chose a low-carb approach. He also explains why long-term maintenance became just as important as achieving remission in the first place, and how he uses continuous glucose monitors to support that process. He also describes his approach to behavioral support, including addressing food addiction.
generated summary
Before low-carb: diabetes care without remission
- For 25 years, type 2 diabetes care focused on blood sugar prescriptions without investigating the causes; chronic disease care frequently misses underlying causes.
- Repeat prescriptions dominated while patients developed ulcers, amputations and escalating medication regimens; the work became management of decline.
- Before 2012, drug-free remission was absent in the practice; higher doses, additional drugs and eventually insulin were the usual progression.
- An NHS low-carb programme later achieved remission in approximately half of participating patients, a major change from earlier outcomes. [1]
- Severe dyslexia made medical training difficult despite a strong commitment to helping people; better patient outcomes renewed that purpose.
Publishing outcomes in a normal NHS surgery
- The first 18-patient low-carb case series documented major improvements and triggered hostility among some dietitians, endocrinologists and doctors. [2]
- Public heckling and hate mail led to baseline measurements, weekly follow-up, inclusion of poor outcomes and continuous programme audit.
- These audits improved clinical methods; observational data follow actual patients, with similar work emerging in multiple countries.
- A subsequent 186-patient NHS service evaluation found about 50% remission without expensive concierge care or a large dedicated team. [1]
How low-carb advice works
- Norwood Surgery diet sheets and protocols are available in BMJ Nutrition papers; no single carbohydrate limit applies to every patient. [1][3]
- With insulin resistance, glucose processing is impaired; lowering foods that raise blood sugar and increasing protein and healthy fats addresses this.
- Research commonly defines low-carb as under 130 g/day, while the effective level depends on individual glucose response.
- Goals and baseline HbA1c, weight, waist or CGM values guide reassessment; drug-free remission requires HbA1c under 48 mmol/mol (6.5%).
- Initial remission or satisfactory weight and long-term maintenance are distinct challenges.
Maintenance through feedback and psychology
- Longer participation at Norwood Surgery coincides with continued average HbA1c improvement; Jen Unwin's psychology input supports maintenance.
- Progress checks around six weeks and immediate CGM feedback connect glucose spikes with recently eaten foods, without waiting three months.
- The DiRECT programme achieved nearly 50% remission after one year, declining to approximately 12% after five years. [4]
- Birthdays, Christmas, holidays, bereavement and stress contribute to lapses, and almost everyone eventually needs renewed support.
- Persistent pressure to eat carbohydrates in the wider food environment makes ongoing support essential.
Food addiction and long-term adherence
- Failure to ask about food addiction left it unrecognized alongside the absence of remission; questioning patients revealed substantial cravings for bread and other carbohydrates.
- A food-addiction study connected addiction with a 670% greater likelihood of type 2 diabetes, making screening important. [5]
- Jen Unwin's CRAVED questionnaire sometimes identifies carbohydrate addiction throughout groups of approximately 30 people with diabetes.
- Severe mental-health symptoms can motivate sustained ketosis, while food addiction can interfere with ketogenic adherence, as Iain Campbell has observed.
- Moderation of bread, potatoes and other problem foods can fail for affected patients; abstinence can be more effective.
Growing acceptance and visible glucose responses
- An initially isolated and unpopular low-carb approach now has an international network, dozens of annual talks, thousands of attendees and continuing critics.
- CGMs expose glucose responses; a small bowl of cereal doubles Unwin's blood glucose and causes illness in his own type 2 diabetes.
- Some criticism attributes low-carb benefits entirely to weight loss, while other data indicate effects on diabetes beyond weight reduction.
- Approximately 30 papers have been published by the team, alongside clinical learning shared across countries.
GLP-1 drugs: benefits, limits and combinations
- Low-carb often lowers hunger and body weight; Isabella Cooper's work links nutritional ketosis to higher endogenous GLP-1. [6]
- Unwin's roughly 15 years of GLP-1 prescribing include reduced cravings for ultra-processed foods and alcohol alongside severe adverse outcomes.
- Two patients required intensive care: one nearly died of pancreatitis, and another needed removal of most of the bowel after stasis and necrosis.
- A minimal effective GLP-1 dose for limited duration with a discontinuation plan addresses escalating doses, adverse effects and weight regain.
- GLP-1 therapy offers an interval for reducing addictive foods and increasing protein, beyond simply decreasing portions of junk food.
- One patient lost 1 kg over five years with a GLP-1 drug and 27 kg over two years with low-carb; efficacy varies for both approaches.
- Real-world GLP-1 evidence indicates up to 50% discontinuation within two years, requiring plans beyond initial weight loss.
- For severe food addiction and poorly controlled diabetes, combining CGM, GLP-1 therapy and low-carb with collaborative decisions can improve adherence.
Medication safety during carbohydrate reduction
- Insulin, sulfonylureas and SGLT2 inhibitors need medication review as carbohydrates fall; practical clinician guidance is available in a published paper. [7]
- With CGM and close support, initial insulin dose reductions of 50%, followed by further reductions, have enabled some long-term users to stop insulin.
- SGLT2 inhibitors can cause euglycemic ketoacidosis, making hydration important on low-carb; doses are sometimes halved and eventually discontinued.
- Glucose in urine can lead to severe thrush; metformin and GLP-1 drugs are compatible with low-carb without intrinsic hypoglycemia risk.
- Individualized, clinician-led adjustments with monitoring are necessary.
The changing food environment
- In earlier medical training, type 2 diabetes was uncommon and absent among patients younger than 60; it now affects younger people.
- Limited genetic change over forty to fifty years implicates the changed food environment in the diabetes epidemic.
- Changing the food environment and addressing underlying causes could make type 2 diabetes rare again without relying only on medication.
- Low-carb is not appropriate for everyone, but ordinary NHS care has yielded remission, lower medication use and savings.
References
- [04:52] 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
- [07:40] Low carbohydrate diet to achieve weight loss and improve HbA1c in type 2 diabetes and pre-diabetes: experience from one general practice — https://doi.org/10.1002/pdi.1835
- [11:14] 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
- [15:32] 5-year follow-up of the randomised Diabetes Remission Clinical Trial (DiRECT) of continued support for weight loss maintenance in the UK: an extension study — https://doi.org/10.1016/S2213-8587(23)00385-6
- [18:19] Food addiction is strongly associated with type 2 diabetes — https://doi.org/10.1016/j.clnu.2023.03.014
- [26:21] Ketosis Suppression and Ageing (KetoSAge) Part 2: The Effect of Suppressing Ketosis on Biomarkers Associated with Ageing, HOMA-IR, Leptin, Osteocalcin, and GLP-1, in Healthy Females — https://doi.org/10.3390/biomedicines12071553
- [32:40] Adapting diabetes medication for low carbohydrate management of type 2 diabetes: a practical guide — https://doi.org/10.3399/bjgp19X704525
Leading health experts examine the history of the U.S. Dietary Guidelines and question decades of dietary advice insisting that saturated fats are bad for us.
Full documentary on youtube - https://www.youtube.com/watch?v=TUADs-CK7vI
Fat makes you thin, and low-fat makes you fat.
One of my favorite programming books.
Filled with gems like this:
Numbers that fool the Fermat test are called Carmichael numbers, and little is known about them other than that they are extremely rare. There are 255 Carmichael numbers below 100,000,000. the smallest few are 561, 1105, 1729, 2465, 2821, and 6601. In testing primality of very large numbers chosen at random, the chance of stumbling upon a value that fools the Fermat test is less than the chance that cosmic radiation will cause the computer to make an error in carrying out a “correct” algorithm. Considering an algorithm to be inadequate for the first reason but not for the second illustrates the difference between mathematics and engineering.
Full Text - https://web.mit.edu/6.001/6.037/sicp.pdf