Fructose and fat synthesis: the sweet path to diabetes and heart disease

Fructose turns into fat as soon as it hits the liver

Fructose makes up 50% of the common table sugar, 50% of the sugar contained even in freshly squeezed juices (even more in apple juices), 75% of honey and up to 55% of high fructose corn syrup (HFCS).

Fructose, in all it's guises, is now known to be detrimental to metabolism and liver health and excessive consumption may eventually lead to diabetes and heart disease.

Unlike glucose, which is found in what we call "carbs" and also comprises the other 50% of the sucrose (common sugar) molecule, fructose does not enter the bloodstream intact, but it undergoes metabolism by the liver and it is converted into fat, from where it finds it's way into the bloodstream and eventually the fat cells.


A parenthesis on "diabetic" foods containing fructose 

Needless to say, that the old-fashioned "diabetic" fructose powder, and "diabetic foods" that contain fructose instead of glucose or sugar, are exactly that": diabetic foods. They actually cause diabetes or make diabetes worse.

It beggars belief that "medical foods" based on erroneous knowledge or decades past still exist and are still sold, even in pharmacies!


Fatty liver, diabetes and insulin resistance

Excessive fructose consumption leads not only to fat accumulation on the hips and especially the waist (the worst possible type of body fat), but also on the liver itself (non alcoholic fatty liver disease) and the pancreas.

Eventually, excessive fructose / sugar / brown sugar / agave / honey / high-fructose corn syrup / fruit juice consumption leads to insulin resistance, whole body inflammation and diabetes, all of which are risk factors for heart disease.

Furthermore, fructose has a very strong pro-glycation action. Glycation is responsible for skin ageing, whole body ageing and cellulite.

Pharmaceutical methods aiming to act not the fructose metabolism are being developed, but the best course of action to avoid fructose-mediated health deterioration is to simply not eat the fructose-containing sweeteners mentioned above (yes, even agave and honey) and to consume whole fruit, rather than fruit juices.


The difference between fruit and fruit smoothies/juices

Fruit is different to fruit juices for three reasons:

  • Fruit is digested more slowly, leading to less severe reactions in the liver.
  • It is difficult to consume excessive amounts of fructose just by eating whole fruits, while it is very easy to do by drinking juices. A 500ml bottle of apple juice, which can be drunk even in seconds, requires 6-7 medium apples, and will still leave you hungry minutes later. On the other hand, it can take more than half an hour to eat 6-7 apples and they will definitely leave you full for several hours.
  • Furthermore, commercial fruit juices are even sweeter than freshly squeezed, to the type of fruit selected for them, and are definitely more unhealthy.



  • Paper: The Sweet Path to Metabolic Demise: Fructose and Lipid Synthesi
  • Abstract: Epidemiological studies link fructose consumption with metabolic disease, an association attributable in part to fructose-mediated lipogenesis. The mechanisms governing fructose-induced lipogenesis and disease remain debated. Acutely, fructose increases de novo lipogenesis through the efficient and uninhibited action of ketohexokinase and aldolase B which yields substrates for fatty-acid synthesis. Chronic fructose consumption further enhances the capacity for hepatic fructose metabolism by activating several key transcription factors (i.e., SREBP1c and ChREBP) which augment the expression of lipogenic enzymes, increasing lipogenesis and further compounding hypertriglyceridemia and hepatic steatosis. Hepatic insulin resistance develops from diacylglycerol–PKCɛ-mediated impairment of insulin signaling and possibly additional mechanisms. Initiatives that decrease fructose consumption and therapies that block fructose-mediated lipogenesis will be necessary to avert future metabolic pandemics. Trends: Fructose comprises ∼50% of the dietary sugars sucrose and high-fructose corn syrup, and when consumed in excess exacerbates cardiometabolic risk factors including dyslipidemia, fatty liver disease, and insulin resistance. Ketohexokinase (KHK) may be a therapeutic target. Complete knockout of all KHK isoforms prevents fructose-induced disease. By contrast, selective knockout of the ubiquitous, low-activity KHK-A isoform exacerbates fructose-induced disease, possibly by increasing flux through the KHK-C isoform expressed in key metabolic tissues such as liver. Fructose contributes to lipogenesis and associated pathologies, including steatosis, dyslipidemia, and hepatic insulin resistance, both by providing substrate and coordinating the expression of lipogenic enzymes via SREBP1c and ChREBP. Limiting fructose intake and regulating fructose metabolism may represent a promising therapeutic strategy to reduce cardiometabolic risk factors.