Insulin resistance is the term researchers use for muscle, liver, and fat cells that respond poorly to insulin, which leaves glucose in the blood longer after a meal. The medical literature describes it as the stage that comes before most cases of prediabetes and type 2 diabetes. What causes insulin resistance is a longer list than diet: published studies also tie it to sleep loss, sitting time, stress hormones, thyroid output, certain medications, and chemical exposures. This article reports what those studies found, then covers the food-order trials, what a 1976 study measured when carbohydrate was removed from the diet, and how much evidence each herb and supplement has behind it.
Key takeaways
- Human studies link sleep restriction, long sitting time, chronic stress hormones, low thyroid function, and some prescription drugs to changes in glucose handling.
- In controlled trials, eating vegetables and protein before starch, taking diluted vinegar before a high-carbohydrate meal, and walking for 10 minutes after eating each improved post-meal glucose or insulin measures.
- In a 1976 clinical study, an 800-calorie diet with no carbohydrate lowered active thyroid hormone (T3) by 47 percent in two weeks. The same calories with at least 50 grams of carbohydrate did not.
- Among the herbs covered here, berberine has the most human trial data. A Cochrane review of bitter melon found no significant effect.
This article is for education only. It does not diagnose, treat, or replace care from a licensed medical provider, and I am a clinical herbalist, not a physician. Do not start, stop, or change a prescribed medication because of anything written here. Herbs and supplements can interact with diabetes drugs and other prescriptions, and combining them can push blood sugar too low. Pregnancy, breastfeeding, liver or kidney conditions, and upcoming surgery all change what is appropriate, and people respond differently to the same herb or food. Bring any change to your prescriber or pharmacist first. If you are in crisis, contact your local emergency number or a crisis line.
What causes insulin resistance
Evidence: randomized crossover trials, meta-analyses of randomized trials, and cross-sectional population data. The seed oil argument is mechanistic and is labeled as such.
Diet
In the food-order trial covered below, the same meal produced a smaller glucose and insulin rise when the carbohydrate was eaten last than when it was eaten first.2 Magnesium is a second dietary factor in the literature: a meta-analysis of nine double-blind trials found that magnesium supplements lowered fasting glucose in people with type 2 diabetes.18
Within the bioenergetic framework, polyunsaturated fats from seed oils are treated as a direct contributor. Ray Peat pointed to P.J. Randle's 1963 work describing how free fatty acids inhibit glucose oxidation, and wrote that the effects of polyunsaturated fatty acids can account for the insulin resistance seen in type 2 diabetes.24 This is a mechanistic argument rather than a clinical trial result, so it belongs in a different evidence tier than the studies above.
Sitting and sleep
Exercise physiology describes skeletal muscle as the largest site of glucose disposal in the body, and contracting muscle takes up glucose without needing insulin. Long stretches of sitting leave that pathway unused. In a randomized crossover trial of adults with type 2 diabetes, a 10-minute walk after each main meal lowered post-meal glucose by 12 percent compared with one 30-minute walk at any time of day, and the effect was largest after the evening meal.1
Sleep loss changed glucose handling within a week in one Lancet study. When 11 healthy young men were restricted to four hours in bed for six nights, glucose tolerance fell, evening cortisol rose, and sympathetic nervous system activity increased.4 The authors compared the resulting metabolic profile to early aging.
Medications
A meta-analysis of 13 randomized statin trials with 91,140 participants found a 9 percent increase in new-onset diabetes among people taking statins.5 The absolute risk was small, one extra case per 255 people treated for four years, and the authors judged it acceptable against cardiovascular benefit. If you take a statin, raise this with your prescriber rather than stopping on your own.
Plastics and endocrine disruptors
Bisphenol A (BPA) is used in the lining of food cans and in some plastics. In a cross-sectional analysis of the US population, each standard-deviation increase in urinary BPA was associated with 39 percent higher odds of a diabetes diagnosis, and the association remained after adjustment for age, sex, body mass, and the other factors the authors measured.6 Cross-sectional data cannot establish cause, so this counts as a consistent association rather than proof.
Nutrients with trial data
Beyond magnesium, chromium and alpha-lipoic acid both have randomized trial evidence in people with diabetes, covered in the supplements section. The record on vitamin D is mixed: observational studies link low blood vitamin D to type 2 diabetes risk, but in a trial of 2,423 adults at high risk, 4,000 IU a day for a median of 2.5 years did not lower new diabetes diagnoses by a statistically significant margin.25
The thyroid link to insulin resistance
Evidence: an endocrinology review and Ray Peat's primary writing. The signs list draws on clinical references and Broda Barnes's book.
A review in the Journal of Thyroid Research lays out how thyroid hormone affects glucose use. In hypothyroidism, muscle and fat take up less glucose, reduced blood flow slows the delivery of glucose to tissues, and less GLUT4 transporter is available at the cell surface.8 The review ties those changes to insulin resistance in people with low thyroid function.
Peat described a connection running the other way as well. In his diabetes article he wrote that liver cells need glucose to produce the active T3 form of thyroid hormone, so a state in which cells absorb glucose poorly will tend to produce hypothyroidism.19 He also noted that adrenaline runs high in hypothyroidism and releases free fatty acids from storage, which connects back to the Randle argument above.19 If you have been told your cholesterol is high, the thyroid connection is covered in detail in this article on cholesterol and thyroid.
Signs of low thyroid function described in clinical references
None of the signs below is specific to the thyroid, and a list cannot diagnose anything.
- Fatigue that persists after a full night of sleep
- Cold hands and feet, or feeling cold when others are comfortable
- Dry skin, brittle nails, and thinning of the outer third of the eyebrows
- Weight gain that does not respond to reasonable diet changes
- Constipation or slow digestion
- Low mood or brain fog
- Low libido or irregular menstrual cycles
- Puffiness in the face, especially on waking
- A slow resting pulse, or a waking underarm temperature below 97.8°F (36.6°C), which Broda Barnes used as a screening marker26
- Hoarseness or a weak voice
- Slow recovery from exercise and frequent muscle aches
These signs overlap with other conditions, so lab testing is how the question gets settled. Panels described as full usually include TSH, free T4, free T3, and reverse T3. A physician can order one, and direct-to-consumer labs sell the same panels in most states, though a result still needs a clinician to read it against symptoms and history. Prescription thyroid hormone, including natural desiccated thyroid, is a physician decision. The current regulatory status of desiccated thyroid is covered in this update.
Stress, trauma, and glucose
Evidence: a meta-analysis of observational studies, a sleep-restriction trial, and two clinical books.
Endocrinology describes cortisol and adrenaline as hormones that raise blood glucose as part of their normal job. They signal the liver to release stored glucose so muscles have fuel for a physical response, and under chronic stress that signal stays on. A meta-analysis pooling studies of adverse childhood experiences found that people who reported neglect in childhood had 92 percent higher odds of type 2 diabetes as adults, with smaller but still significant increases for physical and sexual abuse.7 Those studies are observational, so they show an association and cannot prove cause. The sleep-restriction study above showed the same hormonal pattern, raised evening cortisol alongside worsened glucose tolerance, in healthy men after less than a week.4
Two clinicians have written at length on this. Bessel van der Kolk, in The Body Keeps the Score, describes how unresolved trauma keeps the nervous system in a defensive state that alters hormone output and digestion.20 Gabor Maté, in The Myth of Normal, argues that chronic illness including metabolic disease often tracks back to early adversity and unmet emotional need, and that treatment which ignores this addresses only part of the problem.21 Both are clinical arguments built on case work and the research they cite, not controlled trials of trauma treatment for diabetes. The population data above is what supports their premise.
If this section describes your own history, a licensed therapist trained in trauma is the appropriate support, and the crisis line note in the disclaimer applies.
Food order, vinegar, and the after-dinner walk
Evidence: three randomized crossover trials in adults with insulin resistance or type 2 diabetes.
Biochemist Jessie Inchauspé popularized a set of meal habits in Glucose Revolution that she calls glucose hacks.22 The book is aimed at a general audience, but the habits themselves come from clinical trials, and those trials are what this section reports.
Vegetables and protein before starch. In a crossover study at Weill Cornell, 11 adults with type 2 diabetes ate the same 628-calorie meal on two days one week apart. On one day they ate the bread and orange juice first. On the other they ate the vegetables and chicken first and the carbohydrate last. Eating carbohydrate last cut the glucose rise at 30 minutes by 28.6 percent and at 60 minutes by 36.7 percent, and cut insulin at the 60-minute mark by roughly half, with order as the only variable that changed.2 Meal pace is a separate variable, covered in the article on eating slowly and GLP-1.
Vinegar before a high-carbohydrate meal. Carol Johnston's group at Arizona State gave 20 grams of apple cider vinegar diluted in 40 grams of water before a bagel-and-juice meal to 29 adults, some insulin sensitive, some insulin resistant, and some with type 2 diabetes. Post-meal insulin sensitivity improved by 34 percent in the insulin-resistant group and 19 percent in the diabetes group.3 Vinegar is acidic, and the trial did not give it undiluted.
A 10-minute walk after each meal. In the Reynolds trial from the causes section, 10 minutes of walking after each main meal lowered post-meal glucose more than a single 30-minute walk, with a 22 percent drop after the evening meal.1
Inchauspé also recommends a savory breakfast in place of a sweet one, on the reasoning that a carbohydrate-only first meal sets up a spike-and-crash pattern for the day. That specific claim has less direct trial support than the three habits above, though it follows the same logic as the food-order data.
Keto, glucose readings, and thyroid hormone
Evidence: a 1976 metabolic ward study in humans, plus Ray Peat's primary writing. The final paragraph is my opinion and is labeled as such.
A ketogenic diet removes the fuel that produces the largest glucose spike, so it can flatten readings in the short term. I ate this way for over a year as an experiment and would not do that again. What the readings do not show is what happens to thyroid output when carbohydrate stays low.
In 1976, Spaulding and colleagues put obese adults on 800-calorie diets in which carbohydrate ranged from zero to 100 percent of calories. Total fasting dropped serum T3 by 53 percent. A zero-carbohydrate diet at 800 calories dropped T3 by 47 percent within two weeks, nearly the same as fasting. Diets with the same calories but at least 50 grams of carbohydrate produced no significant change in T3.9 The authors concluded that dietary carbohydrate is a regulatory factor for T3 production in humans. The subjects were calorie restricted, so a well-fed ketogenic diet may not produce a drop of the same size, but the direction of the effect is documented.
Peat's objection ran along the same line: in his article on glycemia he wrote that when sugar is missing from the diet, stored glycogen covers a few hours to a day, after which the body breaks down protein to make glucose. He added that protein eaten without carbohydrate lowers blood sugar and sets off a stress response involving adrenaline and cortisol.27 On that reading, a diet that lowers T3 while improving glucose readings creates a second problem while it addresses the first.
My view, which is an opinion and comes from no trial: if someone uses this diet at all, the version I see as carrying less of that risk is short, high in protein, free of seed oils, and followed by a return to moderate carbohydrate. Over months and years I prefer a balanced-carbohydrate diet built around the food-order habits above. A ketogenic diet prescribed for a medical condition is a matter for the clinician who prescribed it.
What Ray Peat wrote about food, thyroid, and blood sugar
Evidence: Ray Peat's primary writing. These are his positions, with no clinical trial behind them as a set. Prescription thyroid hormone is outside the scope of this article.
Peat's diabetes article describes the diet he favored as high in protein and low in unsaturated fat. He wrote that milk, cheese, eggs, shellfish, fruit, and coconut oil should make up a major part of it, and he named salt among the supplements he considered safest.19 In the same article he wrote that unsaturated oils suppress the thyroid, and that eating fruit, coconut oil, and salt alongside protein reduces the blood sugar drop that protein alone can cause.19 A second article names liver as a rich source of B vitamins and limits it to about one meal a week, because he considered larger amounts suppressive to the thyroid.24
These are food choices, not a treatment protocol, and they do not replace testing or a physician's judgment. If a thyroid panel comes back low, the treatment conversation belongs with your doctor, and the article on hypothyroidism and weight loss covers what to bring to that appointment.
Herbs studied for blood sugar and insulin resistance
Evidence: ranges from a 27-trial meta-analysis (berberine) to a single rat study (kutki). Each entry states which.
Herbs supplement the diet and movement habits above. Several of these lowered glucose further when trials added them to oral diabetes drugs, so the medication check in the disclaimer applies to every entry in this section. The preparation methods referenced below are covered in this guide to herbal preparations.
Most of the trials below tested extracts, and an extract is a different product from the whole herb. Extracts are often standardized to a single constituent, which may not be the one behind the plant's traditional use. The trial record is also thin for a practical reason: whole plants cannot be patented and human trials are expensive, so few get funded. Traditional use counts as data too, and each entry says which kind of evidence it rests on.
Berberine
Evidence tier: meta-analysis of randomized trials. Berberine is an alkaloid extracted from the roots and bark of Oregon grape (Mahonia aquifolium), goldenseal (Hydrastis canadensis), or the Chinese herbs Coptis and Phellodendron. A 2015 meta-analysis pooled 27 randomized trials, 17 of them in type 2 diabetes with 1,366 patients. Berberine combined with lifestyle changes lowered fasting glucose, post-meal glucose, and HbA1c more than lifestyle changes alone, and berberine added to oral diabetes drugs lowered them more than the drugs alone.15 The authors rated the included trials as low to moderate quality, and most were published in Chinese journals, so the pooled result supports the direction of the effect more firmly than its exact size.
Gymnema (Gymnema sylvestre)
Evidence tier: small open-label clinical studies from one research group. The Hindi name gurmar translates as sugar destroyer, and the leaf does block sweet-taste receptors on the tongue for a period after chewing, which is why it appears in craving formulas. The clinical data comes from Madras University in 1990. In 22 adults with type 2 diabetes already on oral medication, 400 mg a day of a water-soluble leaf extract for 18 to 20 months lowered blood glucose and HbA1c.10 The study was not blinded or placebo controlled, and the work has not been replicated at scale, so gymnema has far weaker evidence than berberine.
Ceylon cinnamon (Cinnamomum verum)
Evidence tier: meta-analysis of randomized trials, with a caveat. A 2013 meta-analysis of 10 randomized trials with 543 patients found that cinnamon at 120 mg to 6 grams a day lowered fasting glucose by an average of 24.6 mg/dL, along with total cholesterol, LDL, and triglycerides.11 It found no significant change in HbA1c, and the heterogeneity between trials was high. Most of those trials used cassia cinnamon, not Ceylon. The species affects daily use because cassia bark carries substantial coumarin, a compound that toxicology studies link to liver injury at high chronic intake, while an analysis of authenticated bark samples found only traces in true cinnamon.12 For that reason I reach for Ceylon when cinnamon is used every day. The full monograph is on the cinnamon materia medica page.
Bitter melon (Momordica charantia)
Evidence tier: Cochrane review, no significant effect. Bitter melon has a long history in Ayurvedic and Chinese practice for diabetes, and it contains compounds with insulin-like activity in laboratory work. The human trials have not borne that out. A 2012 Cochrane review found four randomized trials with 479 participants, none longer than three months, and found no statistically significant difference in glucose control between bitter melon and placebo.13 The reviewers rated the risk of bias as high and the preparations as too variable to pool. It is a nourishing bitter vegetable whose blood sugar claims are ahead of its evidence.
Kutki (Picrorhiza kurroa)
Evidence tier: animal studies only. Kutki is a bitter Ayurvedic root used for liver support, and K.P. Khalsa describes its role in blood sugar as helping the liver store glucose as glycogen.23 A rat study from Banaras Hindu University measured liver glycogen directly. Diabetic rats given a standardized aqueous extract for 14 days showed lower fasting glucose, improved lipid profiles, and higher liver glycogen than untreated diabetic rats.14 A follow-up from the same group found higher insulin levels and more GLUT4 transporter in muscle. I have not found a human trial, so kutki is a traditional choice with a plausible mechanism and no clinical data.
Marshmallow root (Althaea officinalis)
Evidence tier: traditional use. Marshmallow root is a demulcent. Its mucilage coats the digestive tract, and in a cold infusion that mucilage stays intact. Viscous fibers in general slow the passage of carbohydrate through the gut, which is the reasoning behind including it here, but I have not found a human trial of marshmallow root on post-meal glucose. Its traditional use is for the gut, and that is how I use it.
Cautions on record for these herbs
Additive glucose lowering. In the berberine meta-analysis, adding berberine to oral diabetes drugs lowered glucose further than the drugs alone.15 That finding is the basis for the concern about blood sugar dropping too low when glucose-lowering herbs and drugs are combined.
Drug metabolism. In a crossover study in healthy men, berberine at 300 mg three times a day for two weeks reduced the activity of CYP2D6, CYP2C9, and CYP3A4, liver enzymes that clear many common medications.28 A pharmacist or clinical herbalist can check any herb in this section against your own medication list.
Supplements with randomized trial data
Evidence: meta-analyses and systematic reviews of randomized controlled trials. Amounts are what the trials used and are not recommendations.
Magnesium. A meta-analysis of nine double-blind trials in 370 adults with type 2 diabetes found that oral magnesium at a median of 360 mg a day for four to 16 weeks lowered fasting glucose, with no significant effect on HbA1c over that short window.18 Magnesium status is something a clinician can test.
Chromium. A systematic review of 41 randomized trials found that chromium supplementation lowered HbA1c by 0.6 percentage points and fasting glucose by 18 mg/dL in people with type 2 diabetes, with no effect in people without diabetes.17 Almost half the trials were rated poor quality, and the larger effects clustered in the weaker studies.
Alpha-lipoic acid. A 2018 meta-analysis of randomized trials in people with metabolic disease found that alpha-lipoic acid improved fasting glucose, insulin, and HOMA-IR, and lowered triglycerides, total cholesterol, and LDL.16 The authors noted wide variation in dose and duration across the included trials.
The 10-minute walk after dinner is the simplest item in this article to try: it costs nothing, and the trial behind it was run in people who already had type 2 diabetes. The rest of the Ray Peat food and thyroid material is on the Ray Peat hub.
Frequently asked questions
What causes insulin resistance?
Published studies tie insulin resistance to more than diet. The trials and population studies covered above link it to sleep restriction, long sitting time, chronic stress hormones, low thyroid function, statin use, and BPA exposure. Each of these is an association or a short-term trial finding, and none of them is a diagnosis.
Can low thyroid cause insulin resistance?
An endocrinology review describes how hypothyroidism reduces glucose uptake in muscle and fat, slows glucose delivery through reduced blood flow, and lowers the amount of GLUT4 transporter at the cell surface.8 A thyroid panel ordered and read by a clinician is how low thyroid function is confirmed.
Does walking after meals lower blood sugar?
In a randomized crossover trial in adults with type 2 diabetes, a 10-minute walk after each main meal lowered post-meal glucose by 12 percent compared with a single 30-minute walk, and by 22 percent after the evening meal.1
Can cinnamon lower blood sugar?
A 2013 meta-analysis of 10 randomized trials found that cinnamon lowered fasting glucose by an average of 24.6 mg/dL in people with type 2 diabetes, with no significant change in HbA1c.11 Most of those trials used cassia cinnamon, which contains far more coumarin than Ceylon.12
Does a keto diet lower thyroid hormone?
In a 1976 study, an 800-calorie diet with no carbohydrate lowered T3 by 47 percent in two weeks, and diets with the same calories and at least 50 grams of carbohydrate did not.9 The subjects were calorie restricted, so that study cannot say how large the effect is on a well-fed ketogenic diet.
Which herb has the most evidence for blood sugar?
Of the herbs covered here, berberine has the most human data: a 2015 meta-analysis of 27 randomized trials.15 The trials were rated low to moderate quality, and a separate study found that berberine slows three liver enzymes that clear medications, so a pharmacist check comes first.28
Sources
- Reynolds AN, Mann JI, Williams S, Venn BJ. Advice to walk after meals is more effective for lowering postprandial glycaemia in type 2 diabetes mellitus than advice that does not specify timing: a randomised crossover study. Diabetologia. 2016;59(12):2572-2578. doi:10.1007/s00125-016-4085-2 ↩
- Shukla AP, Iliescu RG, Thomas CE, Aronne LJ. Food order has a significant impact on postprandial glucose and insulin levels. Diabetes Care. 2015;38(7):e98-e99. doi:10.2337/dc15-0429 ↩
- Johnston CS, Kim CM, Buller AJ. Vinegar improves insulin sensitivity to a high-carbohydrate meal in subjects with insulin resistance or type 2 diabetes. Diabetes Care. 2004;27(1):281-282. doi:10.2337/diacare.27.1.281 ↩
- Spiegel K, Leproult R, Van Cauter E. Impact of sleep debt on metabolic and endocrine function. Lancet. 1999;354(9188):1435-1439. doi:10.1016/S0140-6736(99)01376-8 ↩
- Sattar N, Preiss D, Murray HM, et al. Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet. 2010;375(9716):735-742. doi:10.1016/S0140-6736(09)61965-6 ↩
- Lang IA, Galloway TS, Scarlett A, et al. Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults. JAMA. 2008;300(11):1303-1310. doi:10.1001/jama.300.11.1303 ↩
- Huang H, Yan P, Shan Z, et al. Adverse childhood experiences and risk of type 2 diabetes: a systematic review and meta-analysis. Metabolism. 2015;64(11):1408-1418. doi:10.1016/j.metabol.2015.08.019 ↩
- Brenta G. Why can insulin resistance be a natural consequence of thyroid dysfunction? Journal of Thyroid Research. 2011;2011:152850. doi:10.4061/2011/152850 ↩
- Spaulding SW, Chopra IJ, Sherwin RS, Lyall SS. Effect of caloric restriction and dietary composition on serum T3 and reverse T3 in man. Journal of Clinical Endocrinology and Metabolism. 1976;42(1):197-200. doi:10.1210/jcem-42-1-197 ↩
- Baskaran K, Kizar Ahamath B, Radha Shanmugasundaram K, Shanmugasundaram ERB. Antidiabetic effect of a leaf extract from Gymnema sylvestre in non-insulin-dependent diabetes mellitus patients. Journal of Ethnopharmacology. 1990;30(3):295-300. doi:10.1016/0378-8741(90)90108-6 ↩
- Allen RW, Schwartzman E, Baker WL, Coleman CI, Phung OJ. Cinnamon use in type 2 diabetes: an updated systematic review and meta-analysis. Annals of Family Medicine. 2013;11(5):452-459. doi:10.1370/afm.1517 ↩
- Wang YH, Avula B, Nanayakkara NPD, Zhao J, Khan IA. Cassia cinnamon as a source of coumarin in cinnamon-flavored food and food supplements in the United States. Journal of Agricultural and Food Chemistry. 2013;61(18):4470-4476. doi:10.1021/jf4005862 ↩
- Ooi CP, Yassin Z, Hamid TA. Momordica charantia for type 2 diabetes mellitus. Cochrane Database of Systematic Reviews. 2012;(8):CD007845. doi:10.1002/14651858.CD007845.pub3 ↩
- Husain GM, Singh PN, Kumar V. Antidiabetic activity of standardized extract of Picrorhiza kurroa in rat model of NIDDM. Drug Discoveries and Therapeutics. 2009;3(3):88-92. PMID 22495535 ↩
- Lan J, Zhao Y, Dong F, et al. Meta-analysis of the effect and safety of berberine in the treatment of type 2 diabetes mellitus, hyperlipemia and hypertension. Journal of Ethnopharmacology. 2015;161:69-81. doi:10.1016/j.jep.2014.09.049 ↩
- Akbari M, Ostadmohammadi V, Lankarani KB, et al. The effects of alpha-lipoic acid supplementation on glucose control and lipid profiles among patients with metabolic diseases: a systematic review and meta-analysis of randomized controlled trials. Metabolism. 2018;87:56-69. doi:10.1016/j.metabol.2018.07.002 ↩
- Balk EM, Tatsioni A, Lichtenstein AH, Lau J, Pittas AG. Effect of chromium supplementation on glucose metabolism and lipids: a systematic review of randomized controlled trials. Diabetes Care. 2007;30(8):2154-2163. doi:10.2337/dc06-0996 ↩
- Song Y, He K, Levitan EB, Manson JE, Liu S. Effects of oral magnesium supplementation on glycaemic control in type 2 diabetes: a meta-analysis of randomized double-blind controlled trials. Diabetic Medicine. 2006;23(10):1050-1056. doi:10.1111/j.1464-5491.2006.01852.x ↩
- Peat R. Diabetes, scleroderma, oils and hormones. raypeat.com. raypeat.com/articles/articles/diabetes.shtml ↩
- van der Kolk B. The Body Keeps the Score: Brain, Mind, and Body in the Healing of Trauma. Viking; 2014. ↩
- Maté G, Maté D. The Myth of Normal: Trauma, Illness, and Healing in a Toxic Culture. Avery; 2022. ↩
- Inchauspé J. Glucose Revolution: The Life-Changing Power of Balancing Your Blood Sugar. Simon & Schuster; 2022. ↩
- Khalsa KPS, Tierra M. The Way of Ayurvedic Herbs. Lotus Press; 2008. ↩
- Peat R. Glucose and sucrose for diabetes. raypeat.com. raypeat.com/articles/articles/glucose-sucrose-diabetes.shtml ↩
- Pittas AG, Dawson-Hughes B, Sheehan P, et al. Vitamin D supplementation and prevention of type 2 diabetes. New England Journal of Medicine. 2019;381(6):520-530. doi:10.1056/NEJMoa1900906 Funded by the National Institute of Diabetes and Digestive and Kidney Diseases and others. ↩
- Barnes BO, Galton L. Hypothyroidism: The Unsuspected Illness. Thomas Y. Crowell; 1976. ↩
- Peat R. Glycemia, starch, and sugar in context. raypeat.com. raypeat.com/articles/articles/glycemia.shtml ↩
- Guo Y, Chen Y, Tan ZR, Klaassen CD, Zhou HH. Repeated administration of berberine inhibits cytochromes P450 in humans. European Journal of Clinical Pharmacology. 2012;68(2):213-217. doi:10.1007/s00228-011-1108-2 ↩