Does fruit juice increase triglycerides?

If I have high triglycerides, should I stay away from fruit juice?

Triglycerides are a blood marker that doctors keep an eye on. Elevated triglycerides are associated with cardiovascular risk, however, triglycerides are a neutral storage form. The reason I highlight “associated” is because association doesn’t mean causation.

Regardless, elevated triglycerides of over 150 should deserve attention, but not necessarily by cutting carbs. More on that in just a bit.

First we have to understand what triglycerides are.

What are triglycerides

Triglyceride molecules consist of a glycerol backbone to which three fatty acids are connected (esterified). The positional distribution of these fatty acids within the triglyceride molecule, the so-called triglyceride structure, can be specified by stereospecific numbering (sn) as sn-1, sn-2, and sn-3. Different kinds of fatty acids can attach to different positions on the glycerol backbone, for example, oleic acid on sn-1, palmitic acid on sn-2 and stearic acid on sn-3.

These neutral lipids (triglycerides and cholesterol) can be either stored in cytoplasmic lipid droplets (LDs), or secreted into the bloodstream as VLDL particles.

How are triglycerides created

Triglycerides are created from free fatty acids in the liver, which can come from 1) free fatty acids released from fat stores through lipolysis, 2) short-chain fatty acids from gut bacteria and 3) the conversion of carbohydrates to fat through lipogenesis.

Triglycerides can also come from dietary fat. Dietary fat is broken down into sn-2-monoacylglycerols and free fatty acids before absorption. After absorption, these lipid molecules are taken up by enterocytes and resynthesized into triglycerides. These triglycerides are packaged into chylomicrons, secreted into the lymphatic system and ultimately reach the circulation. Much of the chylomicron triglycerides are taken up by muscle and fat stores due to the activity of lipoprotein lipase (LPL). TGs remaining within the chylomicron remnants are delivered to the liver and the fatty acids are released during lysosomal processing of the particles.

So the point I’m trying to make is that triglycerides can come from a variety of sources and not just carbs.

Elevated triglycerides (TG) can come from:

  • Gut dysbiosis (excess short-chain fatty acid production; especially acetate) (R).
  • Excess consumption of dietary fat (more than the capacity of your body to process them).
  • Excess lipolysis due to insulin resistance and inflammation.
    • Elevated free fatty acids released through lipolysis causes insulin resistance, leads to hyperglycemia, and the elevates insulin stimulates DNL and fat synthesis, which further promotes the formation of TGs.
  • Hyperinsulinemia (insulin stimulates lipogenesis).
    • We concluded from these findings that insulin suppresses VLDL production in insulin-sensitive humans partly by suppressing plasma FFA levels and partly by a non-FFA-mediated (perhaps direct hepatic) mechanism. In addition, we found that chronically insulin-resistant hyperinsulinemic obese individuals were resistant to this suppressive effect of insulin on VLDL apoB production, in keeping with similar findings by others performing in vitro experiments using cultured hepatocytes isolated from insulin-resistant or hyperinsulinemic rats.” (R)
  • Impaired clearance of chylomicrons and/or VLDL.
  • Hypercortisolemia.
    • Cortisol stimulates lipogenesis; cortisol is elevated due to stress and chronic inflammation due to gut irritation and inflammation.
    • Pathways of lipid deposition stimulated by excess glucocorticoids include 1) increase in appetite and high caloric intake; 2) increased blood glucose levels due to GC-induced stimulation of gluconeogenesis; 3) stimulation of de novo lipogenesis that is augmented by the high glucose and insulin levels and by GC itself; and 4) increased release of free fatty acids from adipose stores and stimulation of their uptake by the liver. Pathways that decrease hepatic lipids affected by glucocorticoids include a modest stimulation of very-low-density lipoprotein synthesis and secretion into the circulation and inhibition of β-oxidation of fatty acids” (R).
  • Excess conversion of carbs to fats via de novo lipogenesis (DNL).
    • Fatty acids created through DNL are more likely to be channeled to VLDL-TG production instead of raising circulating TGs (R).
  • Inflammation (R).
  • LPS (endotoxins) (R).
    • As little as 10 ng/100 g body weight induced hypertriglyceridemia and this increase in serum triglyceride levels occurred rapidly (78% increase at 2 h). At high doses of LPS (50 micrograms/100 g body weight), the clearance of triglyceride-rich lipoproteins was decreased… At low doses of LPS (100 ng/100 g body weight), triglyceride clearance was not altered but the hepatic secretion of triglyceride was increased. Low dose LPS stimulated hepatic de novo fatty acid synthesis and lipolysis, both of which provided a source of fatty acids for the increase in hepatic triglyceride production. It’s via promoting inflammation” (R).

So why is everyone afraid of carbs, or more specifically fructose? It’s because fructose goes straight to the liver after absorption and is thought to stimulate DNL much more than glucose. But that has been debunked. Firstly, fructose is absorbed much slower than glucose, secondly, fructose replenishes liver glycogen very effectively, thirdly, fructose speeds up glucose oxidation and fourthly, fructose is the least insulinogenic of all sugars and insulin is a major driver of DNL.

I’ve already written about sugar and flawed science here and sugar, fat gain and DNL here, so I highly recommend you check out those articles.

But let’s dive into the science of drinking fruit juice and the effects on triglycerides.

What the research shows

Here I’m going to quote snippets from multiple studies.

This meta-analysis suggests that high intake of fruit but not vegetables are inversely associated with hypertriglyceridemia.


Total fruit intake was significantly inversely associated with the prevalence of hypertriglyceridemia in Asian populations.


Higher intakes of phytochemical-rich foods (such as fruit juice) are associated with a lower prevalence of metabolic dysregulation (which includes elevated TGs) and consequently, cardiometabolic diseases in Korean adults.


Among Chinese adults, a higher level of fruit consumption was associated with lower blood pressure and blood glucose levels and, largely independent of these and other dietary and nondietary factors, with significantly lower risks of major cardiovascular diseases (which includes lower TGs).


…randomly assigned to follow a low or a high-fruit energy-restricted diet for 8 weeks…The induced weight loss was similar for both diets (6.9 +/- 2% vs. 6.6 +/- 2%, p = 0.785). Both experimental diets similarly improved the lipid plasma profile in the participants, but the cholesterol fall was higher in obese subjects receiving the diet containing more fruit.


The findings of this meta-analysis suggest that the adverse association of SSBs (sugar-sweetened beverages) with MetS (metabolic syndrome) does not extend to other food sources of fructose-containing sugars, with a protective association for yogurt and fruit throughout the dose range and for 100% fruit juice and mixed fruit juices at moderate doses (R).


Although the next one is not with fruit juice, it shows that even sugar can be “protective”. Triglycerides are also high in diabetics.

Although there was no association of total sugars (RR 0.91, 95% confidence interval [CI] 0.76-1.09) or fructose (RR 1.04, 95% CI 0.84-1.29) with type 2 diabetes, sucrose was associated with a decreased risk of type 2 diabetes.


In the following study, participants consumed 1.28 liter of orange juice with or between meals. Although the conclusion says that TGs remained unchanged, if you look at the actual data, TGs actually dropped in the group that had fruit juice with their meals.

TG (triglycerides), postprandial and basal insulin sensitivity remained unchanged with both interventions.


This next one is remarkable. Even doses of 150g of fructose daily didn’t have a negative effect on triglycerides.

We included 14 comparison arms from 11 trials, including 277 patients. The studies varied in length from 2 to 10 wk (mean: 28 d) and included doses of fructose between 40 and 150 g/d (mean: 68 g/d). Fructose substitution in some subgroups resulted in significantly but only slightly lowered fasting blood glucose (-0.14 mmol/L; 95% CI: -0.24, -0.036 mmol/L), HbA1c [-10 g/L (95% CI: -12.90, -7.10 g/L; impaired glucose tolerance) and -6 g/L (95% CI: -8.47, -3.53 g/L; normoglycemia)], triglycerides (-0.08 mmol/L; 95% CI: -0.14, -0.02 mmol/L), and body weight (-1.40 kg; 95% CI: -2.07, -0.74 kg) (R). The substitution of fructose for glucose or sucrose over a wide dose range of 24–150 g/d (mean dose: 68 g/d) in food or beverages improved glycated hemoglobin and fasting glucose without an adverse effect on fasting insulin, blood lipids, or body weight, especially in participants with impaired glucose tolerance or type 2 diabetes.


Fructose (52 g), sucrose (65 g), and sucralose (0.1 g) were delivered as sweet-taste–balanced muffins with a total fat load (66 g)…Fructose, at a moderate dose, did not significantly elevate triglyceride compared with sucrose or sucralose and lowered the glucose iAUC.


Even though the study above said that fructose didn’t significantly elevate trigs compared to sugar or sucralose, if you look at this graph, fructose actually elevated trigs the least.

Why do some studies show that fructose increases triglycerides?

Here’s why. It’s due to slower clearance rate due to lower insulin-mediated stimulation
of lipoprotein lipase, because fructose is less insulinogenic than glucose.

This suggests lower clearance of CM (chylomicrons), rather than elevated
production, contributed to the elevated plasma TAG concentration.


So what’s up?

Why does everyone think carbs and especially fructose is fattening?

It’s definitely not supported by proper science. Now I’m not recommending guzzling sugar, but still stick to natural sources of sugar, such as whole fresh/dried fruit, fruit juice, maple syrup, agave syrup, honey, milk, etc.

If sugar makes you fat, then you are either consuming too many calories, consuming too much fat, have mineral and vitamin deficiencies (e.g. niacin, zinc, copper, magnesium, dairy calcium (R)), have insulin resistance, have inflammation, have excess cortisol, etc. Should you avoid carbs when you have those?

No, natural carb sources can actually help to correct those issues. It can help replenish vitamins and minerals, lower cortisol, lower inflammation, improve insulin sensitivity, etc.

It’s not trigs, it’s free fatty acids

Triglycerides is just a marker to look at, but it’s a “meh” marker. A more important marker to look at is free fatty acids (FFAs).

Physiologic increases in plasma FFA levels cause insulin resistance in both diabetic and nondiabetic subjects by producing several metabolic defects: (1) FFA inhibit insulin-stimulated glucose uptake at the level of glucose transport or phosphorylation (or both); (2) FFA inhibit insulin-stimulated glycogen synthesis; and (3) FFA inhibit insulin-stimulated glucose oxidation.


And also…

FFA probably also cause hepatic insulin resistance, which results in increased rates of endogenous glucose production in relationship to the prevailing degree of hyperinsulinemia. Lastly, FFA support between 30 and 50% of basal insulin secretion and potentiate glucose-stimulated insulin secretion in short-term and long-term settings. The stimulatory action of FFA on b-cells enables obese individuals who do not have a genetic predisposition to develop type 2 diabetes mellitus to compensate for their FFA-potentiated insulin resistance with an increase in FFA-mediated insulin secretion. In contrast, subjects who are genetically predisposed to develop type 2 diabetes may be unable to secrete sufficient amounts of insulin to compensate for their FFA-induced insulin resistance. This situation will lead to an increase in blood glucose concentration and eventually to type 2 diabetes.


So instead of looking only at triglycerides, also have a look at fasting glucose, fasting insulin, FFAs, hsCRP, cortisol, noradrenaline, adrenaline, thyroid (not just TSH) and bowel symptoms (such as bloating, burping, constipation, diarrhea, transit time, stool quality, etc.)


Research shows that fruit juice doesn’t increase triglycerides and that it’s a good idea to have fruit juice daily. Even up to 1.28L per day has been shown to be safe and I don’t believe that is the daily upper limit.

So go forth and don’t feel guilty of thy fruit juice indulgence. 😉

As always, thanks so much for reading my article. Let me know in the comments below if you have any questions. And if you found this article to be insightful and helpful please like and share so this information can help others as well.

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