Early Olezarsen Results Show 50% Reduction in Triglycerides


“The reduction in triglycerides was greater than that currently possible with any available therapy,” reported Brian Bergmark, MD, an interventional cardiologist at Brigham and Women’s Hospital, Boston.

The drug also produced meaningful improvements in multiple other lipid subfractions associated with increased cardiovascular (CV) risk, including ApoC-III, very low–density lipoprotein (VLDL) cholesterol, ApoB, and non-LDL cholesterol. High-density lipoprotein (HDL) cholesterol levels were significantly raised.

The results were presented on April 7 as a late breaker at the American College of Cardiology (ACC) Scientific Session 2024 and published online simultaneously in The New England Journal of Medicine.

No Major Subgroup Failed to Respond

The effect was seen across all the key subgroups evaluated, including women and patients with diabetes, obesity, and severe as well as moderate elevations in TGs at baseline, Bergmark reported.

Olezarsen is a N-acetylgalactosamine–conjugated antisense oligonucleotide targeting APOC3 RNA. The results of this randomized trial, called BRIDGE-TIMI 73a, are consistent with other evidence that inhibiting expression of ApoC-III lowers the levels of TGs and other lipid subfractions to a degree that would predict clinical benefit.

In this study, 154 patients at 24 sites in North America were randomized in a 1:1 ratio to 50 or 80 mg olezarsen. Those in each of these cohorts were then randomized in a 3:1 ratio to active therapy or placebo. All therapies were administered by subcutaneous injection once per month.

Patients were eligible for the trial if they had moderate hypertriglyceridemia, defined as a level of 150-499 mg/dL, and elevated CV risk or if they had severe hypertriglyceridemia (≥ 500 mg/dL) with or without other evidence of elevated CV risk. The primary endpoint was a change in TGs at 6 months. Complete follow-up was available in about 97% of patients regardless of treatment assignment.

With a slight numerical advantage for the higher dose, the TG reductions were 49.1% for the 50-mg dose and 53.1% for the 80-mg dose relative to no significant change in the placebo group (P < .001 for both olezarsen doses). The reductions in ApoC-III, an upstream driver of TG production and a CV risk factor, were 64.2% and 73.2% relative to placebo (both P < .001), respectively, Bergmark reported.

In those with moderate hypertriglyceridemia, normal TG levels, defined as < 150 mg/dL, were reached at 6 months in 85.7% and 93.3% in the 40-mg and 80-mg dose groups, respectively. Relative to these reductions, normalization was seen in only 11.8% of placebo patients (P < .001).

TG Lowering Might Not Be Best Endpoint

The primary endpoint in this trial was a change in TGs, but this target was questioned by an invited ACC discussant, Daniel Soffer, MD, who is both an adjunct professor assistant professor of medicine at Penn Medicine, Philadelphia, and current president of the National Lipid Association.

Soffer noted that highly elevated TGs are a major risk factor for acute pancreatitis, so this predicts a clinical benefit for this purpose, but he thought the other lipid subfractions are far more important for the goal of reducing atherosclerotic cardiovascular disease (ASCVD).

Indeed, he said categorically that it is not TGs that drive ASCVD risk and therefore not what is the real importance of these data. Rather, “it is the non-HDL cholesterol and ApoB lowering” that will drive the likely benefits from this therapy in CV disease.

In addition to the TG reductions, olezarsen did, in fact, produce significant reductions in many of the lipid subfractions associated with increased CV risk. While slightly more favorable in most cases with the higher dose of olezarsen, even the lower dose reduced Apo C-III from baseline by 64.2% (P < .001), VLDL by 46.2% (P < .001), remnant cholesterol by 46.6% (P < .001), ApoB by 18.2% (P < .001), and non-HDL cholesterol by 25.4% (P < .001). HDL cholesterol was increased by 39.6% (P < .001).

These favorable effects on TG and other lipid subfractions were achieved with a safety profile that was reassuring, Bergmark said. Serious adverse events leading to discontinuation occurred in 0%, 1.7%, and 1.8% of the placebo, lower dose, and higher dose arms, respectively. These rates did not differ significantly.

Increased Liver Enzymes Is Common

Liver enzymes were significantly elevated (P < .001) for both doses of olezarsen vs placebo, but liver enzymes > 3× the upper limit of normal did not reach significance on either dose of olezarsen relative to placebo. Low platelet counts and reductions in kidney function were observed in a minority of patients but were generally manageable, according to Bergmark. There was no impact on A1c levels.

Further evaluation of change in hepatic function is planned in the ongoing extension studies.

Characterizing these results as “exciting,” Neha J. Pagidipati, MD, a member of the Duke Clinical Research Institute and an assistant professor at the Duke School of Medicine, Durham, North Carolina, said that identifying a drug effective for hypertriglyceridemia is likely to be a major advance. While elevated TGs are “one of the toughest” lipid abnormalities to manage, “there is not much out there to offer for treatment.”

She, like Soffer, was encouraged by the favorable effects on multiple lipid abnormalities associated with increased CV risk, but she said the ultimate clinical utility of this or other agents that lower TGs for ASCVD requires a study showing a change in CV events.

High Triglycerides Are a Major Risk Factor for Heart Attacks and Diabetes


Having blood triglyceride levels above 150 mg/dL puts you at increased risk for a heart attack, stroke, or heart valve disease, even if your blood cholesterol levels are normal.  Triglyceride levels can be measured with routine blood tests.

Safe triglyceride level are below 130 mg/dL, while levels between 150 and 200g/dL put a person at increased risk for cell damage. Levels higher than 200 mg/dL put person at significant-risk for a heart attack and diabetes. Everyone who has a triglyceride level above 150 mg/dL should be checked for diabetes, kidney and liver disease and low thyroid function.  (Eur Heart J, Dec 2021;42(47):4791-4806).

High triglycerides are often found in people who:
• are diabetic, obese or alcoholic,
• have high blood pressure,
• have liver damage,
• have pancreatic disease,
• have kidney disease,
• have low thyroid function,
• have genetic disorders of fat metabolism,
• take beta-blockers, birth control pills, estrogen, diuretics or drugs that suppress a person’s immunity

You can lower high blood triglyceride levels with lifestyle changes including diet and exercise, and with established prescription treatments such as fibrates, omega-3 fatty acid preparations, and various biological agents (Eur Heart J, 2020;41(1):99-109c).

What Causes High Triglyceride Levels?
When blood sugar levels rise too high after meals, sugar is converted to a type of fat called triglycerides, so high blood triglyceride levels are usually caused by a high rise in blood sugar after meals and usually mean that a person is already diabetic or pre-diabetic (J Clin Endocrinol Metab, Oct 2011;96(10):E1596–E1605). High rises in blood sugar after meals cause sugar to stick to the outer membranes of every type of cell in your body and eventually destroy these cells. Sugar can stick to:
• brain cells, to cause dementia
• nerve cells, to cause pain or loss of feeling
• matrix cells of bones, to weaken bones and cause osteoporosis
• the DNA of cells, which can cause the uncontrolled growth that is cancer
• the inner lining of arteries, to form plaques
• plaques that have already formed, causing them to break off, leading to a heart attack or stroke
This is why diabetes has so many devastating side effects.

Normal fasting blood sugar is below 100, but a normal fasting blood sugar does not rule out diabetes because having a high blood sugar after meals usually happens earlier than having a high fasting blood sugar. You suffer cell damage even if your blood sugar levels are normal when you fast, but rise too high only after you eat. Many studies show that having a blood sugar greater than 140 one hour after eating a meal causes cell damage and indicates that you are already pre-diabetic or diabetic (Atherosclerosis, 2016 Nov 17;256:15-20). A high rise in blood sugar after a meal causes your liver to convert the extra sugar to fatty triglycerides and a triglyceride level >150 usually means that your blood sugar is also too high.

How High Triglycerides Cause a Fatty Liver
When you have high triglycerides, you use up your good HDL cholesterol because it tries to protect you by carrying triglycerides from your bloodstream into your liver. This is the most common cause of a low HDL (below 40). Your HDL has helped you by clearing excess triglycerides from your bloodstream, but the excess fat collects in your liver to eventually form a fatty liver.

Your body tries to protect you from high rises in blood sugar after meals that causes cell damage. Your pancreas releases insulin that lowers blood sugar levels by driving sugar from your bloodstream into your liver. However, if your liver is full of fat, it cannot accept the sugar and the liver then releases even more sugar from its cells to drive blood sugar levels even higher.

How to Predict High Risk for Diabetes
You are at high risk for diabetes if your:
• triglycerides are higher than 150,
• blood sugar is higher than 140 one hour after eating a meal,
• good HDL cholesterol is lower than 40.
A sonogram of your liver can be used to show whether you have excess fat stored there (“fatty liver“).

Triglycerides Can Also Lead Directly to Heart Attacks
Having high blood triglycerides also puts a person at increased risk for a heart attack because triglycerides can penetrate the inner lining of arteries to start plaques forming in them (Arterioscler Thromb, Nov 1994;14(11):1767-74). Once that has happened, the high triglycerides are associated with inflammation that causes plaques to break off and form clots (Circa Res, 2014;114:214–26) that cause heart attacks (Mymensingh Med J, Jul 2004;13(2):185-7).

Other Reasons for High Triglycerides
The ACC document covers the many other medical conditions associated with high triglycerides, such as poorly controlled diabetes, chronic kidney disease, rheumatoid arthritis or low thyroid function. Many medications can also raise triglycerides; check with your health care provider or pharmacist.

Dietary Treatment for High Triglycerides
• Eat lots of vegetables, but limit starchy root vegetables such as potatoes and sweet potatoes
• Eat lots of legumes (beans, lentils, chickpeas, soybeans, peanuts) and nuts
• Eat whole (unground) grains and restrict refined grains (bakery products, pasta, white rice and so forth)
• Restrict mammal meat and processed meats.
• Eat seafood twice a week or more
• Avoid sugar-sweetened and artificially sweetened beverages
• Avoid sugar-added foods
• Restrict salt
• Restrict alcohol

My Recommendations
If your fasting blood triglyceride levels are greater than 150, you are likely to be pre-diabetic or diabetic and susceptible to cell damage from high blood sugar levels. If you have a big belly and small buttocks, the odds are that you are already diabetic.

Beyond Cholesterol: 14 Ways to Lower Triglycerides


Medically Reviewed by Zilpah Sheikh, MD on August 29, 2023

When Triglycerides Inch Up

When Triglycerides Inch Up

1/16

Maybe you’ve put on a few extra pounds. Now your yearly blood work comes back showing high triglycerides. These fats are an important source of energy in your body, but at high levels they can hurt your heart. Like cholesterol, triglyceride troubles can lead to clogged arteries and possibly to a heart attack or stroke. Luckily, there are many ways to lower your triglycerides.

Why Triglycerides Matter

Why Triglycerides Matter

2/16

High triglycerides can be part of an unhealthy condition called metabolic syndrome. Other parts of this illness can include:

  • Low HDL “good” cholesterol
  • High blood pressure
  • Belly fat
  • High blood sugar

Metabolic syndrome greatly increases your chances of developing heart disease, stroke, and diabetes.

Look at How You Eat

Look at How You Eat

3/16

That creamy latte, grilled cheese sandwich, or scoop of ice cream before bed can all lead to high triglycerides. If you often eat more calories than you burn – like many of us do – your triglycerides may start to inch up. The worst offenders are sugary foods and foods high in saturated fat, like cheese, whole milk, and red meat.

Say No to Sugar

Say No to Sugar

4/16

If you have high triglycerides, get your sweet tooth in check. Simple sugars, especially fructose (a sugar often found in fruit), raise triglycerides. Watch out for foods made with added sugar, including soda, baked goodies, candy, most breakfast cereals, flavored yogurt, and ice cream.

Uncover Hidden Sugar

Uncover Hidden Sugar

5/16

Learn to spot added sugars on food labels. Words to look for include brown sugar, corn syrup, words ending in “ose” (dextrose, fructose, glucose, lactose, maltose, sucrose), fruit juice concentrates, cane syrup, cane sugar, honey, malt sugar, molasses, and raw sugar.

Focus on Fiber

Focus on Fiber

6/16

Swap out foods made with refined white flour, and bring on the whole grains. You’ll eat more fiber, which helps lower your triglycerides. For breakfast, have a bowl of steel-cut oats with berries instead of a bagel or sweet cereal. At lunchtime, try a salad loaded with veggies and garbanzo beans. Choose brown rice or quinoa at dinner instead of potatoes or pasta.

Eat the Right Fat

Eat the Right Fat

7/16

A little fat is good for you, when it’s the healthy kind. Choose foods that naturally contain mono- and polyunsaturated fats: avocados, walnuts, chicken without the skin, canola oil, and olive oil. Avoid trans fats, which are found in many processed foods, French fries, crackers, cakes, chips, and stick margarine. Don’t eat much saturated fat, found in red meat, ice cream, cheese, and buttery baked goods.

Choose Fish Instead of Red Meat

Choose Fish Instead of Red Meat

8/16

The same omega-3 fats that are good for your heart can help lower your triglycerides, too. Next time you eat out, get the fish instead of a burger or steak. Eat fish at least twice a week. Salmon, mackerel, herring, lake trout, albacore tuna, and sardines are all high in omega-3s.

Eat Your Nuts and Greens

Eat Your Nuts and Greens

9/16

Other good sources of omega-3s:

  • Walnuts
  • Flaxseeds
  • Spinach
  • Kale
  • Brussels sprouts
  • Salad greens
  • Beans
Do You Need an Omega-3 Supplement?

Do You Need an Omega-3 Supplement?

10/16

Ask your doctor. Capsules can give you a concentrated amount of omega-3s, but not everyone needs them. You may be able to lower triglycerides by making healthier choices in your life. And high doses of omega-3s can cause bleeding in some people. If your doctor says it’s OK, look for capsules with EPA and DHA, two powerful types of omega-3.

Cut Back on Alcohol

Cut Back on Alcohol

11/16

Do you unwind with wine, beer, or a cocktail? Switch to sparkling water with a squeeze of lime juice. Or try a tangy herbal iced-tea blend that tastes great without added sugar. Excess drinking is one cause of high triglycerides. That means more than one drink a day for women and two drinks a day for men. For some people, even small amounts of alcohol can raise triglycerides.

Skip the Sweet Drinks

Skip the Sweet Drinks

12/16

One of the easiest things you can do to lower your triglycerides is to cut out sweetened drinks. Sodas and other sugary drinks are packed with fructose, a known offender when it comes to boosting triglycerides. Drink no more than 36 ounces of sweet sippers per week — that means three 12-ounce cans of soda.

Lose Weight

Lose Weight

13/16

Extra weight, particularly around your waist, raises triglycerides. One of the biggest things you can do to bring your levels down is to take it off. It doesn’t have to be dramatic, either. 

Get Moving

Get Moving

14/16

If you’re carrying around a few extra pounds, starting regular workouts can get you in shape and lower your triglycerides at the same time. Aim for 30 minutes of exercise five days a week, and be sure to break a sweat and get your heart pumping. You can cut your triglycerides by 20% to 30%. If you’re new to exercise, try a dance class, go for a swim, or take a brisk walk each day.

Get a Checkup

Get a Checkup

15/16

A simple blood test can spot high triglycerides. Your doctor may also look for related health problems. These include kidney disease, a slow thyroid gland, diabetes, and obesity.  Here’s how triglyceride test numbers stack up:

  • Normal – Less than 150 mg/dL
  • Borderline – 150-199 mg/dL
  • High – 200-499 mg/dL
  • Very high – 500mg/dL and up 
When Habits Need a Helping Hand

When Habits Need a Helping Hand

16/16

If lifestyle changes haven’t helped enough, your doctor may suggest adding a prescription medicine. Fibrates, niacin, statins, and high-dose fish oil are a few of the options. Your doctor will look at all your blood fats — triglycerides and all types of cholesterol — to decide the best way to protect your heart.

Omega-3 Meds Not Effective After MI, EMA Panel Concludes


The European Medicine Agency’s (EMA’s) Committee for Medicinal Products for Human Use (CHMP) has concluded that omega-3 fatty acid medicines are not effective for secondary prevention after myocardial infarction (MI).

Omega-3 fatty acid medicines at a dose of 1 g per day have been authorized in several European Union countries since 2000 for preventing heart disease or stroke after MI and for lowering high triglycerides.

When they were authorized, the available data showed “some benefits in reducing serious problems with the heart and blood vessels, although the benefits were considered modest,” the EMA said in a news release. “Further data that have become available since then have not confirmed the beneficial effects of these medicines for this use.”

The CHMP’s conclusion, released at their December meeting, means that these medicines will no longer be authorized for such use.

Their review included results of the open-label GISSI Prevenzione study from 1999, which supported the initial authorization of these products, as well as retrospective cohort studies, more recent randomized controlled trials, and results of meta-analyses.

“The review concluded that, while a small relative risk reduction was seen in the original open label GISSI Prevenzione study, such beneficial effects were not confirmed in more recent randomized controlled trials,” the EMA said. The review found no new safety concerns.

The Committee’s decision does not affect the authorization of omega-3 fatty acid medicines for the treatment of hypertriglyceridemia.

The CHMP opinion will now be forwarded to the European Commission, which will issue a final legally binding decision applicable in all EU member states.

Support for the CHMP decision comes from results of the large VITAL trial, which found little benefit from omega-3 supplements (or vitamin D supplementation) for the prevention of cardiovascular disease, as reported by Medscape Medical News.

In the ASCEND trial, a 1 g dose of omega-3 fatty acids had no effect on serious vascular events (or cancer or mortality) when used for primary prevention in patients with diabetes.

However, in the REDUCE-IT trial, a high-dose purified form of the omega-3 oil, eicosapentaenoic acid (EPA), in patients with elevated triglycerides who had cardiovascular disease or diabetes and one additional risk factor did show significant benefit, with a 25% relative risk reduction in major adverse

Overweight Individuals with T2DM | Keto Diet vs Plate Method Diet


Recently a study was conducted by Saslow LR and colleagues to study whether a very low carbohydrate ketogenic diet with lifestyle factors (intervention) or a “Create Your Plate” diet (control) recommended by the American Diabetes Association (ADA) would improve glycemic control and other health outcomes among overweight individuals with type 2 diabetes mellitus (T2DM).

This article was published in February 2017 in a very reputed journal ‘Journal of Medical Internet Research’. In 2017, the impact factor of this journal was 4.671. For those of you who don’t know what an impact factor is or have never heard of, it simply means the number of times recent articles published in that journal in a year was cited by others. If the impact factor is high, it is considered to be a highly ranked journal.

Now coming back to the study, it was a parallel-group, balanced randomization (1:1) trial. This trial was approved by the University of California, San Francisco, Institutional Review Board and registered with ClinicalTrials.gov (NCT01967992).

In this study, glycemic control, operationalized as the change in glycated hemoglobin (HbA1c) was the primary outcome.

They also assessed body weight, cholesterol, triglycerides, diabetes-related distress, subjective experiences of the diet, and physical side effects.

During the study, the participants were asked to measure urinary acetoacetate (one type of ketone bodies that can be measured in urine) test kits (KetoStix). Basically, there are three types of ketone bodies. Other two types of ketone bodies are acetone and beta-hydroxybutyrate.

The other group i.e. the control group were asked to follow “Create Your Plate” diet recommended by ADA. What does this ADA diet consist of? Well, ADA recommends a low-fat diet which includes green vegetables, lean protein sources, and limited starchy and sweet foods. Most of the doctors worldwide follow ADA guidelines and recommend this particular diet to their patients.

As mentioned earlier the investigators divided the eligible participants into two groups (intervention group and control group).

In fact, when I was diagnosed with T2DM my diabetologist also recommended a low-fat diet with a caloric restriction of 1800 calories. But he never advised me how to restrict my calories to 1800 or what should I eat.  I was totally confused.

Also, he prescribed a couple of oral antidiabetic drugs and a statin. I followed his instructions for a couple of weeks and the result was that within 2 weeks I developed side effects of the drugs. I immediately STOPPED all my medications and started following a keto diet. Finally, I was able to reverse my T2DM. Anyway, that’s a separate story.

Coming back to the study, all the parameters were measured at baseline before randomization in both the groups. Again, all the parameters were measured after 16 and 32 weeks of intervention.

So what conclusions were drawn from this study. Let me list the results of this study in bullet points for better understanding.

  • The investigators observed that there were significantly greater reductions in HbA1cthose who followed the ketogenic diet after 16 as well as 32 weeks
  • Similarly, those who were on keto diet lost more weight than those who followed conventional ADA diet (12.7 kg versus 3 kg)
  • Also, triglycerides level was much lower in the ketogenic group compared to ADA diet followers

This study showed that those who followed a ketogenic diet had several health benefits including lower HbA1c, body weight, and triglyceride levels.

There were few limitations in this study. The number of participants was very less (25 participants) and the follow-up duration of the study was not long.

Despite all limitations, the conclusion we can draw from this study is that low-carbohydrate ketogenic diet and lifestyle changes are beneficial in individuals who are overweight with T2DM.

If you have any queries or any experience to share please type in the comment box. I will try to reply to all your queries.

If you have enjoyed reading this article, I would request you to share with your friends and colleagues who are diagnosed with T2DM. I am sure by reading this article, they will be motivated that it’s not the end of the world if they are diagnosed with T2DM.

With dietary and lifestyle modifications, it is possible to reverse your T2DM.

Omega-3 Meds Not Effective After MI, EMA Panel Concludes


The European Medicine Agency’s (EMA’s) Committee for Medicinal Products for Human Use (CHMP) has concluded that omega-3 fatty acid medicines are not effective for secondary prevention after myocardial infarction (MI).

Omega-3 fatty acid medicines at a dose of 1 g per day have been authorized in several European Union countries since 2000 for preventing heart disease or stroke after MI and for lowering high triglycerides.

When they were authorized, the available data showed “some benefits in reducing serious problems with the heart and blood vessels, although the benefits were considered modest,” the EMA said in a news release. “Further data that have become available since then have not confirmed the beneficial effects of these medicines for this use.”

The CHMP’s conclusion, released at their December meeting, means that these medicines will no longer be authorized for such use.

Their review included results of the open-label GISSI Prevenzione study from 1999, which supported the initial authorization of these products, as well as retrospective cohort studies, more recent randomized controlled trials, and results of meta-analyses.

“The review concluded that, while a small relative risk reduction was seen in the original open label GISSI Prevenzione study, such beneficial effects were not confirmed in more recent randomized controlled trials,” the EMA said. The review found no new safety concerns.

The Committee’s decision does not affect the authorization of omega-3 fatty acid medicines for the treatment of hypertriglyceridemia.

The CHMP opinion will now be forwarded to the European Commission, which will issue a final legally binding decision applicable in all EU member states.

Support for the CHMP decision comes from results of the large VITAL trial, which found little benefit from omega-3 supplements (or vitamin D supplementation) for the prevention of cardiovascular disease, as reported by Medscape Medical News.

In the ASCEND trial, a 1 g dose of omega-3 fatty acids had no effect on serious vascular events (or cancer or mortality) when used for primary prevention in patients with diabetes.

However, in the REDUCE-IT trial, a high-dose purified form of the omega-3 oil, eicosapentaenoic acid (EPA), in patients with elevated triglycerides who had cardiovascular disease or diabetes and one additional risk factor did show significant benefit, with a 25% relative risk reduction in major adverse cardiovascular events.

Omega-3 Meds Not Effective After MI, EMA Panel Concludes


The European Medicine Agency’s (EMA’s) Committee for Medicinal Products for Human Use (CHMP) has concluded that omega-3 fatty acid medicines are not effective for secondary prevention after myocardial infarction (MI).

Omega-3 fatty acid medicines at a dose of 1 g per day have been authorized in several European Union countries since 2000 for preventing heart disease or stroke after MI and for lowering high triglycerides.

When they were authorized, the available data showed “some benefits in reducing serious problems with the heart and blood vessels, although the benefits were considered modest,” the EMA said in a news release. “Further data that have become available since then have not confirmed the beneficial effects of these medicines for this use.”

The CHMP’s conclusion, released at their December meeting, means that these medicines will no longer be authorized for such use.

Their review included results of the open-label GISSI Prevenzione study from 1999, which supported the initial authorization of these products, as well as retrospective cohort studies, more recent randomized controlled trials, and results of meta-analyses.

“The review concluded that, while a small relative risk reduction was seen in the original open label GISSI Prevenzione study, such beneficial effects were not confirmed in more recent randomized controlled trials,” the EMA said. The review found no new safety concerns.

The Committee’s decision does not affect the authorization of omega-3 fatty acid medicines for the treatment of hypertriglyceridemia.

The CHMP opinion will now be forwarded to the European Commission, which will issue a final legally binding decision applicable in all EU member states.

Support for the CHMP decision comes from results of the large VITAL trial, which found little benefit from omega-3 supplements (or vitamin D supplementation) for the prevention of cardiovascular disease, as reported by Medscape Medical News.

In the ASCEND trial, a 1 g dose of omega-3 fatty acids had no effect on serious vascular events (or cancer or mortality) when used for primary prevention in patients with diabetes.

However, in the REDUCE-IT trial, a high-dose purified form of the omega-3 oil, eicosapentaenoic acid (EPA), in patients with elevated triglycerides who had cardiovascular disease or diabetes and one additional risk factor did show significant benefit, with a 25% relative risk reduction in major adverse cardiovascular events.