The recent headlines about erythritol and its possible association with cardiovascular disease has led to a heavy stream of questions flooding my inbox. As always, there’s so much more to this story than the headlines suggest. I’d like to use this study as another opportunity to highlight the serious issues with premature conclusions released to the media.

Endogenous vs Exogenous Erythritol

Erythritol is either exogenous, meaning it comes from outside sources through your diet or endogenous, meaning it is produced naturally inside your body. This is similar to exogenous dietary cholesterol versus the endogenous cholesterol our liver naturally produces. Dietary erythritol is a sweetener that has become ubiquitous in many low carb and keto-friendly foods, while also being a household sugar substitute to add to coffee, tea, or used to prepare low carb baked goods.

Even if you have never eaten a speck of dietary erythritol, your body naturally produces erythritol every single day. It’s a metabolic byproduct of a biochemical pathway called the pentose phosphate pathway or shunt which I’m going to cover in detail in an upcoming podcast. It’s actually one of my favorite biochemical pathways which I planned to discuss and this headline pushed this to the top of my list.

P3 is an essential anabolic pathway, which means it’s used to build important things like fatty acids, DNA, RNA, and an important antioxidant molecule called glutathione. I’ll explain this in more detail in my podcast. Metabolic diseases are typically due to an essential pathway or mechanism like P3  that’s either less active or running on hyperdrive.

In individuals who are overeating and/or inactive, the P3 pathway is revved up. See the image below. Glycolysis is the linear process in the light blue box on the left that turns glucose at the top into pyruvate. The pyruvate then enters (red arrow) the mitochondria (blue oval at bottom), which is our metabolic engine that produces ATP energy. When that engine is overwhelmed with more glucose fuel than it can handle, it takes an abrupt right turn into the P3 anabolic, biosynthetic pathway represented by the red box.


Erythritol is one of the metabolic byproducts that increases in your bloodstream when P3 is in hyperdrive. Your body is desperately trying to stash away all the excess nutrients and P3 is also trying to produce lots of glutathione, our natural antioxidant, to combat all of the free radicals that result from our modern day lifestyle habits. Free radicals are unstable molecules that damage cells and cause chronic inflammation, resulting in common health conditions like heart disease, cancer, etc., along with causing premature aging.

So key point here is that blood levels of erythritol are elevated in individuals who have chronic health issues like diabetes, heart disease, stroke, etc.

Endogenous, not exogenous dietary erythritol, thus serves as a chemical signal or alarm marking a highly diseased state.

The Erythritol Study

With the above background, now we can dig into the study published in the journal Nature Medicine a bit more. The most important thing for you to understand is that the study did not expose individuals to dietary erythritol and measure risk going forward. That would have been a more compelling result. The researchers in this study actually weren’t even targeting erythritol. They decided to look at over 4,000 patients in the US and Europe who mostly had conditions like heart attack, stroke, diabetes, etc. and then observe various blood markers to see if they could find any abnormal signals. Not surprisingly, elevated blood levels of erythritol was one of these signals for the very reasons we already discussed.

What the researchers did next is that they took just 8 study subjects and gave them dietary erythritol and noted that their blood levels of erythritol stayed “markedly elevated” for days. The final step is that they added erythritol to either whole blood or isolated platelets, and found that they clumped together, similar to what happens during the formation of a heart attack causing clot. This final experiment was done outside of the body. Researchers will tell you that what happens outside of the body in a test tube or petri dish often does not mimic or mirror what happens inside the human body, which is a far more complex biological system.

Using the 3 major independent lines of evidence were as follows:

  1. Higher endogenous erythritol levels found in diseased individuals, for the reasons discussed above (overactive P3)
  2. Persistently elevated erythritol levels after dietary consumption. The exact blood concentrations were not shared in the study findings.
  3. A clumping effect when erythritol was exposed to blood or platelets ex vivo (outside the body), suggesting increased blood clotting.

Are these 3 independent findings sufficient to stitch together a bold statement that dietary erythritol is linked to cardiovascular disease with a weak disclaimer that “more studies are needed?” In my opinion, absolutely not. I agree that these findings do warrant further research, but in my opinion, this study did not meet the minimal criteria for being leaked to the press, which not surprisingly turned this into an alarmist headline.

There are actually studies that show erythritol may have cardiovascular benefit such as this one done in 24 human subjects with type 2 diabetes who were given an orange flavored beverage containing 36 grams of erythritol, and using fingertip arterial tonometry, they found beneficial effects on the health of arteries. This is also not a conclusive study, but at least they actually had the subjects consume exogenous erythritol. This study is an overview of erythritol and mentions some of the beneficial effects on blood glucose and insulin resistance, while pointing out how plasma erythritol levels are expected to go up due to P3 and are likely not an indicator of it being an unsafe sweetener. It also mentions how long term erythritol used in rodent studies results in lower body fat. Unlike the Cleveland Clinic study, these human and animal studies are assessing the impact of exogenous dietary erythritol, rather than drawing conclusions by measuring endogenous erythritol production.

The line of logic used for erythritol feels eerily similar to what was used for cholesterol. Cholesterol is a component of heart-attack causing plaque, thus blood cholesterol, influenced by dietary cholesterol is a major culprit to causing heart disease. That hypothesis has been thoroughly disproved and has led to the elimination of specific dietary cholesterol target recommendations from dietary guidelines.

Consequences of this Study

Why would a research team release these claims to the public when their study hardly meets what I consider scientific rigor? The study came out of the prestigious Cleveland Clinic, which made the results feel even more legitimate. I don’t know the research authors and have to  believe part of their intent was to protect the public with these preliminary findings. However, keep in mind that these headlines bring lots of sought after attention to research teams. One of the lead authors, Dr.Stanley Hazen, has been extensively interviewed and quoted by various news outlets, and as a consequence his lab’s work has received global attention.

The downside of this research is that there are so many well meaning individuals who use sweeteners like erythritol to reduce their consumption of sugar. Is someone who is exercising, eating a balanced diet, and using erythritol to sweeten their coffee or prepare a baked good every now and then truly at risk for increased heart disease based on the lines of evidence I presented to you? Regardless of my answer, many people are throwing out their erythritol and also questioning the role of all sweeteners, many of which don’t have any convincing studies to indicate harm.

I also think that if dietary erythritol was truly atherogenic (plaque causing), we would have likely picked up on some type of signal in the low carb/keto community of unexpectedly increased heart disease incidence.

I’m not aware of any such red flag in lower carb erythritol consumers. These findings also impact businesses of all sizes who genuinely have created food products to help consumers find a healthier alternative to beat their sugar dependence.

What Am I Doing?

I used to sweeten my coffee with erythritol a few years back and naturally migrated to using honey. I had nothing against using a teaspoon of sugar, but grew to like the flavor of honey in my coffee and tea. Other than occasional indulgences for sweet things during social occasions, my overall appetite for sweet things has gone down quite a bit. Even if my wife bakes a lower carb dessert, she’ll just use less sugar or honey or fruit rather than an artificial sweetener. We still have erythritol in the house and if a recipe calls for its use, I’ll use it for now.

What should you do? It’s perfectly fine for you to wait for further studies to come out and stick to using other sweeteners or lower amounts of sugar, honey, etc. There are clearly lots of other alternatives out there that you can use. At the same time, if you decided to continue using erythritol in the context of a healthy lifestyle, I wouldn’t be calling you a major risk taker.

In fact, if erythritol is helping people consume less sugar and fewer overall calories, then it’s actually helping to remove the primary driver for P3 overactivation and chronic disease, which is overnutrition.

In the end, the decision is yours and should be based on your risk tolerance. If I thought there was more substance to this study, I would have made a stronger recommendation against using erythritol, but for now all I can say is stay tuned.