Sugar usually means sucrose (half Glucose, half Fructose). Mainstream nutrition often treats all sugars as metabolic villains. For Ray Peat, sucrose supports oxidative metabolism when thyroid, protein, and minerals are adequate, and starch-heavy, seed-oil-rich diets do more harm than plain sugar.[1][2]

Sugar
Sucrose (table sugar) molecular structure
Sucrose (table sugar) molecular structure
Molecular formula C₁₂H₂₂O₁₁ (sucrose)
Type Disaccharide (glucose + fructose)
Glycemic index Moderate, lower than pure glucose or starch
Metabolism Hydrolyzed to glucose and fructose in the small intestine before absorption
Food sources Table sugar, fruit, honey, milk (as lactose, a different disaccharide)
Synonyms Sucrose, table sugar
Ray's verdict Generally helps
Supports oxidative metabolism when thyroid, protein, and minerals are adequate; sugar craving is usually a sign of hypothyroidism, not addiction

There is a great anti-sugar cult, with even moralistic overtones, equating sugar craving with morphine addiction. Sugar craving is usually caused by the need for sugar, generally caused by hypothyroidism.

— Ray Peat[3]

Fructose inhibits the stimulation of insulin by glucose, so this means that eating ordinary sugar, sucrose (a disaccharide, consisting of glucose and fructose), in place of starch, will reduce the tendency to store fat.

— Ray Peat[4]

Peat cited nineteenth-century physicians P. A. Piorry and William Budd, who added large amounts of sucrose to diabetic diets, as historical counterexamples to the idea that eating sugar causes diabetes.[2][1] See Fructose, Starch, Glucose, Harm reduction.

Dosing

[edit]

A daily diet that includes two quarts of milk and a quart of orange juice provides enough fructose and other sugars for general resistance to stress, but larger amounts of fruit juice, honey, or other sugars can protect against increased stress, and can reverse some of the established degenerative conditions.

I think a total for sugar up to ten ounces can be o.k., depending on your metabolic rate and needs. Budd and Piorry used up to 12 ounces per day therapeutically.

Appetite for sugar after stress is a reasonable guide to replenishing glycogen.[7]

Refined granulated sugar is very pure but carries no essential nutrients, making it a temporary support or winter substitute when good fruit or tolerable honey is scarce.[7] Brown sugar's mineral traces come with impurities he considered slightly toxic or allergenic; bleaching washes away Molasses residue, and the whitest grades were least likely to provoke reactions in his experience.[7] Coconut sugar heated dark may be more allergenic; unheated forms suit some people. Fruit remains his first choice when quality is good.[7]

When relying on refined sugar in poor fruit seasons, the priority is Milk, cheese, eggs, fruit, and occasional liver and seafood over starchy Vegetables; cooked greens and mushrooms could replace starchy sides.[7]

History/Etymology

[edit]

Sugar refining from sugarcane dates back over 2,000 years in South Asia, but sucrose wasn't isolated and characterized as a specific chemical compound until the work of 18th and 19th century chemists, including Andreas Marggraf's 1747 identification of the same sugar in beets as in cane. "Sucrose" itself, from French sucre plus the "-ose" sugar suffix, became the standard chemical name only in the late 19th century, once glucose, fructose, and sucrose were understood as chemically distinct.

The premise that meat, not sugar, built the human brain is itself contested. A 2026 modeling study spanning 4 million years of hominin evolution found dietary sugars from fruit and honey were positioned to supply the brain's obligatory glucose demand before cooking made starch digestible, putting sugars at over 25% of dietary energy across that span and making carbohydrate foods as central to brain evolution as animal foods.[8]

Structure/Chemical properties

[edit]

Sucrose (C₁₂H₂₂O₁₁) is a disaccharide formed from one glucose and one fructose unit joined by a glycosidic bond between their anomeric carbons, a linkage that makes sucrose a "non-reducing" sugar, unlike most other disaccharides. This bond is readily hydrolyzed by the enzyme sucrase in the small intestine, releasing free glucose and fructose for absorption.

Function/Mechanism of Action

[edit]

The body converts very little dietary carbohydrate to fat under normal conditions. A classic overfeeding study found that even with massive carbohydrate intake (up to 5000 kcal/day, 86% carbs), de novo lipogenesis only became substantial after glycogen stores were saturated at ~500 g; even then, fat gain from carbohydrate was far less than from dietary fat itself.[9] Under typical mixed-diet conditions, net de novo lipogenesis accounts for <5% of daily fat storage, meaning the fear that dietary sugar is efficiently converted to body fat is not supported by the metabolic evidence.[9]

When yeasts lack sugar they can send filaments into the intestinal wall; in very weak people they may reach the bloodstream.[7] Adequate sugar with Milk, cheese, and Fruit was his preferred pattern. Meat as the main protein can skew phosphorus high relative to Calcium in his notes.[7]

If the rest of your diet is good, the energy bursts from sugar should level off, and become a steady increased metabolic rate.

— Ray Peat[10]

The references on Robert Lustig's charts do not support his framing of fructose as uniquely toxic.[7]

Medical uses/Effects

[edit]
  • Sugar is addictive: Peat equated the moral panic with misread craving from Hypothyroidism, not morphine-like addiction.[7] A 2016 review found little evidence for sugar addiction in humans; addiction-like bingeing in animals appeared only with intermittent access to sweet food.[11][12]
  • Sugar and thinking: in a systematic review of 11 neuroimaging studies, a glucose drink changed brain markers of episodic memory and attention in all but one, though only five showed measurable cognitive gains.[13]
  • Sugar makes kids hyperactive: A 1995 JAMA meta-analysis (23 experiments, 16 papers) found no consistent effect on behavior or cognition.[14]
  • Sugar causes diabetes: Peat traced the belief to pre-Bernard medicine; hyperglycemia in obesity overlaps cortisol and insulin-resistance patterns he tied more to PUFA and chronic stress than to sucrose alone.[2][1]
  • Avoid fruit when dieting: Peat cited inverse associations between fruit intake and diabetes versus positive associations for bread and pasta in epidemiology he reproduced.[1]
  • Sugar causes cancer: Cancer cells are adapted to run on protein and fats, not on glucose alone.[15] Cancer Research UK states there is no evidence that a sugar-free diet lowers cancer risk or improves survival.[16] Mouse work on ketogenic diets and metastasis has been reported in university press coverage; mechanisms remain contested.[17] In mice carrying human breast cancer xenografts, a ketone body increased tumor growth about 2.5-fold and lactate increased lung metastases about 10-fold.[18]

Artificial sweeteners

[edit]

Non-nutritive sweeteners (aspartame, sucralose, saccharin, and others) taste sweet without sugar calories. Metabolic and gut effects are debated; they do not replace sugar's fuel role under stress. A randomized controlled trial in 120 healthy adults given saccharin, sucralose, aspartame, or stevia for 2 weeks (at doses below the acceptable daily intake) found each sweetener distinctly altered the gut and oral microbiome and plasma metabolome, and that saccharin and sucralose specifically impaired glucose tolerance, an effect that tracked with each person's individual microbiome shift rather than hitting everyone equally.[19]

Stevia

[edit]

Stevia (Stevia rebaudiana) leaf extracts and steviol glycosides such as rebaudioside A are used as non-sugar sweeteners. Commercial extracts can be arsenic-contaminated; interview notes otherwise often treat it as comparatively low-risk among non-sugar sweeteners.[20] In a one-week crossover study of 16 healthy volunteers, whole-leaf stevia raised systolic blood pressure from 114.5 ± 12.7 to 119.9 ± 12.9 mmHg and diastolic from 70.8 ± 9.4 to 75.7 ± 9.6 mmHg. Urinary free cortisol rose from 91.8 ± 49.1 to 125.7 ± 60.5 nmol/day; the urinary free cortisol/cortisone ratio rose from 1.73 ± 0.78 to 2.65 ± 1.03. Morning salivary cortisol also rose after stevia; sugar placebo did not. Authors suggested possible inhibition of 11β-HSD2 (less conversion of cortisol to cortisone).[21] This is a small, short trial of whole-leaf stevia, not purified rebaudioside A alone; broader steviol-glycoside blood-pressure meta-analyses often report null or blood-pressure-lowering effects, so the cortisol finding should be weighed against dose, preparation, and duration.

Sucralose

[edit]

Sucralose is a chlorinated sucrose derivative. Heat stability makes it common in processed foods. Same preference hierarchy applies: real sugar for fuel, novelty sweeteners optional. Gut and metabolic data are mixed across studies.

Xylitol

[edit]

Xylitol is a sugar alcohol. It has dental benefits in some studies and GI side effects in excess. Not a whole-food sugar; GI distress and metabolic ambiguity make fruit sugar, sucrose, and honey cleaner defaults when calories from carbs are the goal.

Aspartame

[edit]

Aspartame breaks down to phenylalanine, aspartate, and methanol in small amounts. Prefer sugar from fruit, sucrose, and honey when calories and metabolic support are the goal; diet soda habits can maintain sweet preference without fueling oxidation.

Cinnamon

[edit]

Cinnamon is a bark spice used for flavor and blood-sugar marketing. Cassia cinnamon carries more coumarin than Ceylon cinnamon; food-level amounts are the practical guide.

Side/Adverse effects

[edit]

Refined sugar's main real drawback isn't sugar toxicity itself but nutrient dilution: it supplies energy without the minerals, protein, or other nutrients that whole foods like fruit or milk carry alongside their sugar content, which is why it's treated here as a temporary or supplementary source rather than a dietary foundation.[7] Impure brown or dark forms carry the added risk of allergenic/irritant residues from incomplete refining.[7]

High-carb framing

[edit]

"High carb" in this framework means ample carbohydrate from fruit, juice, sugar, honey, sucrose, and safe starches, set against modern low-carb fashion, not unlimited processed sweets. Mainstream nutrition treats sucrose and starch-heavy diets as metabolic villains without good evidence; adequate carbohydrate supports oxidative metabolism when thyroid, protein, and minerals are also adequate. He also cited 19th-century physicians who added large amounts of sucrose to diabetic patients' diets as a historical counterexample to the modern assumption that sugar intake causes diabetes.[22] Adequate carbohydrate lowers the stress-hormone need that shows up when the body has to run on free fatty acids instead; see Keto for the contrast case. Pair carbohydrate with protein and minerals rather than eating it in isolation.

Blood sugar

[edit]

Blood sugar is circulating glucose. Both lows and highs cause symptoms; continuous monitors make patterns visible.

Context

[edit]

High blood sugar appears alongside high blood pressure and obesity in Cushing's syndrome, driven by excess cortisol - the same cluster now called metabolic syndrome. The common explanation blames obese type 2 diabetes on eating too much sugar, especially fructose, though starch is the only common carbohydrate with no fructose at all.[23]

Stable glucose from regular mixed meals supports temperature and mood. Extreme low-carb swings into adrenaline are common. Medical diabetes care remains mandatory when diagnosed.

Practice

[edit]

A stable glucose supply matters more than any single reading. Peat cited Bernardo Houssay's finding that animals fed once a day got fatter and more diabetic on the same calories than animals fed three or more times a day. A modern human trial found the same pattern: 9 healthy women followed a randomized crossover diet, eating either 6 regular meals a day or an irregular 3-9 meals a day for two weeks each. The irregular pattern produced a significantly higher insulin response (peak and total insulin output) to a test meal, plus higher fasting total and LDL cholesterol, despite fasting glucose and insulin being unaffected.[24] A much larger cross-sectional study of over 4,000 UK schoolchildren found those who skipped breakfast had 26% higher fasting insulin and 27% greater insulin resistance than daily breakfast-eaters, independent of body fat.[25]

The famous Argentine biologist Bernardo ... in the 1940s, I think he was the first one to show that if he fed his animals only once a day, they not only tended to get fat on the same amount of calories, but they had a high incidence of diabetes. But if you fed them at least three times a day or more, then they were very resistant to diabetes and were less fattened on a given number of calories. So more or less nibbling all the time is the safest thing. But if you have a really good diet and aren't under emotional pressure, then the person can get along on one or two meals a day.

On sugar-vs-starch timing, Peat's framing runs opposite the common low-carb advice: fruit sugar (mostly fructose plus potassium) triggers less insulin and less downstream cortisol than starch or a large meat-heavy meal does, because fructose metabolism doesn't require insulin the way glucose from starch does.

One of the reasons that the single meal eaters tend to get fat and diabetic is that it triggers a great surge of insulin and the insulin then triggers cortisol. And so if you can eat foods that don't trigger insulin, that's the ideal thing. And fruit happens to be the the best single type of food for not triggering the stress reaction because it combines very small amounts of protein with large amounts of sugar. And the minerals potassium happens to handle sugar in place of insulin. And the fructose component of, of fruit. Sugar doesn't require insulin. So eating a lot of fruit, even in one meal a day, produces a much smaller amount of insulin, obesity and cortisol than eating, for example, just one big meal of meat and potatoes.

— Ray Peat[27]

Practical takeaway: eat something every few hours rather than relying on one or two large meals, favor fruit/orange juice over starch as the carbohydrate source at a given meal when the goal is a smaller insulin/cortisol response, and treat "going long without eating" as tolerable only once temperature and pulse are already solid, not as a routine goal.

The stress cascade

[edit]

Falling blood sugar is an upstream stress signal. When liver glycogen is depleted, adrenaline mobilizes fatty acids and cortisol converts tissue protein into amino acids that can be used to make glucose. The response helps preserve glucose for vital organs. Persistent activation raises the metabolic cost of maintaining blood sugar.[28]

The liver and thyroid form a feedback loop. Available glucose supports the liver's production of active T3, while low thyroid function reduces glycogen storage and makes overnight drops more likely. Low temperature, cold extremities, hunger, and early waking can occur together in hypothyroid states.[29][30]

Free fatty acids add a second part to the cycle. The Randle effect can inhibit glucose oxidation, so a high blood glucose reading may coexist with poor glucose use inside cells.[31] Niacinamide lowers free fatty acids. Aspirin has broad anti-inflammatory actions. Diabetes treatment should be managed with a qualified clinician.[32][33]

Glycemia is blood glucose level and its regulation. Mainstream diabetes care centers insulin and the glycemic index of foods.

Degenerative diseases linked to hyperglycemia are only indirectly related to insulin, and the glycemic index has little physiological meaning as a clinical tool, according to Ray Peat's article Glycemia, starch, and sugar in context.[34]

Insulin itself has been found to account for only about 8% of the "insulin-like activity" of the blood, with potassium being probably the largest factor.

— Ray Peat[35]

Starch and the glycemic index

[edit]

Dietitians promoted "complex carbohydrates" as slower and safer than sugars; in 1981 David Jenkins' glycemic index measurements put starch above sucrose for many foods.[36][37] The ideology that diabetes is caused by eating too much sugar diverted attention from PUFA-driven insulin resistance and pancreatic damage.[38]

Orange juice and sucrose have a lower glycemic index than white bread in published glycemic index tables, yet dietitians often oppose juice while promoting bread.[39] Fruit consumption associates inversely with diabetes in epidemiology; bread and pasta associate positively.[40]

Protein, stress hormones, and blood sugar

[edit]

Glucagon, Cortisol, adrenalin, growth hormone, and Thyroid hormone raise blood sugar; hyperglycemia is often labeled "diabetes" without measuring these factors.[41] Large protein without carbohydrate can drop blood sugar sharply, triggering adrenalin and cortisol that mobilize fatty acids and break down tissue protein.[42]

Unsaturated fatty acids, adrenalin, and cortisol cause insulin resistance.[43] Bernardo Houssay's work and Philip Randle's fat-glucose antagonism support coconut oil and sugar as protective themes in animal models Peat cited.[44]

Soft drinks

[edit]

Coca-Cola is a sucrose- (or high-fructose-corn-syrup-) sweetened soda that shows up repeatedly in Ray Peat's writing as a practical source of quick sugar and sodium, not as a food to avoid on principle. Its sugar content, not its brand or "junk food" status, is what matters metabolically.

Metabolic effects

[edit]

Feeding animals a normal diet with added Coca-Cola, or an equivalent amount of sucrose, let them increase calorie intake by 50% without increasing weight gain (Bukowiecki, et al., 1983).[45] A separate experiment found the same pattern directly: rats fed sucrose or Coca-Cola alongside standard chow, allowed to eat freely, consumed 50% more calories than rats on the standard diet alone without gaining extra weight.[46] Sugar in this context raises metabolic rate rather than simply adding calories, which is why the extra intake doesn't translate to extra fat.

Dietitians commonly argue against orange juice because its glycemic index matches Coca-Cola's, without extending the same logic to argue for substituting either one for white bread or other starches, which have a comparable or higher glycemic index.[47]

Practical uses

[edit]

Coca-Cola (like orange juice and ice cream) can provide fast relief from the hypoglycemia symptoms of liver malfunction. Its sodium content helps absorb the sugar and supports blood volume restoration. Pepsi specifically has been recommended by the World Health Organization for rehydrating babies with diarrhea, where hypovolemia (blood thickening from water loss) is a concern.[48]

Peat also relayed anecdotal reports of people recovering from depression and migraines simply by adding fruit juice or Mexican Coca-Cola (cane-sugar-sweetened, unlike U.S. high-fructose-corn-syrup Coca-Cola) to their diet, framing these as signs of reversing a slowed, inhibited metabolism rather than a specific drug-like effect of the beverage itself.

Currently I'm hearing reports from several people who just by introducing fruit juice or even Mexican Coca-Cola suddenly they recovered from various things, depression, migraines, all signs of slowing inhibited metabolism.

— Ray Peat[49]

Research notes

[edit]

A 15-day study gave mice free access to undiluted Coca-Cola or Pepsi. Testosterone levels nearly doubled and testicle size/volume increased in the undiluted-soda groups, with androgen receptor mRNA expression in the testes up 60-78%. The study authors proposed caffeine as the mechanism, but the caffeine dose involved (~1 mg/kg human-equivalent) is far below doses of 80-100mg/day that have never been shown to produce this scale of effect in males, leaving sugar content as the more plausible driver. Other research links sugar intake to improved male fertility.[50]

Fruit

[edit]

Fruit is plant sugar with water, potassium, vitamin C, and fiber. In the bioenergetic pattern it is a primary fuel: fructose and glucose that support oxidation and end stress lipolysis when protein and minerals are present.

Evolutionary role

[edit]

Fruit sugars may have been the main fuel behind brain growth across hominin evolution, not just a modern dietary preference. See Human evolution.

Ranking

[edit]

Ripe fruit and juice beat dry cereal and seed-oil snacks for anti-stress carbohydrate. Industrial "fruit snacks" with oil and starch are not fruit. See Sugar, Fructose, Orange juice, Honey. The China Kadoorie Biobank, following 462,342 adults free of chronic disease for about 7 years, found that people who ate fresh fruit 4 or more days a week had 27% lower all-cause mortality than those who almost never ate fruit, with 34% lower cardiovascular mortality and 42% lower COPD mortality, and the benefit scaled with how much fruit was eaten.[51]

Sugar composition and blood sugar

[edit]

Fruits contain about the same ratio of fructose to glucose as table sugar, whereas grains, beans, starches and potatoes are almost all glucose.[52] Pure fructose and sucrose produce less glycemia than glucose and starch, and the different health effects of fruits and grains cannot be reduced to their effect on blood sugar; pasta consumption is strongly associated with diabetes while fruit consumption has a strong inverse association.[53] The potassium and other minerals in fruit bypass much of the glycemic issue, and potassium itself has an insulin-like action.[54]

Whole fruit and diabetes

[edit]

In three large US cohorts, total whole fruit intake was only slightly protective against type 2 diabetes, and the association varied by fruit, from clearly protective for blueberries to slightly adverse for cantaloupe; fruit juice was associated with a higher risk.[55]

Ripeness and allergens

[edit]

Bananas and jackfruit are strong allergens, mangos, apples and pears are allergenic to some people, and poorly ripened fruit of any kind is best avoided.[56]

Tropical fruits such as papaya, pineapple and the custard apple family, together with tropical oils, are an ideal calorie source: low in iron, rich in vitamins and a good source of magnesium.[57] Many fruit juices supply minerals and antioxidants, grape juice, guava and mango among them, while carrot juice is best kept small because its carotene antagonizes thyroid function.[58]

Practice (fruit)

[edit]

Eat ripe fruit with meals or between them. Pair with milk, cheese, or eggs when a full meal is needed.

Glycogen

[edit]

Glycogen is stored glucose in chains, mainly in liver and muscle. Liver glycogen buffers blood sugar between meals. When it empties, the body liberates amino acids and free fatty acids and stress hormones rise.

Buffer against stress

[edit]

Full glycogen supports steady oxidation and lower adrenaline and cortisol demand. Empty glycogen is the door into fasting chemistry: tryptophan and cysteine release, lower thyroid effect, higher free fatty acids.[59] A human trial measured this directly: 16 patients scheduled for gallbladder surgery were randomized to receive or skip an overnight glucose infusion, and those given glucose entered surgery with 65% more liver glycogen than the overnight-fasted group, alongside lower circulating free fatty acids and a gluconeogenesis-favoring enzyme shift that was absent in the glucose-supported group.[60]

Practice (glycogen)

[edit]

Refill glycogen with regular carbohydrate: fruit, juice, honey, sucrose, milk. Protein without carbohydrate does not refill glycogen well.

Night snacks of milk and sugar or ice cream help some people hold glycogen through sleep. See Sugar, Milk, Ice cream, Thyroid.

Honey

[edit]

Honey is a mix of Fructose and Glucose with enzymes, minerals, and antimicrobial peptides. For Ray Peat, raw honey is a convenient metabolic fuel supporting Liver glycogen and Thyroid when paired with protein and Salt.[61]

In glycemic tables Peat reproduced, honey has moderate glycemic index, below pure glucose though context matters more than index alone.[62]

Simply eating sucrose was recently discovered to restrain the stress hormone system ("A new perspective on glucocorticoid feedback: relation to stress, carbohydrate feeding and feeling better," J Neuroendocrinol 13(9), 2001, KD Laugero).

Prefer traditional honey over high-fructose corn syrup industrial sweets. See Roadmap/03 - Diet, Sugar, Harm reduction.

Recipes

[edit]
Honey Cinnamon Iced Coffee
From ReciPeatsHoney Cinnamon Iced Coffee

Honey as a practical sweetener alongside coffee.

Coconut Oil Honey Chocolate
From ReciPeatsCoconut Oil Honey Chocolate

Honey paired with saturated fat.

All honey recipes

Anti-inflammatory effects

[edit]

Natural honey reduces C-reactive protein (CRP) and improves cardiovascular risk markers. A clinical trial comparing honey to sucrose in healthy and hyperlipidemic subjects found that honey significantly lowered CRP, homocysteine, cholesterol, and triglycerides compared to sucrose or dextrose.[64] A separate study confirmed that honey consumption lowered CRP by over 50% in subjects with elevated baseline levels, along with improvements in blood sugar and homocysteine.[65]

Wound healing and pain

[edit]

Treating deep wounds with honey or granulated sugar has been studied in controlled settings, including diabetic ulcers, infected wounds after heart surgery and the wounds of lepers; the treatment clears bacterial infection and speeds healing with little scarring.[66] In Africa, surgeons without antibiotics filled chest cavities with sugar, and the wounds did not become infected.[67]

Sucrose, and sometimes honey, is used to reduce pain in newborns during minor procedures such as injections, and it works in adults too.[68]

Some honey is allergenic, so a mild one is preferable; white sugar is similar with less allergy risk.[69]

Hypoglycemia

[edit]

Hypoglycemia is low blood sugar. In Ray Peat's framework it is not an isolated glucose problem but a direct driver of stress-hormone output, closely tied to hypothyroidism.

Adrenaline and cortisol

[edit]

Hypothyroid people are especially prone to hypoglycemia, and hypoglycemia itself directly triggers adrenaline release:[70]

Hypothyroid people are susceptible to hypoglycemia, and hypoglycemia increases adrenaline.

— Ray Peat[71]

A specific overnight pattern follows: because hypothyroid people store very little glycogen, blood sugar falls as soon as they stop eating for the night, triggering a stress-hormone response almost immediately after going to bed:

Blood sugar falls at night, and...hypothyroid people store very little sugar. As a result, adrenalin and cortisol begin to rise almost as soon as a person goes to bed.

— Ray Peat[72]

That overnight adrenaline/cortisol rise is part of why this framework treats night sweats, waking in the middle of the night, and poor sleep as blood sugar/thyroid problems as often as psychological ones.

Hypothyroidism

[edit]

Hypoglycemia was a recognized symptom of hypothyroidism in older endocrinology but is largely absent from modern textbooks and clinical workups.[73] A case report describes a type 2 diabetic patient with recurrent hypoglycemia that resolved entirely once undiagnosed hypothyroidism was treated with levothyroxine, after other causes (drug dosing, renal or hepatic impairment) were ruled out.[74] Broda Barnes made the same point clinically: a sluggish liver in hypothyroid patients cannot produce enough sugar from protein during stress, and restoring thyroid function corrects the hypoglycemia without needing special frequent-feeding diets.[75] Thyroidectomized rats show the same pattern experimentally: given daily doses of 0, 0.1, 2, or 25 mcg thyroxine per 100 g body weight, after 48-hour starvation the blood glucose drop and ketone-body rise were greatest in the group given no thyroxine, while the 25 mcg dose kept plasma insulin at the fed-state level even during starvation.[76]

Reactive hypoglycemia and violence

[edit]

Habitually violent and impulsive male offenders show a tendency toward reactive hypoglycemia on glucose tolerance testing, with a more rapid drop from hyperglycemia and faster rebound to baseline in those with intermittent explosive disorder specifically.[77] An 8-year follow-up of 49 violent offenders found the same underlying defect: those who reoffended violently had markedly lower non-oxidative glucose metabolism, meaning less glucose was being stored as glycogen, than those who did not reoffend. Substances that increase glycogen formation, rather than carbohydrate restriction, could lower hypoglycemia risk and reduce impulsive violence.[78]

Practice (hypoglycemia)

[edit]

Regular food, especially before bed, with protein and carbohydrate together, reduces the overnight blood sugar drop that drives this cascade. Supporting thyroid function to restore normal glycogen storage addresses the underlying susceptibility rather than just the symptom.

Within an hour or two of sleep the body may call for more sugar and turn on the stress hormones; a little salty snack helps the intestine absorb sugar and lowers those hormones, and a tablespoon of sugar or honey in a glass of milk usually restores sleep for a couple of hours.[79]

A sauna or hot bath raises the metabolic rate and can quickly deplete liver glycogen, and protein eaten without enough carbohydrate can also cause hypoglycemia, so frequent snacks of orange juice and milk help.[80] Acute hypoglycemia may call for a lot of sugar and suggests depleted adrenals, which need pantothenic acid, vitamin C, vitamin A, magnesium and potassium.[81]

Estrogen contributes to hypoglycemia by impairing the counterregulatory system, and serotonin, like noradrenalin, rises with hypoglycemia.[82]

Ketogenic diets

[edit]

Ketogenic diets cut carbohydrate until the body runs on ketones and free fatty acids instead of glucose. Marketing sells it as a metabolic cure-all; in Ray Peat's framework, sustained low blood sugar is itself a stress state. Chronically low glucose keeps cortisol elevated.[83]

The basic worry is that the cortisol level is going to be kept up, if you keep your glucose too low.

— Ray Peat[84]

The same stress state pulls cells away from oxidative metabolism.

The whole shift of stress and cancer is away from oxidation towards reduction.

— Ray Peat[85]

He identified free fatty acids specifically as blocking glucose oxidation at the enzyme level:

Fatty acids are right at the center of that by blocking the pyruvate dehydrogenase.

— Ray Peat[86]

A controlled trial found 3 days on a ketogenic diet (50% fat, 45% protein, 5% carbohydrate) raised resting beta-hydroxybutyrate to about 2.0 mmol/L and free fatty acids to about 1.0 mmol/L, with both pre- and post-exercise adrenaline, noradrenaline, and cortisol enhanced compared to a normal diet.[87]

A JAMA-published controlled feeding trial comparing three diets during weight-loss maintenance in previously obese young adults (low-fat/high-carbohydrate, low-glycemic-index, and very-low-carbohydrate/ketogenic) found the very-low-carbohydrate group had the highest urinary cortisol (71 vs. 50 μg/day on low-fat) and the lowest T3 (108 vs. 121 ng/dL on low-fat), despite also having the highest total energy expenditure; the low-fat, high-carbohydrate group had the lowest cortisol and the highest T3 of the three diets.[88]

In ten lean women who had eaten a ketogenic diet for at least six months, three weeks of adding carbohydrate back (about 199 g a day, same calories) raised free T3 by about 43%, and it fell again after three weeks back on the diet. TSH, T4, reverse T3 and resting metabolic rate did not change.[89]

In six healthy men fed the same calories and protein for 11 days per diet, cutting carbohydrate to 2% of energy lowered plasma T3 and raised urinary nitrogen, a marker of protein breakdown, compared with 85% or 44% carbohydrate.[90]

A 2022 systematic review and meta-analysis of 27 studies (309 male participants) found low-carbohydrate diets (under 35% of calories from carbohydrate) raised cortisol and lowered testosterone, with post-exercise cortisol staying elevated longer than on higher-carbohydrate diets, a pattern that would work against muscle protein synthesis and recovery.[91]

In a crossover trial in 14 male recreational athletes, 90 minutes of cycling raised cortisol most after 2 days on a diet under 10% carbohydrate, and the gap from a high-carbohydrate diet narrowed by 2 weeks. Resting cortisol did not differ between diets, and work output stayed lower on the low-carbohydrate diet.[92]

Case report: fatal kidney failure

[edit]

In 2020, 27-year-old Indian actress Mishti Mukherjee died of bilateral kidney failure while following a standard ketogenic diet, a case widely reported in Indian media as a caution against unsupervised keto use, particularly for anyone with existing kidney vulnerability.[93] This is a single reported case, not a controlled study, but it illustrates the real-world downside risk beyond the chronic-cortisol mechanism Peat describes above.

Practice (ketogenic diets)

[edit]

Prefer sugar/glucose oxidation supported by protein and salt over sustained carbohydrate restriction. See Sugar, Free fatty acids, Randle cycle, Cortisol.


See also

[edit]

References

[edit]
  1. ↑ 1.0 1.1 1.2 1.3 "Glycemia, starch, and sugar in context," Ray Peat article
  2. ↑ 2.0 2.1 2.2 "Sugar issues," Ray Peat article
  3. ↑ Ray Peat, email correspondence, Sugar, raypeatemails.com
  4. ↑ Ray Peat, Glycemia, starch, and sugar in context, raypeat.com
  5. ↑ Sugar issues, raypeat.com
  6. ↑ Sugar, raypeatemails.com
  7. ↑ 7.00 7.01 7.02 7.03 7.04 7.05 7.06 7.07 7.08 7.09 7.10 Ray Peat, email correspondence, "Sugar," raypeatemails.com.
  8. ↑ Brand-Miller J, Hardy K, Raubenheimer D, Copeland L. "A central role for dietary sugars in human evolution," Science. 2026;373(6811). PMID 42561068.
  9. ↑ 9.0 9.1 Acheson KJ, Schutz Y, Bessard T, Anantharaman K, Flatt JP, Jéquier E. "Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man," Am J Clin Nutr. 1988 Aug;48(2):240-7. PMID 3165600.
  10. ↑ Ray Peat, email correspondence, Sugar, raypeatemails.com
  11. ↑ Westwater ML, Fletcher PC, Ziauddeen H. "Sugar addiction: the state of the science," Eur J Nutr. 2016;55(Suppl 2):55-69. PMID 27372453.
  12. ↑ "Even mainstream medicine admits many claims about sugar are myths"
  13. ↑ Peters R, White D, Cleeland C, Scholey A. "Fuel for thought? A systematic review of neuroimaging studies into glucose enhancement of cognitive performance," Neuropsychol Rev. 2020;30(2):234-250. PMID 32162177.
  14. ↑ Wolraich ML, Wilson DB, White JW. "The effect of sugar on behavior or cognition in children: a meta-analysis," JAMA. 1995. PMID 7474248.
  15. ↑ Ray Peat, "Lactate vs. CO2 in wounds, sickness, and aging; the other approach to cancer," raypeat.com.
  16. ↑ "Even mainstream medicine admits many claims about sugar are myths"
  17. ↑ "New Study Links the Keto Diet to Cancer Metastasis"
  18. ↑ Bonuccelli G et al., "Ketones and lactate "fuel" tumor growth and metastasis: Evidence that epithelial cancer cells use oxidative mitochondrial metabolism," Cell cycle (Georgetown, Tex.), 2010
  19. ↑ Suez J, Cohen Y, Valdés-Mas R, et al. "Personalized microbiome-driven effects of non-nutritive sweeteners on human glucose tolerance,"Cell. 2022;185(18):3307-3328.e19. doi:10.1016/j.cell.2022.07.016.
  20. ↑ Email on stevia arsenic contamination, collected in Ephemera.
  21. ↑ E. A. S. Al-Dujaili, H. Twaij, Y. A. Bataineh, U. Arshad, and F. Amjid, "Effect of Stevia Consumption on Blood Pressure, Stress Hormone Levels and Anthropometrical Parameters in Healthy Persons," American Journal of Pharmacology and Toxicology 12, no. 1 (2017): 7-17, https://doi.org/10.3844/ajptsp.2017.7.17. Reported significance: systolic p < 0.001; diastolic p < 0.01; urinary free cortisol p < 0.01; cortisol/cortisone ratio p < 0.0001.
  22. ↑ Ray Peat, "Glucose and sucrose for diabetes," raypeat.com.
  23. ↑ Ray Peat, "Sugar issues," raypeat.com.
  24. ↑ Farshchi HR, Taylor MA, Macdonald IA. "Regular meal frequency creates more appropriate insulin sensitivity and lipid profiles compared with irregular meal frequency in healthy lean women," Eur J Clin Nutr. 2004;58(7):1071-1077. Insulin response difference p<0.01.
  25. ↑ Donin AS, et al., "Regular breakfast consumption and type 2 diabetes risk markers in 9- to 10-year-old children in the child heart and health study in England (CHASE)," PLoS Med. 2014;11(9):e1001703. PMID 25181492.
  26. ↑ Ray Peat, "Effects of Stress and Trauma on the Body", ELUV, 6:37
  27. ↑ Ray Peat, "Effects of Stress and Trauma on the Body", ELUV, 8:59
  28. ↑ "Glycemia, starch, and sugar in context," Ray Peat
  29. ↑ "Glucose and sucrose for diabetes," Ray Peat
  30. ↑ "TSH, temperature, pulse rate, and other indicators in hypothyroidism," Ray Peat
  31. ↑ "Glucose and sucrose for diabetes," Ray Peat
  32. ↑ "Glucose and sucrose for diabetes," Ray Peat
  33. ↑ "Glucose and sucrose for diabetes," Ray Peat
  34. ↑ "Glycemia, starch, and sugar in context," Ray Peat article
  35. ↑ "Glycemia, starch, and sugar in context," Ray Peat article
  36. ↑ "Glycemia, starch, and sugar in context," Ray Peat article
  37. ↑ Jenkins DJ, Wolever TM, Taylor RH, et al., "Glycemic index of foods: a physiological basis for carbohydrate exchange," American Journal of Clinical Nutrition. 1981;34(3):362-6. PMID 6259925.
  38. ↑ "Glycemia, starch, and sugar in context," Ray Peat article
  39. ↑ "Glycemia, starch, and sugar in context," Ray Peat article
  40. ↑ "Glycemia, starch, and sugar in context," Ray Peat article
  41. ↑ "Glycemia, starch, and sugar in context," Ray Peat article
  42. ↑ "Glycemia, starch, and sugar in context," Ray Peat article
  43. ↑ "Glycemia, starch, and sugar in context," Ray Peat article
  44. ↑ "Glycemia, starch, and sugar in context," Ray Peat article
  45. ↑ Peat, Raymond. "Glucose and Sucrose for Diabetes."
  46. ↑ Peat, Raymond. "Sugar Issues."
  47. ↑ Peat, Raymond. "Glycemia, Starch, and Sugar in Context."
  48. ↑ Peat, Raymond. "Eclampsia in the Real Organism: A Paradigm of General Distress Applicable in Infants, Adults, etc."
  49. ↑ Ray Peat, "Your Health Questions Answered: Melanoma, COVID-19, Polyps, Inversion Therapy & More", One Radio Network, 53:06
  50. ↑ Gong Z et al., "CARBONATED BEVERAGES AFFECT LEVELS OF ANDROGEN RECEPTOR AND TESTOSTERONE SECRETION IN MICE," Acta Endocrinol (Buchar), 2022
  51. ↑ Du H, Li L, Bennett D, et al. "Fresh fruit consumption and all-cause and cause-specific mortality: findings from the China Kadoorie Biobank,"Int J Epidemiol. 2017;46(5):1444-1455. doi:10.1093/ije/dyx042.
  52. ↑ Ray Peat, "Sugar Myths II," Ask the Herb Doctor, 2011-10-21.
  53. ↑ Ray Peat, "Glycemia, starch, and sugar in context," raypeat.com.
  54. ↑ Ray Peat, "Sugar II," Ask the Herb Doctor, 2010-10-15.
  55. ↑ Muraki I, Imamura F, Manson JE, Hu FB, Willett WC, van Dam RM, Sun Q. "Fruit consumption and risk of type 2 diabetes: results from three prospective longitudinal cohort studies," BMJ. 2013;347:f5001. 187,382 people, 3.5 million person-years, 12,198 cases. HR per three servings a week: whole fruit 0.98; blueberries 0.74, grapes and raisins 0.88, apples and pears 0.93, bananas 0.95, oranges 0.99, cantaloupe 1.10; fruit juice 1.08.
  56. ↑ Ray Peat, "Allergenic Fruits," email exchange, in Ephemera: Emails & Exchanges from the Archives (2012-2024).
  57. ↑ Ray Peat, "Thyroid Function," interview with Gary Null, 1996.
  58. ↑ Ray Peat, "Ask the Herb Doctor: Weight Gain", Ask the Herb Doctor, 52:50
  59. ↑ Ray Peat, "Gelatin, stress, longevity," raypeat.com.
  60. ↑ Thorell A, Alston-Smith J, Ljungqvist O. "The effect of preoperative carbohydrate loading on hormonal changes, hepatic glycogen, and glucoregulatory enzymes during abdominal surgery,"Nutrition. 1996;12(10):690-5. doi:10.1016/s0899-9007(96)00167-0.
  61. ↑ "Glycemia, starch, and sugar in context," Ray Peat article
  62. ↑ "Glycemia, starch, and sugar in context," Ray Peat article
  63. ↑ Glycemia, starch, and sugar in context
  64. ↑ Yaghoobi N, Al-Waili N, Ghayour-Mobarhan M, et al. "Natural honey and cardiovascular risk factors; effects on blood glucose, cholesterol, triacylglycerole, CRP, and body weight compared with sucrose," ScientificWorldJournal. 2008 Apr 20;8:463-9. PMID 18454257.
  65. ↑ Al-Waili NS. "Natural honey lowers plasma glucose, C-reactive protein, homocysteine, and blood lipids in healthy, diabetic, and hyperlipidemic subjects: comparison with dextrose and sucrose," J Med Food. 2004 Spring;7(1):100-7. PMID 15117561.
  66. ↑ Ray Peat, "Glucose and sucrose for diabetes," raypeat.com.
  67. ↑ Ray Peat, "Ask the Herb Doctor: Cellular Repair", Ask the Herb Doctor, 34:37
  68. ↑ Ray Peat, "Sugar issues," raypeat.com.
  69. ↑ Ray Peat, email, Sugar, raypeatemails.com.
  70. ↑ Ray Peat, "TSH, temperature, pulse rate, and other indicators in hypothyroidism," raypeat.com.
  71. ↑ Preventing and Treating Cancer with Progesterone, Ray Peat newsletter
  72. ↑ Preventing and Treating Cancer with Progesterone, Ray Peat newsletter
  73. ↑ "The hypoglycemic side of hypothyroidism," Indian J Endocrinol Metab. 2014;18(1). A diabetic patient with a sudden, unexplained increase in hypoglycemic episodes should be evaluated for hypothyroidism.
  74. ↑ Kumar A. "Recurrent hypoglycaemia in type 2 diabetic patient due to hypothyroidism," J Diabetes Metab Disord. 2015. doi:10.1186/s40200-015-0149-y.
  75. ↑ Ray Peat, "Hope For Hypoglycemia", PeatySharing (1989)
  76. ↑ Aranda A, Montoya E, Herrera E. "Effects of hypo- and hyper-thyroidism on liver composition, blood glucose, ketone bodies and insulin in the male rat," Biochem J. 1972;128(3):597-604. PMID 4634830.
  77. ↑ Virkkunen M. "Insulin secretion during the glucose tolerance test among habitually violent and impulsive offenders," Aggress Behav. 1986;12(4):303-310.
  78. ↑ Virkkunen M, Rissanen A, Franssila-Kallunki A, Tiihonen J. "Low non-oxidative glucose metabolism and violent offending: an 8-year prospective follow-up study," Psychiatry Res. 2009;168(1):26-31. PMID 19446886.
  79. ↑ Ray Peat, "One Radio Network: Fats and Questions", One Radio Network, 11:03
  80. ↑ Ray Peat, Ephemera: Emails & Exchanges from the Archives (2012-2024).
  81. ↑ Ray Peat, "Nutrition for Women", p. 31
  82. ↑ Ray Peat, "Hot flashes, energy, and aging," raypeat.com.
  83. ↑ Ray Peat and Bud Weiss, "Ray Peat and Bud Weiss on Ketogenic Diets," interview transcript, raypeat.rodeo.
  84. ↑ Ray Peat and Bud Weiss on Ketogenic Diets
  85. ↑ Ray Peat and Bud Weiss on Ketogenic Diets
  86. ↑ Ray Peat and Bud Weiss on Ketogenic Diets
  87. ↑ Langfort J, Pilis W, Zarzeczny R, Nazar K, Kaciuba-Uściłko H, "Effect of low-carbohydrate-ketogenic diet on metabolic and hormonal responses to graded exercise in men," J Physiol Pharmacol. 1996;47(2):361-71. PMID 8807563.
  88. ↑ Ebbeling CB, Swain JF, Feldman HA, et al. "Effects of dietary composition on energy expenditure during weight-loss maintenance," JAMA. 2012;307(24):2627-2634. doi:10.1001/jama.2012.6607. PMID 22735432.
  89. ↑ Cooper ID, Sanchez-Pizarro C, Norwitz NG, et al. "Thyroid markers and body composition predict LDL-cholesterol change in lean healthy women on a ketogenic diet: experimental support for the lipid energy model," Front Endocrinol (Lausanne). 2023;14:1326768. doi:10.3389/fendo.2023.1326768. PMID 38189051. Three-phase crossover, n=10, 21 days per phase; carbohydrate 58.5, 198.6 and 57.0 g/day; energy intake 1,834, 1,830 and 1,757 kcal/day; free T3 3.85, 5.5 and 3.9 pmol/L (p<0.001).
  90. ↑ Bisschop PH et al. 2001. "Isocaloric carbohydrate deprivation induces protein catabolism despite a low T3-syndrome in healthy men." Clin Endocrinol (Oxf) 54(1):75-80. n=6 men, 11 days per diet, 15% protein, 85%, 44% or 2% carbohydrate at equal calories; plasma T3 1.78 ± 0.09, 1.71 ± 0.07 vs 1.33 ± 0.05 nmol/L (P < 0.01); urinary nitrogen 10.91 ± 0.67, 12.79 ± 1.14 vs 15.89 ± 1.10 g/24 h (P = 0.03); reverse T3 and free T4 rose, TSH and resting energy expenditure unchanged. doi:10.1046/j.1365-2265.2001.01158.x. PMID 11167929.
  91. ↑ Whittaker J, Harris M. "Low-carbohydrate diets and men's cortisol and testosterone: Systematic review and meta-analysis," Nutr Health. 2022. doi:10.1177/02601060221083079. PMID 35254136.
  92. ↑ Terink R, Witkamp RF, Hopman MTE, Siebelink E, Savelkoul HFJ, Mensink M. "A 2 Week Cross-over Intervention with a Low Carbohydrate, High Fat Diet Compared to a High Carbohydrate Diet Attenuates Exercise-Induced Cortisol Response, but Not the Reduction of Exercise Capacity, in Recreational Athletes," Nutrients. 2021;13(1):157. doi:10.3390/nu13010157. PMID 33418951. PMCID PMC7825040. Randomized crossover, n=14 men; cycle ergometry 90 min at 60% Wmax; post-exercise cortisol LCHF 822 ± 215 (day 2) and 669 ± 243 nmol/L (week 2), p = 0.004; HC 609 ± 208 and 555 ± 173 nmol/L, both p < 0.001 vs LCHF; post-exercise rise 83% vs 31% (LCHF) and 28% vs 19% (HC); baseline cortisol not different; lower workload and higher perceived exertion on LCHF.
  93. ↑ "Did Eating Keto Contribute to Mishti Mukherjee's Death?," Diet Doctor, 2020.