Fructose
Fructose is a monosaccharide in fruit, honey, and sucrose (paired with Glucose). Mainstream nutrition often groups all sugars together. Ray Peat distinguished whole-fruit fructose from industrial high-fructose corn syrup and from sugars eaten with excess PUFA in processed food.[1]
History/Etymology
[edit]Fructose was first isolated in pure form in 1847 by French chemist Augustin-Pierre Dubrunfaut. Its name, from the Latin fructus ("fruit") plus the "-ose" suffix used for sugars, was coined later in the 19th century once it was recognized as the sweetest of the common sugars and a major component of ripe fruit.
Structure/Chemical properties
[edit]Fructose (C₆H₁₂O₆) shares glucose's molecular formula but not its structure: fructose is a ketohexose (ketone-bearing six-carbon sugar) rather than an aldohexose, and predominantly forms a five-membered ring (furanose) in solution rather than glucose's six-membered ring. That structural difference is what routes it through a different initial metabolic pathway in the liver.
Function/Mechanism of Action
[edit]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
Eating starch, by increasing insulin and lowering the blood sugar, stimulates the appetite, causing a person to eat more, so the effect on fat production becomes much larger than when equal amounts of sugar and starch are eaten.
— Ray Peat
Fructose metabolism bypasses phosphofructokinase regulation, which can support CO₂ production when glucose oxidation is efficient.[1]
Medical uses/Effects
[edit]When better foods are available, they should be used instead of starches. Fruit has advantages over grains besides the sugar-starch difference. Bread and pasta consumption correlate with diabetes incidence in epidemiology he cites, while fruit consumption shows inverse association.[1]
Orange juice and sucrose have lower glycemic index than white bread in David Jenkins's measurements, though the glycemic index is physiologically crude as a measure.[1] Whole fruit adds water, minerals, and pulp unlike HFCS in seed-oil-rich junk food. A 25-year cohort of 25,749 people found sugar-sweetened beverages and fruit juice raised hypertension risk (52% and 35% higher at the highest intake levels), while whole fruit intake showed no such association, supporting the distinction between fructose sources rather than a blanket fructose effect.[2]
Dosing
[edit]Pair fructose with adequate protein, salt, and minerals, as found in whole fruit, rather than as isolated HFCS. See Roadmap/03 - Diet, Liver.
Side/Adverse effects
[edit]Peat's argument is physiological (insulin, appetite, storage), not a license for unlimited sweets. Concerns about fructose specifically (as opposed to whole fruit) center on industrial HFCS consumed apart from the water, minerals, and pulp that accompany fructose in whole fruit, and on sugar eaten alongside excess PUFA in processed food.[1]
See also
[edit]References
[edit]- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 "Glycemia, starch, and sugar in context," Ray Peat article
- ↑ Ma X, et al. "Consumption of Fructose-Containing Food and Beverage Sources in Childhood Through to Adulthood and Risk of Hypertension: A Prospective Cohort Study," Circulation. 2026. doi:10.1161/CIRCULATIONAHA.125.077666.