omega-3 fatty acids Archives - Health Tips From The Professor

Are Omega-3 Supplements Safe?

July 9, 2024 by Dr. Steve Chaney

The Flaws And Blind Spots In This Study

Author: Dr. Stephen Chaney

Has the omega-3 pendulum swung again? The recent headlines are downright scary. For example:

“Fish Oil May Increase the Risk of Stroke and Heart Conditions.”

“Fish Oil Supplements May Cause Harm, Study Finds. Is It Time to Ditch Them?”

“Fish Oil Supplements May Lead to Heart Problems”.

“Regular Use of Fish Oil Supplements Might Increase, Rather Than Lessen, The Risk of First Time Heart Disease and Stroke Among Those in Good Cardiovascular Health.”

Yikes! That sounds bad. Should we be thinking about giving up our omega-3 supplements?

But wait. Just a few weeks earlier we were reading headlines about the benefits and lack of side effects from omega-3 supplements. That’s confusing. Which headlines are correct?

To answer these questions:

I will review the study (G Chen et al, BMJ Medicine 2024; 3e000451.doi.10.1136/bmjmed-2022-000451) behind the headlines.

I will point out the flaws and blind spots in the study.

I will strip away the hyperbole and put the headlines into perspective.

How Was The Study Done?

The investigators made use of data from the UK Biobank Study. The UK Biobank Study is a large, long-term study in the United Kingdom which was designed to investigate the contributions of genetic predisposition and environmental exposure [including diet and supplementation] to the development of disease.

The UK Biobank Study enrolled 502,461 participants, aged 40-69 years, between January 1^st, 2006 and December 31^st, 2010. Participants were followed from entry into the program until March 31^st 2021, an average of 11.9 years.

The current study excluded any participants who had a diagnosis of atrial fibrillation, heart failure, heart attack, stroke, or cancer at entry into the study, leaving 415,737 participants.

The participants were:

55% women.
Average age of 56 years, with 83.4% of them below 65 years old at entry into the study.
94.5% white.

The study was designed in a unique manner, in that it was designed to test the effect of omega-3 supplements on 6 specific transitions:

Primary prevention. This measured the transition of healthy (no diagnosed heart disease) people to either atrial fibrillation, major cardiovascular events, or death.

Secondary prevention. This measured the transition from atrial fibrillation to either major cardiovascular events or death.

Tertiary prevention. This measured the transition from major cardiovascular events to death.

Major cardiovascular events were further broken down to heart attacks, stroke and heart failure.

Participants were asked whether they used fish oil supplements when they entered the study and were categorized as either regular users or non-users. [Note: The users were not asked the dose or brand of fish oil supplements they used.]

Deaths were obtained from the national death registry and disease diagnosis from the National Health Service.

Are Omega-3 Supplements Safe?

Here is what the study found.

Primary Prevention – For healthy individuals (defined as having no diagnosed heart disease) using omega-3 supplements for an average of 11.9 years:

Increased the risk of atrial fibrillation by 13%.

Did not affect the risk of major cardiovascular events and death were unaffected by omega-3 supplementation.

When major cardiovascular events were broken down to their component parts, omega-3 supplementation:

- Decreased the risk of heart failure by 8%.

- Increased the risk of stroke by 5% (this was just barely statistically significance).

- Did not affect the risk of heart attack.

Secondary Prevention – For individuals with atrial fibrillation omega-3 supplementation:

Decreased the risk of major cardiovascular events by 9%.

Decreased the risk of death by 8%.

When major cardiovascular events were broken down into their component parts, omega-3 supplementation:

Decreased the risk of heart attacks by 15%.

Had no effect on the risk of stroke or heart failure.

Tertiary Prevention – For people who suffered major cardiovascular events during the study omega-3 supplementation:

Decreased the risk of death by 8%.

Since this is a very complex set of data, I have coded positive results in green and negative results in red.

And as if these complexities were not enough, when the investigators broke these effects down by population groups:

Omega-3 supplementation decreased the transition from healthy to death for men (7% decrease) and participants older than 65 (9% decrease).

I will discuss the significance of these observations below.

The authors concluded, “Regular use of fish oil supplements might be a risk factor for atrial fibrillation and stroke among the general population but could be beneficial for [reducing] progression of cardiovascular disease from atrial fibrillation to major adverse cardiovascular events, and from atrial fibrillation to death.”

In short, they were suggesting that omega-3 supplements should be avoided by the general population because they have no positive benefits and might increase the risk of atrial fibrillation and stroke. But omega-3 supplements may be useful for those who already have heart disease.

Some of the articles you may have read about the study repeated this message. Others just emphasized the negative aspects of the study.

But is this message accurate? Let me start by discussing the flaws, blind spots, and hidden data in this study. Then I will summarize the 3 key findings of the study and tell you what they mean for you.

The Flaws, Blind Spots, And Hidden Data In This Study

Flaws: As I said above, there were two major flaws in the study.

Flaw #1: The study did not identify the dose of supplement used. This is important because the increased risk of atrial fibrillation and stroke is primarily seen in clinical trials using high dose omega-3 supplements.

Flaw #2: This was an association study which cannot prove cause and effect. However, the authors of this study reported it as showing that omega-3 supplement use caused atrial fibrillation and stroke – and all the news reports on the study have repeated that claim.

Flaw #3: Other experts have pointed out that the authors inflated the risks associated with omega-3 supplementation by reporting relative risk rather than absolute risk. Let me try to simplify the distinction.

The risk of atrial fibrillation was 4.24% in the non-supplement users and 4.80% in the omega-3 supplement users. That is an absolute increase in risk of 0.56% (4.80% – 4.24%). This is the increase in risk you actually experience. In contrast, 4.80% is 13% greater than 4.24%, which is how relative risk is calculated.

In response to the questions you are probably thinking:

Yes, this is a perfect example of the Mark Twain quote, “There are lies. There are damn lies. And then there are statistics.”

Yes, all the percentages reported in this study are based on relative risk and are, therefore, inflated. However, I do not have access to their data, so I cannot tell you the absolute risk associated with their other observations.

Blind Spots: In their paper the investigators recommended against the use of omega-3 supplements to prevent heart disease because their data showed:

No benefit of omega-3 supplementation for preventing major cardiovascular events and deaths in a healthy population.

But did suggest an increased risk of atrial fibrillation and stroke in that same population.

However, their blind spot was in underestimating the difficulty of showing the benefit of any intervention in a healthy population. The example I always use is statin drugs. Statin Drugs:

Dramatically reduce the risk of a second heart attack and/or death in people who have already had a heart attack.

Reduce the risk of heart attacks in people who are at high risk of heart attacks.

Cannot be shown to reduce the risk of heart attacks in a healthy population.

This study suggests that omega-3 supplements are no different. In this study, omega-3 supplements:

Reduced the risk of death in people who had already experienced a major cardiovascular event like a heart attack or stroke.

Reduced the risk of major cardiovascular events and death in people with atrial fibrillation, which puts them at high risk for a heart attack or stroke.

Could not be shown to reduce the risk of major cardiovascular events or deaths in a healthy population.

Hidden Data: There are some important data that were buried in the text and supplemental figures but were ignored in the concluding remarks of this study and all the articles written about it. For example:

The original study and all articles written about the study reported that omega-3 supplementation increased the risk of stroke in otherwise healthy individuals but ignored the observation that omega-3 supplementation decreased the risk of heart failure in that same group.

The second example of hidden data likely represents another blind spot of the authors. They concluded that omega-3 supplementation had no benefit for healthy individuals without asking whether omega-3 supplements might benefit higher-risk subpopulations within this group. To help you understand this statement let me start by giving you some perspective.

As I said above, statin drugs cannot be shown to reduce the risk of heart attacks in a healthy population. But when you include people at high risk of heart disease with healthy people in the dataset, you start to see a reduced risk of heart attacks.

Similarly, with supplements you often see no benefits with the general population, which is what is usually reported in the media. But when you look at higher risk groups within that population, the benefits of supplementation emerge.

This study is no different:

For healthy individuals, omega-3 supplementation had no effect on deaths during the 12-year follow-up period.

However, omega-3 supplementation reduced the risk of death by 9% for both men and people ≥ 65. These represent two groups with elevated risk of heart disease within the otherwise healthy population.

Once again, these data were completely ignored.

What Does This Study Mean For You?

This study made 3 major points:

Point #1: Let me start with the one you’ve heard the most about. The risk of atrial fibrillation and stroke associated with omega-3 supplementation is real. We should not ignore it.

But what this study and most of the reports on the study didn’t tell you is that the risk is dose dependent. The risk is primarily seen with high doses of omega-3s. While no one has done a comprehensive dose response analysis, I can tell you that these side effects are:

Seldom reported in clinical studies at doses of 1 gm/day or less.
Sometimes reported in clinical studies at doses of ≥2 gm/day.
Frequently reported in clinical studies at doses of ≥4 gm/day.

However, atrial fibrillation and stroke occur in a very small percentage of omega-3 users, even at 4 gm/day. At this point we have no idea why some people are susceptible to these side effects and others are not. More research in this area is clearly needed.

Until we know more about who is at risk, my recommendation for people who are trying to reduce the risk of heart disease is to rely on something called the Omega-3 Index to determine your individual omega-3 needs rather than using high-dose omega-3 supplements.

The Omega-3 Index measures the amount of omega-3 fatty acids in your tissues. It is determined by the amount of omega-3s you consume and how you metabolize them, so it is individualized to you.

An Omega-3 Index of 4% is associated with a high risk of heart disease, while an Omega-3 Index of 8% is associated with a low risk of heart disease. There is no evidence that more than 8% provides additional benefit.

Most importantly, it only takes 1-1.6 gm/day of omega-3s to raise your Omega-3 Index from 4% to 8%. At these doses your risk of atrial fibrillation and stroke is extremely small.

For example, a recent meta-analysis of 29 studies with a total of 183,292 participants reported that people with an 8% Omega-3 Index had:

Decreased risk of ischemic stroke (stroke due to blood clots) with no detectable increased risk of hemorrhagic stroke (stroke due to bleeding), and…

No detectable increased risk of atrial fibrillation.

I recommend getting your Omega-3 Index determined, and if it is low, increasing your omega-3 intake to get it into the 8% range. Some people go from 4% to 8% more rapidly than others, so you may need to repeat the test several times to optimize your Omega-3 Index.

If your health professional doesn’t have access to the Omega-3 Index test, you can order it from https://omegaquant.com (I have no financial stake in this company, but I know it as a reputable source of the Omega-3 Index test).

Does The Professor Plan To Reduce His Intake Of Omega-3 Fatty Acids? Three weeks ago, I shared that my wife and I have been taking around 3 gm/day of omega-3 supplements for the past 40 years. Now that the association of atrial fibrillation and stroke with high dose omega-3 intake has been firmly established, some of you may be wondering whether we plan to decrease our intake of omega-3 supplements.

The answer is, “No”. Remember that the increased risk of atrial fibrillation and stroke is only seen for a small subset of people taking high-dose omega-3 supplements. If we were part of that subset, we would likely have experienced one of those side effects by now.

However, if you are considering omega-3 supplementation for the first time, you don’t know whether you are part of that subset or not. So, my advice remains the same. Rely on optimizing your Omega-3 Index rather than high-dose omega-3 supplementation.

Point #2: Healthy individuals (those with no symptoms of heart disease) do not benefit from omega-3 supplementation. As I pointed out above, this ignores data from their study, namely.

Omega-3 supplementation reduced the risk of heart failure in healthy subjects.

Omega-3 supplementation reduced the risk of death in higher risk groups within the healthy population (namely men and people 65 and older).

As I discussed above, this is a pattern seen with statin drugs and most nutritional supplements. Simply put, you can’t show any benefit of statin drugs or most nutritional supplements in a “healthy” population, but you can show benefit when you focus on higher risk individuals within the “healthy” population.

The problem, of course, is that most of us don’t really know whether we are “healthy” or not. For millions of Americans the first indication that they are at risk from heart disease is sudden death from a heart attack or stroke.

With that in mind, I will leave the decision about whether you want to supplement with omega-3s up to you. But if you decide to supplement, I recommend you optimize your Omega-3 Index rather than using a high dose omega-3 supplement.

Point #3: People with heart disease benefit from omega-3 supplementation. This recommendation is becoming non-controversial, so I won’t comment further other than to say high dose omega-3 supplements are probably not needed unless prescribed by your health professional.

The Bottom Line

You have been asking me about recent headlines saying that omega-3 supplements may increase rather than decrease the risk of heart disease. So, I analyzed the study behind the headlines. The study makes 3 claims:

Omega-3 supplements increase the risk of atrial fibrillation and stroke when taken by healthy people.

Omega-3 supplements are of no benefit for healthy individuals.

Omega-3 supplements are beneficial for people who have heart disease.

In the article above I review the flaws, blind spots, and hidden data in the article and discuss what it means for you.

For more details about this study and what it means for you read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease.

______________________________________________________________________________

My posts and “Health Tips From the Professor” articles carefully avoid claims about any brand of supplement or manufacturer of supplements. However, I am often asked by representatives of supplement companies if they can share them with their customers.

My answer is, “Yes, as long as you share only the article without any additions or alterations. In particular, you should avoid adding any mention of your company or your company’s products. If you were to do that, you could be making what the FTC and FDA consider a “misleading health claim” that could result in legal action against you and the company you represent.

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

_______________________________________________________________________

About The Author

Dr. Chaney has a BS in Chemistry from Duke University and a PhD in Biochemistry from UCLA. He is Professor Emeritus from the University of North Carolina where he taught biochemistry and nutrition to medical and dental students for 40 years. Dr. Chaney won numerous teaching awards at UNC, including the Academy of Educators “Excellence in Teaching Lifetime Achievement Award”. Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading biochemistry text books for medical students.

Since retiring from the University of North Carolina, he has been writing a weekly health blog called “Health Tips From the Professor”. He has also written two best-selling books, “Slaying the Food Myths” and “Slaying the Supplement Myths”. And most recently he has created an online lifestyle change course, “Create Your Personal Health Zone”. For more information visit https://chaneyhealth.com.

For the past 45 years Dr. Chaney and his wife Suzanne have been helping people improve their health holistically through a combination of good diet, exercise, weight control and appropriate supplementation.

Does EPA Reduce Migraine Frequency?

June 11, 2024 by Dr. Steve Chaney

What Causes Migraines And The Role Of Omega-3s In Prevention

Author: Dr. Stephen Chaney

Migraines can be debilitating. And they affect millions of Americans. According to a recent survey 17.1% of women and 5.6% of men in the United States suffer migraine symptoms.

Symptoms range from frequent headaches to visual disturbances, nausea and vomiting, extreme light and sound sensitivity, brain fog, and debilitating pain. Sometimes all a migraine sufferer can do is retreat to a dark, quiet room and wait out the symptoms. This makes it virtually impossible to work, socialize, and interact with family.

For example, work absenteeism due to migraines is thought to cost US businesses up to $13 billion dollars annually. And, of course, there is no way to estimate the psychological cost of lost interactions with family and friends. And people who experience frequent migraines are more likely to suffer from depression, anxiety, and sleep disorders.

Medications can provide some relief from migraine symptoms, but they all have side effects. Various natural approaches for migraine relief have been proposed, but none of them are proven.

What Causes Migraines And The Role Of Omega-3s In Prevention

Our understanding of migraines is complicated by the fact there appear to be multiple causes of migraines. It’s almost as if what we call “migraines” are really a variety of diseases with different causes but similar symptoms.

Migraines can be triggered by:

Hormonal fluctuations.
Weather changes.
Foods
- The top 3 food triggers of migraines are caffeine, red wine, and chocolate.
- Other common food triggers are artificial sweeteners, foods containing MSG, cured meats, aged cheeses, pickled and fermented foods, frozen foods, and salty foods.
Stress
Lack of sleep.
Certain drugs.
Missed meals.

Migraine triggers vary from person to person. And multiple neurophysiological pathways have been proposed to explain how each of these triggers progresses to a full-blown migraine.

To simplify a very complex subject, there are three main factors that influence each of these proposed pathways:

Susceptibility to migraines clearly runs in families.

75% of migraine sufferers are women.

Inflammation.

Because inflammation plays a strong role in progression and severity of migraines, there has been a strong interest in the use of long-chain omega-3s like EPA and DHA as nutraceuticals to reduce the frequency and severity of migraines.

However, previous studies have had mixed results. Some have suggested that omega-3s reduce the risk of migraines while others have come up empty.

The authors of the current study (H-F Wang, et al, Brain, Behavior, and Immunity 118, 459-467, 2024) postulated that some previous studies failed to find a benefit of omega-3 supplementation because they were too short in duration, used a mixture of omega-3s, or were poorly designed.

They noted that high dose EPA alone had proven to be effective in reducing the risk of heart disease and depression. So, they performed a 12-week randomized, double-blind, placebo-controlled clinical trial with migraine sufferers using 1.8 grams of EPA per day.

How Was This Study Done?

This was a double-blind, placebo-controlled clinical trial, the gold standard for clinical studies. The investigators recruited 70 patients (15 men and 55 women) with episodic migraines (defined as migraines with or without aura occurring fewer than 15 days per month) from the neurology clinic of Kuang Tien General Hospital in Taiwan. The average age of the patients was 39 years old.

The subjects were randomly assigned to use either 1.8 gm/day of EPA or a soybean oil placebo for 12 weeks. Both were formulated with an orange flavoring to hide the taste difference. Neither the patients nor the physicians conducting the study knew who got the EPA and who got the placebo.

The patients filled out an extensive questionnaire about their migraines and related issues at entry into the study and at the end of 12 weeks. They were also asked to maintain headache diaries for at least 4 weeks prior to the study and for every 4 weeks of the 12-week study. They received training from the study coordinator on how to fill out the diaries and were encouraged to contact the coordinator if they had any questions about how to accurately fill out the diary.

The primary outcome of the study was the decrease in migraine frequency from baseline to 12 weeks. The study also assessed changes in:

Headache severity.

The need to use headache medicines.

Migraine-specific disability (The extent to which migraines resulted in disability).

Migraine-specific quality of life index (The extent to which migraines affected the quality of life).

Anxiety and depression (These are often side effects of chronic migraines).

While some of those outcomes appear to be overlapping, they are all well-established assessments used in migraine research. The questionnaire the doctors used was designed to provide a numerical rating for each of these outcomes.

Does EPA Reduce Migraine Frequency?

As expected, there were no significant changes in the placebo group. But in the group taking 1.8 gm/day of EPA:

Migraine frequency decreased by 60%.

Frequency that headache medication was needed decreased by 45%.

Headache severity decreased by 14%.

Sleep quality increased by 17%, but that increase was not statistically significant.

Migraine-related disability decreased by 73%.

Migraine-related quality of life improved by 31%.

Anxiety and depression decreased by 53%.

These differences were statistically significant for the women in the study, but not for men – probably because of the small number of men in the study.

The study also assessed side effects from EPA supplementation in this group. Side effects were minimal and were not different from the placebo group.

The authors concluded, “High-dose EPA significantly reduced migraine frequency and severity. Improved psychological symptoms and quality of life in migraine patients, and showed no adverse events [effects], suggesting its potential for prophylactic use for migraine patients.”

They went on to say, “The results of this study may not only serve as a valuable reference for future large-scale randomized clinical trials to investigate the optimal dosing and components of omega-3 fatty acids for migraine prevention but also underscore the need for replication of these findings in adequately powered and controlled studies.”

In other words, this study needs to be confirmed by additional studies. And future studies need to determine the optimal dose of EPA and the optimal ratio of EPA to DHA.

What This Study Means For Us And For You

The topic of omega-3s and migraines is of special significance for us. About 40 years ago my wife and I started taking a high purity omega-3 supplement containing both EPA and DHA to control inflammation. We didn’t have noticeable inflammation at the time, but we both had parents who suffered from rheumatoid arthritis and wished to avoid their suffering later in life.

In just a few weeks the migraines my wife had been experiencing for years disappeared. That piqued my interest, so I searched the literature and found several studies showing that omega-3 fatty acids reduce migraine symptoms. I have followed the twists and turns of omega-3 – migraine research ever since, which is how I came across this study.

As for our original purpose in taking an omega-3 supplement, all I can say is that we are now in our 80s, and neither of us suffer from the rheumatoid arthritis that plagued our parents.

And for my wife the disappearance of her migraines was an unexpected side benefit.

This study is a strong validation of the effect of omega-3s on reducing migraine symptoms. However, it is not the end of the story. As the authors said:

It needs to be confirmed by larger, well controlled studies.

The optimal dose of omega-3s needs to be determined.

The optimal ratio of EPA to DHA and possibly other long chain omega-3s needs to be determined.

This study used 1.8 grams/day of pure EPA. My wife takes 3 grams of EPA and 2 grams of DHA each day. But we don’t know whether she would experience the same benefit from a lower dose or whether that is the optimal ratio of EPA to DHA. We do know that EPA and DHA have different health benefits, so we plan to continue taking a supplement that contains both.

And finally, as I said above, it is almost as if what we call migraines are really a cluster of diseases with similar symptoms. There are multiple migraine triggers and multiple proposed explanations of how these triggers lead to full-blown migraines.

So, we shouldn’t think of omega-3s as a magic bullet. Rather, we should think of them as one of many approaches that may provide you with some migraine relief.

The Bottom Line

A recent double-blind, placebo controlled clinical study with migraine sufferers reported that when they were given 1.8 gm/day of EPA for 12 weeks:

Migraine frequency decreased by 60%.

Frequency that headache medication was needed decreased by 45%.

Headache severity decreased by 14%.

Migraine-related disability decreased by 73%.

Migraine-related quality of life improved by 31%.

Anxiety and depression decreased by 53%.

In other words, this study needs to be confirmed by additional studies. And future studies need to determine the optimal dose of EPA and the optimal ratio of EPA to DHA.

For more details about this study and what it means for you read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease.

______________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

____________________________________________________________________________

About The Author

Do Omega-3s Reduce Osteoarthritis Pain?

April 16, 2024 by Dr. Steve Chaney

How Do Rheumatoid And Osteoarthritis Differ?

Author: Dr. Stephen Chaney

This week I am concluding my series on recent omega-3 advances by reviewing a meta-analysis that asks whether omega-3s are beneficial for people with osteoarthritis.

This is an important question because osteoarthritis affects around 32.5 million adults in the United States, and that number is increasing each year as our population ages. Osteoarthritis causes pain and disabilities that can significantly affect quality of life.

And the costs are high. Health care costs due to osteoporosis are around $140 billion/year. And when you include lost workdays, the annual cost is around $468 billion.

There are several medications for reducing symptoms of osteoarthritis. But they each have side effects and some patients cannot tolerate them. Joint replacement surgery is the final resort. But the recovery period is long, and the surgery isn’t always effective. For both reasons many patients with osteoarthritis are looking for natural solutions.

Most of the research on omega-3s and arthritis has been done with patients who have rheumatoid arthritis. Omega-3 supplements have been shown to reduce the pain, swelling of the joints, and inflammation associated with rheumatoid arthritis for many people with the disease.

Based on several dose-response studies, the NIH says the optimal dose is around 2.7 gm/day of EPA + DHA but cautions not to go above 3 gm/day without your doctor’s OK.

The evidence is less clear for omega-3s and osteoarthritis. Some studies suggest that EPA + DHA reduce the pain and inflammation associated with osteoarthritis. But other studies have come up empty. There is no consensus as to whether omega-3s are beneficial for people with osteoarthritis.

When there is disagreement between individual studies, a meta-analysis of the studies is often helpful. By pooling the data from multiple studies, a meta-analysis can smooth out some of the differences between the studies and accumulate enough data points to discover effects that would not have been statistically significant with the smaller data sets from individual studies.

With that in mind, the authors of this manuscript (W Den et al, Journal of Orthopaedic Surgery and Research, 18: 381, 3023) performed a meta-analysis on the data obtained from 9 double-blind, placebo-controlled studies looking at the effect of omega-3s versus a placebo on both pain and joint mobility in osteoarthritis patients.

How Do Rheumatoid And Osteoarthritis Differ?

While the causes of rheumatoid arthritis and osteoarthritis are very different, there are some underlying similarities between the two diseases that suggest both might benefit from omega-3 supplementation.

Rheumatoid Arthritis: Rheumatoid arthritis is thought to be an autoimmune disease, which means that our immune system attacks our cells rather than foreign invaders. It results in chronic inflammation that attacks our joints and can affect other tissues in our body.

It initially affects the lining of our joints which can result in painful, swollen joints. As the disease progresses it can also lead to bone erosion and joint deformity.

Osteoarthritis:Osteoarthritis is generally thought of as a “wear and tear” disease. It is associated with sports injuries and accidents. It is also associated with stress to particular joints due to repeated motions associated with either sports or a job. Obesity also increases wear and tear of the joints because it increases the load on the joints.

The wear and tear causes the cartilage that cushions the junction between bones to deteriorate. Eventually, the cartilage deteriorates to the extent that bone is grinding against bone, which can lead to bone loss and deformities.

Eventually, this results in an inflammation of the joint lining which causes pain and accelerates bone loss. It also causes deterioration of the connective tissue which holds bones together and connects them to muscle.

What Do These Diseases Have In Common? Inflammation is the common factor associated with both rheumatoid and osteoarthritis, and many studies suggest that omega-3s reduce inflammation. In the simplistic description of the two diseases I shared above, it sounds like inflammation occurs much earlier in the disease process for rheumatoid arthritis than for osteoarthritis. This might suggest that omega-3s could be more effective at reducing the symptoms and progression of rheumatoid arthritis than of osteoarthritis.

However, we know that the risk of developing osteoarthritis is increased by chronic inflammation caused by obesity, diseases like diabetes, and/or an inflammatory diet.

How Was This Study Done?

This study was a meta-analysis of 9 double-blind, placebo-controlled clinical studies looking at the effect of omega-3 fatty acids on the pain and loss of joint mobility associated with osteoarthritis. These studies were performed in countries from around the world and included a total of 2,070 participants.

The criteria for inclusion in the meta-analysis were:

1) The articles were written in English.

2) The studies had to be double-blind, placebo-controlled studies (The gold standard for clinical studies).

3) Patients with osteoarthritis were randomly assigned to an intervention group receiving omega-3 supplementation or a placebo group receiving olive oil or another plant oil.

4) The studies measured efficacy and safety outcomes including joint pain (efficacy), joint mobility (efficacy), and treatment-related adverse events (safety).

5) Patients in both the omega-3 and placebo groups were using medications to reduce osteoarthritis symptoms when they were enrolled in the study and were advised to continue with their prescribed medicines for the duration of the study.

The characteristics of the clinical studies included in this meta-analysis were:

Sample size (47-1221), Average = 230.

Mean age (55.9-68), Average = 63.

% men (13.8-45.1%), Average = 31%.

Omega-3 (EPA + DHA) dose (350 mg/day – 2,400 mg/day), Average = 1,085 mg/day.

Do Omega-3s Reduce Osteoarthritis Pain?

When the data from all 9 studies were combined in a single meta-analysis, omega-3 (EPA + DHA) supplementation:

Reduced joint pain by 29% compared to the placebo.

Increased joint mobility by 21% compared to the placebo.

Was not associated with any adverse effects.

The authors concluded, “The results of the meta-analysis indicate that supplementation with omega-3 fatty acids is effective to relieve pain and improve joint function in patients with osteoarthritis, without increasing the risk of treatment-related adverse events. These findings support the use on omega-3 fatty acid supplementation as an alternative treatment for osteoarthritis.”

What Are The Strengths and Limitations Of This Study?

Strengths:

All the studies included in this meta-analysis were randomized, double-blind, placebo-controlled studies (the gold standard for clinical trials).

All the individual studies that qualified for this meta-analysis found that omega-3 supplementation reduced joint pain and improved joint mobility. This improves confidence that the conclusions of the meta-analysis are correct. The meta-analysis simply improved the statistical significance of this conclusion by combining the data from the individual studies.

Limitations:

The biggest limitation was that the individual studies included in this meta-analysis were not performed under the guidelines of the “Fatty Acids and Outcomes Research Consortium” that I discussed in last week’s issue of “Health Tips From the Professor”.

- The “Fatty Acids and Outcomes Research Consortium” guidelines harmonize the designs of individual studies, which strengthens the meta-analysis.

- - In contrast, the design of the individual studies within this meta-analysis was very different, which prevented the meta-analysis from being able to determine the optimal dose of omega-3 supplements and the minimum time required for omega-3 supplementation to significantly reduce the symptoms of osteoarthritis.

- The “Fatty Acids and Outcomes Research Consortium” guidelines would have also required these studies to measure tissue levels of omega-3s (something called Omega-3 Index) at the beginning and end of each study. This was not done in any of these studies.

- - This is important because if a patient’s tissue levels of omega-3s at the beginning of the study were already in the optimal range, you would expect little additional benefit from supplementation for that patient.

All the individual studies were very small. This limits the ability of these studies to provide definitive conclusions. Unfortunately, this is probably unavoidable.

- Double blind, placebo-controlled clinical studies are expensive. Only major pharmaceutical companies have the multi-million-dollar budgets required to conduct large double blind, placebo-controlled clinical studies that would provide more definitive evidence that omega-3 supplementation reduces the symptoms of osteoarthritis – and the follow-up studies that would determine the optimal dose of omega-3 supplements and the minimum time required to show an effect of omega-3 supplementation.

The patients in these studies were already taking medications to reduce their osteoarthritis symptoms prior to entering the study and were instructed to continue taking those medications during the study. This means that the studies were not asking whether omega-3s alone were effective at reducing osteoarthritis symptoms. They were asking whether omega-3 supplementation provided any additional benefits for people who were already taking medications to reduce symptoms.

- Unfortunately, this is also probably unavoidable. Current guidelines consider it unethical to withhold the medical “standard of care” from any patient in a clinical trial.

What Does This Study Mean For You?

This study, while not definitive, strengthens the evidence that omega-3 supplements containing EPA + DHA may reduce joint pain and improve joint mobility for people with osteoarthritis. It also shows that the doses required to achieve these benefits are not associated with any significant side effects.

While large scale double blind, placebo-controlled clinical studies to confirm these conclusions would be nice, they are unlikely to occur for the reasons discussed above.

The investigators said, “[This study shows that] supplementation of omega-3 fatty acids is effective to relieve pain and improve joint function in patients with osteoarthritis…These findings support the use of omega-3 fatty acid supplementation as an alternative treatment for osteoarthritis.”

This might lead you to believe that omega-3 fatty acids can potentially replace medications for reducing osteoarthritis pain and loss of joint mobility. That may be true, but that is not what the study showed.

Patients in both the omega-3 and placebo group continued their prescribed medicines for osteoarthritis. In reality, the study only shows that omega-3s provide additional benefit for people already taking osteoarthritis medications. The effect of omega-3 supplements by themselves has not been tested and, as I discussed above, is not likely to be tested in the foreseeable future.

However, the use of omega-3 supplements may allow you to reduce or eliminate the medications you are on for osteoarthritis and may delay the need for joint replacement surgery. Of course, if you wish to reduce/eliminate your medications and/or delay joint replacement surgery, I recommend consulting with your doctor first.

Finally, this study provides no information on the optimal dose of omega-3s. Some studies suggest the dose of omega-3s needed to reduce osteoarthritis symptoms may be less than that required to reduce rheumatoid arthritis symptoms, but that evidence is weak.

In the absence of good dose response data, I recommend you aim for an omega-3 index of 8%. You will find a more detailed discussion of the Omega-3 Index and how to use it in last week’s “Health Tips From the Professor” article .

The Bottom Line

A recent meta-analysis looked at the effect of omega-3 supplementation on the pain and lack of joint mobility associated with osteoarthritis.

The study showed that omega-3 (EPA + DHA) supplementation:

Reduced joint pain by 29% compared to the placebo.

Increased joint mobility by 21% compared to the placebo.

Was not associated with any adverse effects.

For more details about the study and what it means for you, read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease.

_____________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

_______________________________________________________________________

About The Author

The Good News About Omega-3s And Stroke

April 9, 2024 by Dr. Steve Chaney

How Do Omega-3s Affect The Two Types Of Stroke?

Author: Dr. Stephen Chaney

I am continuing my series on recent omega-3 breakthroughs. Last week I reviewed a study showing that the omega-3s EPA and DHA lowered blood pressure. Since high blood pressure is a major contributing factor to stroke risk, it only makes sense that EPA and DHA would also decrease the risk of strokes.

In last week’s article I mentioned that high blood pressure is called a silent killer. That is because the symptoms of high blood pressure are easy to ignore and often confused with other illnesses.

For many people the first indication they have a problem is when they have a stroke, which either kills them or forever impacts their quality of life. Let me share some statistics with you.

Every 40 seconds someone in the United States has a stroke. One in four adults over the age of 25 will have a stroke in their lifetime.
Every 4 minutes someone in the United States dies from a stroke. For many of them sudden death is the first indication they had a health problem.
The overall incidence of strokes has increased 60% in the last 20 years with most of that increase (65%) coming from younger adults (ages 20 to 45)
The cost of treatment, rehabilitation, and lost wages from stroke was $891 billion in 2020 and is projected to increase to $2.3 trillion in 2050.

Any way you look at it, the personal and financial costs of strokes are immense.

How Do Omega-3s Affect The Two Types Of Stroke?

There are two major kinds of stroke – ischemic stroke, which is caused by a thrombus (blood clot) in the carotid arteries leading to the brain, and hemorrhagic stroke, which is caused by bleeding from small blood vessels in the brain. Ischemic stroke accounts for around 85% of all strokes.

Ischemic strokes are caused by atherosclerosis, the buildup of fatty plaques in the walls of the carotid arteries, followed by the formation of a blood clot which lodges in the narrowed arteries. As you might expect, the prevention and treatment of ischemic strokes are similar to the prevention and treatment of heart attacks.

EPA and DHA have been shown to:

Reduce inflammation, which is associated with increased risk of heart disease and stroke.

Reduce blood pressure. High blood pressure damages the endothelial lining of blood vessels, which can lead to either build up of atherosclerotic plaque or rupturing of the blood vessels.

Reduce platelet aggregation and blood viscosity, which reduces the potential for inappropriate blood clots forming in the carotid arteries.

[When you cut yourself, you want a blood clot to form to stop the bleeding. That is an example of appropriate blood clot formation. However, when a blood clot forms within your arteries, it can prevent blood from reaching surrounding tissues. This is an example of inappropriate blood clot formation.]

Reduce the risk of atherosclerotic plaques rupturing. Rupturing of atherosclerotic plaques triggers blood clot formation, so this also decreases the risk of inappropriate blood clots forming in the carotid arteries.

Based on the known effects of EPA and DHA, it is not surprising that they would decrease the risk of ischemic strokes. But what about hemorrhagic strokes? Here the answer is not as clear cut.

In a previous clinical study 4 gm/day of purified EPA without DHA was associated with a slightly increased risk of bleeding events but did not increase the risk of hemorrhagic stroke.

High doses of pharmaceutical grade EPA have also been associated with a slightly increased risk of atrial fibrillation (Afib). In contrast, previous studies have shown that higher dietary intake of EPA + DHA are associated with a lower risk of Afib.

At present, we don’t know whether the increased risk of bleeding events and Afib are only seen at very high doses of omega-3s or are due to the use of pharmaceutical grade EPA without DHA and any of the other naturally occurring omega-3s.

However, this uncertainty has led some experts to warn that omega-3s may be a two-edge sword. They might increase the risk of hemorrhagic stroke while decreasing the risk of ischemic stroke. This uncertainty was part of the rationale for the study (JH O’Keefe et al, Stroke, 55: 50-58, 2024) I am describing today.

How Was This Study Done?

This study was a meta-analysis of 29 clinical studies looking at the effect of omega-3 fatty acids on the risk of both ischemic and hemorrhagic stroke. These studies were performed in 15 countries from around the world and included a total of 183,291 participants.

One major drawback of many meta-analyses is that each study in the meta-analysis is independently designed. Sometimes the studies are so different that it is difficult to fit them together in a coherent pattern.

A major strength of this meta-analysis is that all the studies were conducted within the “Fatty Acid and Outcome Research Consortium” which specifies a general protocol for the design of each study within that consortium.

For example, estimates of dietary omega-3 intake can be inaccurate and the uptake and utilization of both dietary and supplemental omega-3s vary from person to person. Because of that the Fatty Acid and Outcomes Research Consortium guideline specifies that studies rely on biomarkers of omega-3 levels in the body rather than the amount of omega-3s consumed.

The most frequently used biomarker was the percentage of omega-3s incorporated into the fatty portion of red blood cell membranes. Some studies used other biomarkers, such as the percentage of omega-3s incorporated into the fatty portion of plasma phospholipids or cholesterol-containing phospholipid particles (LDL and HDL for example).

In each case, the percentage of omega-3s is used to calculate something called an “Omega-3 Index”. Previous studies have shown that an Omega-3 Index of 4% or less correlates with a high risk of heart disease, and an Omega-3 Index of 8% or more correlates with a low risk of heart disease. In essence, this study correlated Omega-3 Index with the risk of stroke.

The Fatty Acids and Outcomes Research Consortium harmonized the studies included in this meta-analysis in several other ways, but the use of Omega-3 Index rather than omega-3 consumption was the most important.

Other key characteristics of the studies included in this meta-anaysis were:

The average age of participants was 65 years.
82% of the participants were white and 53% were women.
The average length of follow-up was 14 years (range = 5-30 years).
10,561 participants (5.8%) suffered a stroke during follow-up (78% ischemic, 11% hemorrhagic, and 11% unspecified).

The Good News About Omega-3s and Stroke

The participants in these studies were divided into quintiles based on their Omega-3 Index. When those in the highest quintile (≥ 8%) were compared with those in the lowest quintile (≤ 4%):

Risk was reduced by 17% for total stroke and 18% for ischemic stroke. There was no effect on hemorrhagic stroke.

When the effect of individual components of the Omega-3 Index were analyzed:

For EPA + DHA risk was reduced by 17% for total stroke and 18% for ischemic stroke. There was no effect on hemorrhagic stroke.

For EPA risk was reduced by 17% for total stroke and 18% for ischemic stroke. There was no effect on hemorrhagic stroke. (You are probably starting to detect a pattern).

For DHA the results were only slightly different. Risk reduction was 12% for total stroke and 16% for ischemic stroke. There was no effect on hemorrhagic stroke.

For DPA, a minor component of the Omega-3 Index, there was no significant effect on total, ischemic, or hemorrhagic stroke.

There was a linear dose-response for the effect of EPA, DHA, and the two combined on the reduction in risk for both total and ischemic stroke.

When they looked at subgroups within the analysis, the results were the same for:

Age (<65 compared to >65).
Gender.
Studies that lasted less than 10 years and studies that lasted more than 10 years.
The presence of preexisting Afib.
The presence of preexisting cardiovascular disease.

The authors concluded, “In summary, this harmonized and pooled analysis of prospective studies showed that long-chain omega-3 levels were inversely associated with risk of total and ischemic stroke but were unrelated to risk of hemorrhagic stroke. Thus, higher dietary intake of DHA and EPA would be expected to lower risk of stroke.”

What Does This Study Mean For You?

Key Takeaways From This Study: The most important takeaway from this study is that reasonable amounts of EPA and DHA from either diet or supplementation are unlikely to increase your risk of hemorrhagic stroke (I will define reasonable below).

That is important to know because this and several other studies show that EPA and DHA decrease the risk of ischemic stroke, which accounts for around 85% of total strokes. This study shows you can reduce your risk of ischemic stroke without fearing that you will increase your risk of hemorrhagic stroke.

This study also reaffirms the importance of relying on Omega-3 Index rather than the dosage of omega-3s in a supplementation. Previous studies have shown there is significant individual variability in the uptake and utilization of dietary omega-3s.

Finally, this study shows you don’t need huge amounts of EPA and DHA to significantly decrease your risk of stroke and cardiovascular disease in general. An Omega-3 Index of ≥ 8% is sufficient to accomplish both.

How Much Omega-3s Do You Need? The authors of this manuscript are experts on the Omega-3 Index, and they estimated that:

To raise your Omega-3 Index from 5.4% (the median Omega-3 Index in these studies) to 8% would require about 1,000 mg/d of EPA + DHA.

To raise your Omega-3 Index from 3.5% (the lowest Omega-3 Index quintile in these studies) to 8% would require about 1,600 mg/d of EPA + DHA.

These intakes are well within the American Heart Association recommendations for reducing the risk of stroke and cardiovascular disease and are easily achievable from diet and supplementation.

But these estimates are based on averages, and, as I noted above, none of us are average. We differ in our ability to absorb and utilize omega-3s. So, I recommend relying on your Omega-3 Index rather than a dose of omega-3s that’s right for the average person but may not be right for you.

My recommendation would be to start with an Omega-3 test. If you are below 8%, start with the dosage of EPA + DHA the authors of today’s study recommended. Then retest in 6 months and adjust your dose based on the results of that test.

How Much Is Too Much? As I mentioned above, the dose response was linear for Omega-3 Index versus reduction in risk of total and ischemic strokes. So, the question becomes whether you might wish to increase your Omega-3 Index above 8% to achieve an even better reduction in stroke risk.

That is a very personal decision that only you can make but let me share some facts to help you make that decision.

As I mentioned above, a previous clinical trial showed an increased risk of bleeding events and Afib at a dosage of 4 gm/day of pure EPA. We don’t know whether that was because of the dose or the use of a formulation that contained only EPA without DHA and other naturally occurring long-chain omega-3s.

In that study the increase in bleeding events and Afib was observed in <5% of participants, which suggests that those side effects may be limited to certain high-risk individuals.

- In this context, high risk might include individuals with preexisting Afib, individuals with a tendency towards excess bleeding, and patients on blood thinning medications.

- However, only your physician knows all your risk factors. If you have health issues or are on medications, it is always a good idea to check with your physician before changing your omega-3 intake. And if you are considering high-dose omega-3 supplementation or exceeding an 8% Omega-3 Index, I strongly recommend that you consult with your physician first.

The Bottom Line

A recent study looked at the effect of omega-3 levels in red blood cells and other tissues (something called Omega-3 Index) on the risk of various types of stroke.

When individuals with an Omega-3 Index ≥ 8% were compared with those with an Omega-3 Index of ≤ 4%:

Risk was reduced by 17% for total stroke and 18% for ischemic stroke (stroke caused by blood clots in the carotid arteries). There was no effect on hemorrhagic stroke (stroke caused by bleeding from small blood vessels in the brain).

This study represents an important breakthrough. There is good evidence that increased EPA + DHA from food and/or supplements reduces the risk of ischemic stroke. But some experts have cautioned it might also increase the risk of hemorrhagic stroke. This study puts that fear to rest.

For more details about the study and what it means for you, read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease.

_______________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

About The Author

How Much Omega-3s Are Best For Blood Pressure?

April 2, 2024 by Dr. Steve Chaney

What Does This Study Mean For You?

Author: Dr. Stephen Chaney

I am continuing my series on recent omega-3 breakthroughs. Today I am going to cover a recent systematic review and meta-analysis (X Zhang et al, Journal of the American Heart Association, 11: e025071, 2022) that analyzed 71 double blind, placebo-controlled clinical studies with 4,973 subjects to determine the optimal dose of omega-3s needed to lower blood pressure.

But first, I will cover why this study is so important.

High blood pressure is called a “silent killer”. For most of us our blood pressure creeps up year after year, decade after decade. Factors like inactivity, obesity, smoking, poor diet, and excess alcohol consumption speed the increase.

Unfortunately, the symptoms of high blood pressure – things like headaches, anxiety, fatigue, and blurred vision – are easy to ignore or confuse with other health problems. And if these symptoms are ignored long enough, the result can be sudden death due to a stroke or heart attack.

Alternately, the consequence could be things like congestive heart failure, kidney failure, vision loss, and memory loss that change your quality of life forever. And once the genie is out of the bottle, it can never be put back again. The damage is permanent.

Omega-3s are often recommended for keeping blood pressure in the normal range. In fact, in 2019 the FDA approved a qualified health claim stating, “Consuming eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) omega-3 fatty acids in food or dietary supplements may reduce the risk of hypertension (high blood pressure) and coronary heart disease.”

But the amount of omega-3s needed to reduce the risk of high blood pressure is uncertain. Previous studies have come up with conflicting results. That is the question the study I will discuss today was designed to answer.

How Was This Study Done?

The investigators included 71 studies published between 1987 and 2020 with a total of 4,793 subjects ranging in age from 22 to 86 years in their systematic review and meta-analysis. The studies were all randomized, placebo-controlled trials looking at the effectiveness of omega-3 intake (primarily in the form of food or supplements containing both EPA and DHA) at lowering blood pressure. The placebo used in these studies was olive oil or other vegetable oils.

The studies included in this meta-analysis:

Included omega-3 intake from both diet (mackerel, salmon, trout, or tuna) and supplements (fish oil, algal oil, or purified omega-3 ethyl esters).

Were conducted in populations from Europe, North America, Australia and other Pacific islands, and Asia.

Included subjects with normal blood pressure as well as those with high blood pressure.

Ranged in length from 5 to 52 weeks (the average was 10 weeks).

Included approximately equal numbers of men and women.

The meta-analysis excluded studies that:

Lacked a placebo.

Lasted less than 4 weeks.

Included blood pressure medications.

Included individuals with preexisting cardiovascular events.

The data from these trials was analyzed by a statistical method called a 1-stage cubic spline regression model. This is a recently developed statistical method which the investigators stated was superior to the statistical methods used in previous studies because it reduces the likelihood the results are influenced by investigator bias.

How Much Omega-3s Are Best For Blood Pressure?

When the investigators combined the data from all 71 studies:

The maximum reduction in both systolic and diastolic blood pressure was observed between 2g/d and 3 g/d.

The dose response was non-linear. Doses above 3 g/d offered no additional benefit.

When the investigators looked at subgroups within the studies:

Reduction in blood pressure was seen in both subjects with normal blood pressure and those with high blood pressure.

- However, reduction in blood pressure and the dose response were different in the two groups.

- - In subjects with normal blood pressure the dose response was non-linear with the optimum reduction between 2 and 3 g/d.

- - In subjects with high blood pressure the reduction in blood pressure was greater and the dose response was linear. The authors recommended a dose ≤ 3 g/d EPA + DHA for people with high blood pressure.

Subjects with hyperlipidemia had a greater reduction in blood pressure than subjects with normal lipid levels, and the dose-response was linear.

Subjects over the age of 45 had a greater reduction in blood pressure than subjects under the age of 45, and the dose response was linear.

There were no significant differences between:

- Diet versus supplementation.

- Type of omega-3 supplement (natural fish oil versus purified ethyl ester).

- Sex.

The authors concluded, “This dose-response meta-analysis demonstrates that the optimal combined intake of omega-3 fatty acids for blood pressure lowering is likely between 2 g/d and 3 g/d. Doses of omega-3 fatty acid intake above the recommended 3 g/d may be associated with additional benefits in lowering blood pressure among groups at high risk of cardiovascular disease.”

I should probably explain the reasoning behind this conclusion.

79% of the studies included in this meta-analysis were performed with subjects who had normal blood pressure. This group had a non-linear reduction in blood pressure with an optimal reduction between 2 and 3 g/d EPA + DHA.

- Because of its size this group exerted a major influence on the results, which explains why the average results for the entire group showed a non-linear reduction in blood pressure with an optimal reduction between 2 and 3 g/d EPA + DHA.

- Subjects with normal blood pressure and normal lipid levels are at low risk of cardiovascular disease. The high-risk groups (high blood pressure, high cholesterol and/or triglyceride levels, and over 45) all had a linear dose response suggesting that doses above 3 g/d EPA + DHA may be optimal.

The authors also said, “We found associations [between omega-3 intake and blood pressure] among both hypertensive (high blood pressure) and nonhypertensive (normal blood pressure) groups, suggesting that omega-3 fatty acids could be beneficial for controlling blood pressure even before the onset of hypertension.

This means that the intake of omega3 fatty acids could have implications on a person’s future risk of stroke, ischemic heart disease, and all-cause mortality.”

In other words, they are saying their data suggests that EPA + DHA intakes in the 2-3 g/d range may prevent high blood pressure and the effects it can have on our health.

What Does This Study Mean For You?

The authors of this study claim their data support a dose of 2-3 mg/d of EPA + DHA to prevent a future increase in blood pressure and all its associated health consequences. They also say that an EPA+ DHA dose ≥ 3g/d may be optimal for people who already have high blood pressure and/or other risk factors for heart disease.

I am not an expert on statistics, so I cannot evaluate the author’s claim that their statistical method was superior to the methods used in earlier studies that gave conflicting results.

However, their results are consistent with recommendations of several major health and government agencies.

For example, the European Food Safety Authority has said, “An intake of EPA and DHA of ~3 g/d is required to bring out the claimed hypotensive (blood pressure lowering) effect”.

The FDA has approved qualified health claims stating that consuming EPA and DHA in foods or dietary supplements may reduce the risk of hypertension (high blood pressure) and coronary heart disease but did not recommend a dose to achieve these results.

The American Heart Association has recommended ~ 1 g/d of EPA + DHA for patients with documented coronary heart disease and 2–4 g/day of EPA + DHA to lower triglycerides.

And the American Heart Association features this article on their website with the headline, “Consuming about 3 grams of omega-3 fatty acids a day may lower blood pressure.”

When we contrast that with the fact that the average American gets less than 100 mg/d of EPA + DHA from their diet it is obvious that many Americans would likely benefit from increasing the amount of EPA and DHA in their diet.

The Rest Of The Story

There are four additional points I would like to make:

In trying to explain the differences between dose response in high and low risk subjects, the authors said, “There could be mechanistic differences in bioavailability and efficacy of omega-3 fatty acid intake in these populations.”

In last week’s “Health Tips From the Professor” article I reviewed a study that measured individual differences in the utilization of EPA and DHA and concluded that a blood measurement called Omega-3 Index was a more reliable indicator of health outcomes than the dose of omega-3s consumed.

For that reason, I recommend personalizing your dose of EPA + DHA to reach an Omega-3 Index of 8%, which appears to be optimal for heart health and provides significant blood pressure reduction. This is an iterative process which will require frequent measurement of your omega-3 index and adjustment of EPA + DHA dose until you find the level of EPA + DHA supplementation you need to achieve an Omega-3 Index of 8%.

This study and similar studies measure the health benefits of the long chain omega-3 fatty acids EPA and DHA. Short chain omega-3s from nuts, seeds, and plant oils are healthy, but their conversion to EPA and DHA is very inefficient.

Both the FDA and American Heart Association recommend that doses of EPA + DHA above 3 g/d should be taken under a physician’s supervision because high doses can cause bleeding problems.

This is another reason for basing your intake of EPA + DHA on Omega-3 Index rather than on the dose recommended by a clinical study. Based on dozens of clinical studies, an Omega-3 Index of 8% appears to be safe unless you have a bleeding disorder or are on a blood-thinning medication (see below).

If you are on a medication to thin your blood, you should consult with your physician before increasing or decreasing your omega-3 intake because changes in dietary omega-3s can affect the optimal dose of medication they prescribe.

The Bottom Line

A recent study looked at the dose of EPA + DHA needed to lower blood pressure.

The study concluded that a dose of 2-3 mg/d of EPA + DHA was optimal for preventing a future increase in blood pressure and all its associated health consequences.

It also concluded that an EPA+ DHA dose ≥ 3g/d was optimal for lowering blood pressure in people who already have high blood pressure and/or other risk factors for heart disease.

Based on previous studies, I recommend optimizing your omega-3 index rather than relying on a dose of EPA + DHA that may not be right for you.

For more details about this study and what it means to you read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease.

______________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

About The Author

Do Omega-3s Improve Recovery From A Heart Attack?

March 26, 2024 by Dr. Steve Chaney

Where Do We Go From Here?

Author: Dr. Stephen Chaney

Despite years of controversy, the benefits of omega-3s remain an active area of research. Over the next few weeks, I will review several groundbreaking omega-3 studies. This week I will focus on omega-3s and heart health.

I don’t need to tell you that the effect of omega-3s on heart health is controversial. One month a new study is published showing an amazing health benefit from omega-3 supplementation. A month or two later another study comes up empty. It finds no benefit from omega-3 supplementation.

That leads to confusion. On one hand you have websites and blogs claiming that omega-3s are a magic elixir that will cure all your ills. On the other hand, there are the naysayers, including many health professionals, claiming that omega-3 supplements are worthless.

I have discussed the reasons for the conflicting results from omega-3 clinical studies in previous issues of “Health Tips From the Professor”. You can go to https://www.chaneyhealth.com/healthtips/ and put omega-3s in the search box to read some of these articles.

Or if you prefer, I have also put together a digital download I call “The Omega-3 Pendulum” which briefly summarizes all my previous articles. It’s available on my Chaney Health School Teachable website.

Today I will discuss a study (B Bernhard et al, International Journal of Cardiology, 399; 131698, 2024) that asks whether 6 months of high dose omega-3 supplementation following a heart attack reduced the risk of major cardiovascular events over the next 6.6 years.

You might be wondering why the study didn’t just look at the effect of continuous omega-3 supplementation for 6 years following a heart attack. There are two very good reasons for the design of the current study.

1) The investigators wanted to do a double blind, placebo controlled clinical trial, the gold standard for clinical studies. However, that kind of study is impractical for a multi-year clinical trial. It would be prohibitively expensive, and patient compliance would be a big problem for a study that long.

2) The months immediately after a heart attack are critical in determining the long-term recovery of that patient. There is often a period of massive inflammation following a heart attack. And that can lead to further damage to the heart and reclosing of the arteries leading to the heart, both of which increase the risk of future adverse cardiac events.

Previous studies have shown that high dose omega-3s immediately following a heart attack can reduce inflammation and damage to the heart. However, those studies did not determine whether the cardioprotective effect of omega-3 supplementation immediately after a heart attack lead to improved long-term outcomes, something this study was designed to determine.

How Was The Study Done?

The investigators enrolled 358 patients who had suffered a heart attack from three Boston area medical centers between June 2008 and August 2012.

The patient demographics were:

Gender = 70% female.
Average age = 59
Average BMI = 29 (borderline obese).
Patients with high blood pressure = 64%
Patients with diabetes = 25%.

The patients were divided into two groups. The first group received capsules providing 4 gm/day of EPA, DHA, and other naturally occurring omega-3 fatty acids. The other group received a placebo containing corn oil. This was a double-blind study. Neither the patients nor the investigators knew which patients received the omega-3 fatty acids and which ones received the placebo.

The patients were instructed to take their assigned capsules daily for 6 months. At the beginning of the study, blood samples were withdrawn to determine the percentage of omega-3s in the fatty acid content of their red cell membranes (something called omega-3 index). Patients were also tested for insulin resistance and given a complete cardiovascular workup. This was repeated at the end of the 6-month study.

[Note: Previous studies have shown that an omega-3 index of 4% or lower is associated with high risk of heart disease, and an omega-3 index of 8% or above is associated with a low risk of heart disease.]

At 2-month intervals the patients were contacted by staff using a scripted interview to determine compliance with the protocol and their cardiovascular health. Once the 6 months of omega-3 supplementation was completed, the patients were followed for an additional 6.6 years. They were contacted every 6 months for the first 3 years and yearly between 3 years and 6 years.

The investigators quantified the number of major cardiac events (defined as recurrent heart attacks, the necessity for recurrent coronary artery bypass grafts, hospitalizations for heart failure, and all-cause deaths) for each patient during the 6.6-year follow-up period.

Patients in both groups were treated according to current “standard of care” protocols which consisted of diet and exercise advice and 5-6 drugs to reduce future cardiovascular events.

Do Omega-3s Improve Recovery From A Heart Attack?

When the investigators looked at the incidence of adverse cardiac events during the 6.6-year follow-up period, there were three significant findings from this study.

1) There were no adverse effects during the 6-month supplementation period with 4 gm/day of omega-3s. This is significant because a previous study with 4 gm/day of high purity EPA had reported some adverse effects which had led some critics to warn that omega-3 supplementation was dangerous. More study is needed, but my hypothesis is that this study did not have side effects because it used a mixture of all naturally occurring omega-3s rather than high purity EPA only.

However, this could also have been because of the way patients were screened before entering this study. I will discuss this in more detail below.

2) When the investigators simply compared the omega-3 group with the placebo group there was no difference in cardiovascular outcomes between the two groups. This may have been because this study faced significant “headwinds” that made it difficult show any benefit from supplementation. I call them “headwinds” rather than design flaws because they were unavoidable.

- It would be unethical to deny the standard of care to any patient who has just had a heart attack. That means that every patient in a study like this will be on multiple drugs that duplicate the beneficial effects of omega-3 fatty acids – including lowering blood pressure, lowering triglycerides, reducing inflammation, and reducing plaque buildup and blood clot formation in the coronary arteries.

That means that this study, and studies like it, cannot determine whether omega-3 fatty acids improve recovery from a heart attack. They can only ask whether omega-3 fatty acids have any additional benefit for patients on multiple drugs that duplicate many of the effects of omega-3 fatty acids. That significantly reduces the risk of a positive outcome.

- As I mentioned above, it would have been impractical to continue providing omega-3 supplements and placebos during the 6.6-year follow-up.

And the study was blinded, meaning that the investigators did not know which patients got the omega-3s and which patients got the placebo. That meant the investigators could not advise the omega-3 supplement users to continue omega-3 supplementation during the follow-up period.

Consequently, the study could only ask if 6 months of high-dose omega-3 supplementation had a measurable benefit 6.6 years later. I, for one, would be more interested in knowing whether lower dose omega-3 supplementation continued for the duration of this study reduced the risk of major coronary events.

3) When the investigators compared patients who achieved a significant increase in their omega-3 index during the 6-month supplementation period with those who didn’t, they found a significant benefit of omega-3 supplementation.

This was perhaps the most significant finding from this study.

If the investigators had stopped by simply comparing omega-3 users to the placebo, this would have been just another negative study. We would be wondering why it did not show any benefit of omega-3 fatty acid supplementation.

However, these investigators were experts on the omega-3 index. They knew that there was considerable individual variability in the efficiency of omega-3 uptake and incorporation into cell membranes. In short, they knew that not everyone taking a particular dose of omega-3s will achieve the same omega-3 index.

And that is exactly what they saw in this study. All the patients in the 6-month omega-3 group experienced an increase in omega-3 index, but there was considerable variability in how much the omega-3 index increased over 6 months.

So, the investigators divided the omega-3 group into two subgroups – ones whose omega-3 index increased by ≥ 5 percentage points (sufficient to move those patients from high risk of heart disease to low risk) and ones whose omega-3 index increased by less than 5 percentage points.

When the investigators compared patients with ≥ 5% increase in omega-3 index to those with <5% increase in omega-3 index:

Those with an increase in omega-3 index of ≥ 5% had a 2.9% annual risk of suffering major adverse cardiac events compared to a 7.1% annual risk for those with an increase of <5%.

That’s a risk reduction of almost 60%, and it was highly significant.

The authors concluded, “In a long-term follow-up study, treatment with [high dose] omega-3s for 6 months following a heart attack did not reduce adverse cardiac events compared to placebo. However, those patients who were treated with omega-3s and achieved ≥ 5% rise in omega-3 index experienced a significant reduction of adverse cardiac events after a median follow-up period of 6.6 years…Additional studies are needed to confirm this association and may help identify who may benefit from omega-3 fatty acid treatment following a heart attack.”

What Does This Study Mean For You?

I should start by saying that I do not recommend 4 gm/day of omega-3 fatty acids following a heart attack without checking with your doctor first.

If you are on a blood thinning medication, the dose of either the medication or the omega-3 supplement may need to be reduced to prevent complications due to excess bleeding.

In addition, the investigators excluded patients from this study who might suffer adverse effects from omega-3 supplementation. This is a judgement only your doctor can make.

With that advice out of the way, the most important takeaway from this study is that uptake and utilization of omega-3 fatty acids varies from individual to individual.

The omega-3 index is a measure of how well any individual absorbs and utilizes dietary omega-3s. And this study shows that the omega-3 index is a much better predictor of heart health outcomes than the amount of omega-3 fatty acids a person consumes.

This is not surprising because multiple studies have shown that the omega-3 index correlates with heart health outcomes. It may also explain why many studies based on omega-3 intake only have failed to show a benefit of omega-3 supplementation.

Vitamin D supplementation is a similar story. There is also considerable variability in the uptake of vitamin D and conversion to its active form in the body. 25-hydroxy vitamin D levels in the blood are a marker for active vitamin D. For that reason, I have long recommended that you get your 25-hydroxy vitamin D level tested with your annual physical and, with your doctor’s help, base the dose of the vitamin D supplement you use on that test.

This study suggests that we may also want to request an omega-3 index test and use it to determine the amount of supplemental omega-3s we add to our diet.

Where Do We Go From Here?

The idea that we need to use the omega-3 index to determine the effectiveness of the omega-3 supplement we use is novel. As the authors suggest, we need more studies to confirm this effect. There are already many studies showing a correlation of omega-3 index with heart health outcomes. But we need more double blind, placebo-controlled studies like this one.

More importantly, we need to understand what determines the efficiency of supplemental fatty acid utilization so we can predict and possibly improve omega-3 utilization. The authors suggested that certain genetic variants might affect the efficiency of omega-3 utilization. But the variability of omega-3 utilization could also be affected by:

Diet, especially the presence of other fats in the diet.

Metabolic differences due to obesity and diseases like diabetes.

Gender, ethnicity, and age.

Design of the omega-3 supplement.

We need much more research in these areas, so we can personalize and optimize omega-3 supplementation on an individual basis.

The Bottom Line

A recent study asked whether high dose omega-3 supplementation for 6 months following a heart attack reduced major cardiac events during the next 6.6 years.

When they simply compared omega-3 supplementation with the placebo there was no effect of omega-3 supplementation on cardiac outcomes.

However, when they based their comparison on the omega-3 index (a measure of how efficiently the omega-3s were absorbed and incorporated into cell membranes), the group with the highest omega-3 index experienced a 60% reduction in adverse cardiac events over the next 6.6 years.

This is consistent with multiple studies showing that the omega-3 index correlates with heart health outcomes.

More importantly, this study shows there is significant individual variation in the efficiency of omega-3 absorption and utilization. It also suggests that recommendations for omega-3 supplementation should be based on the omega-3 index achieved rather than the dose or form of the omega-3 supplement.

For more information on this study and what it means for you read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

______________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

_______________________________________________________________________

About The Author

Dr Chaney also ran an active cancer research program at UNC and published over 100 scientific articles and reviews in peer-reviewed scientific journals. In addition, he authored two chapters on nutrition in one of the leading biochemistry text books for medical students.

Is HDL Good For Your Heart?

June 13, 2023 by Dr. Steve Chaney

Is Everything You Knew About HDL Wrong?

Author: Dr. Stephen Chaney

In last week’s “Health Tips From the Professor” I talked about one of the greatest strengths of the scientific method – namely that investigators constantly challenge, and occasionally disprove, existing paradigms. That allows us to discard old models of how things work and replace them with better ones.

Last week I shared a study that disproved the paradigm that low to moderate alcohol consumption is healthier than total abstinence. This week I share several studies that challenge the belief that HDL cholesterol is good for your heart.

The belief that HDL is good for your heart has all the hallmarks of a classic paradigm.

It is supported by multiple clinical studies.

Elaborate metabolic explanations have been proposed to support the paradigm.

It is the official position of most medical societies, scientific organizations, and health information sites on the web.

It is the recommendation of most health professionals.

It has been repeated so often by so many trusted sources that everyone assumes it must be true.

Once we accept the HDL/heart health paradigm as true, we can construct other hypotheses on that foundation. For example:

Raising your HDL levels naturally takes effort. Pharmaceutical companies have been pursuing the “magic pill” that raises HDL levels without any effort on your part.

Low carb diets like the Keto and Paleo diets are high in saturated fat. The low carb enthusiasts claim this is a good thing because saturated fat raises HDL levels, and HDL is good for your heart.

But what if the underlying HDL/heart health paradigm weren’t true? These hypotheses would be like the parable of a house built on a foundation of sand. The paradigm will be washed away as soon as it is critically tested.

So, let’s look at experiments that have challenged the HDL/heart health paradigm.

Do Drugs That Increase HDL Levels Work?

The first hint that the HDL/heart health paradigm might be faulty happened when a pharmaceutical company developed a drug that selectively increased HDL levels.

The drug company thought they had found the goose that laid golden eggs. Just imagine. People wouldn’t have to lose weight, exercise, or change their diet. They could simply take a pill and dramatically decrease their heart disease risk. A drug like that would be worth $billions.

The problem was that when they tested their drug (torcetrapib) in clinical trials, it had absolutely no effect on heart disease outcomes (AR Tall et al, Atherosclerosis, Thrombosis, and Vascular Biology 27:257-260, 2007).

The pharmaceutical company couldn’t believe it. Raising HDL levels just had to reduce heart disease risk. They concluded they didn’t have the right drug, and they continued to work on developing new drugs.

That was 16 years ago, and no HDL-increasing drug has made it to market. Have they just not found the right drug, or does this mean the HDL/heart health paradigm is incorrect?

Does Saturated Fat Decrease Heart Disease Risk?

Now let’s turn to two claims of low carb enthusiasts.

#1: Saturated fats decrease your risk of heart disease in the context of a low carb diet. I have debunked that claim in several previous issues of “Health Tips From The Professor”. But let me refer you to two articles here – one on saturated fat and heart disease risk and one on low-carb diets.

#2: Saturated fats decrease heart disease risk because they raise HDL levels. This is the one I will address today.

The idea that saturated fats decrease heart disease risk because they raise HDL levels is based on a simplistic concept of HDL particles. The reality is more complex. Several clinical studies have shown:

The type of fat determines the property of the HDL particles.

- When polyunsaturated fats predominate, the HDL particles have an anti-inflammatory effect. When saturated fats predominate, the HDL particles have a pro-inflammatory effect.

Anti-inflammatory HDL particles relax the endothelial cells lining our blood vessels. That makes the lining of our blood vessels more pliable, which improves blood flow and reduces blood pressure.

- Anti-inflammatory HDL particles also help reduce inflammation of the endothelial lining. This is important because an inflamed endothelial lining is more likely to accumulate fatty plaques and to trigger blood clot formation that can lead to heart attacks and strokes.

So, the question becomes, “What good is it to raise HDL levels if you are producing an unhealthy, pro-inflammatory HDL particle that may increase the risk of high blood pressure, heart attacks, and strokes?”

In short, these studies suggest it isn’t enough to just focus on HDL levels. You need to ask what kind of HDL particles you are creating.

Is HDL Good For Your Heart?

Once the studies were published showing that…

Drug-induced increase of HDL levels without any change in health habits is not sufficient to decrease heart attack risk, and…

Not all HDL particles are healthy. There are anti-inflammatory or pro-inflammatory HDL particles, which likely have opposite effects on heart attack risk…

…some people started to question the HDL/heart health paradigm. And one group came up with the perfect study to test the paradigm.

But before I describe the study, I need to review the term “confounding variables”. I described the term and how it affects clinical studies in last week’s article. Here is a brief synopsis:

The studies supporting the HDL/heart health paradigm are association studies. Association studies measure the association between a single variable (in this case, increase in HDL levels) and an outcome (in this case, heart disease events, heart disease deaths, and total deaths).

Associations need to be corrected for other variables known to affect the same outcome (things like age, gender, smoking, and diabetes would be examples in this case).

Confounding variables are variables that also affect the outcome but are unknown or ignored. Thus, they are not used to correct the associations, which can bias the results.

The authors of this study (M Briel et al, BMJ 2009:338.b92) observed that most interventions that increase HDL levels also lower LDL levels. Lowering LDL is known to decrease the risk of heart disease deaths. But this effect had been ignored in most studies looking at the association between HDL and heart disease deaths.

They hypothesized that the change in LDL levels was a confounding variable that had been ignored in previous studies and may have biased the results.

To test this hypothesis the authors searched the literature and identified 108 studies with 299,310 participants that:

Compared the effect of drugs, omega-3 fatty acids, or diet with either a placebo or usual care.
Measured both HDL and LDL levels.
Measured reduction in cardiovascular risk.
Had a randomized control design.
Lasted at least 6 months.

They found that every 10 mg/dl decrease in LDL levels in these studies was responsible for a:

7.1% reduction in heart disease events (both heart disease deaths and non-fatal heart attacks).

7.2% reduction in heart disease deaths.

4.4% reduction in total deaths.

After correcting for the effect of decreased LDL levels on these heart disease outcomes, the increase in HDL levels had no statistically significant effect on any of the outcomes.

The authors concluded, “Available data suggest that simply increasing the amount of circulating HDL cholesterol does not reduce the risk of coronary heart disease events, coronary heart disease deaths, or total deaths. The results support reduction in LDL cholesterol as the primary goal for lipid modifying interventions.”

In other words, this study:

Supports the author’s hypothesis that LDL levels were a confounding variable that biased the studies supporting the HDL/heart health paradigm.

Concludes that increasing HDL levels has no effect on heart disease outcomes, thus invalidating the HDL/heart health paradigm.

Is Everything You Knew About HDL Wrong?

Does that mean that everything you knew about HDL is wrong? Not exactly. It just means that you need to change your perspective.

Don’t focus on HDL levels. Peek behind the curtain and focus on what’s behind the HDL levels. For example:

Losing weight when overweight increases HDL levels. But the decrease in heart disease outcomes is more likely due to weight loss than to the increase in HDL levels.

Exercise increases HDL levels. But the decrease in heart disease outcomes is more likely due to exercise than to the increase in HDL levels.

Reversing pre-diabetes or type 2 diabetes increases HDL levels. But the decrease in heart disease outcomes is more likely due to the reversal of diabetes than to the increase in HDL levels.

High-dose omega-3 fatty acids increase HDL levels. But the decrease in heart disease outcomes is more likely due to the omega-3 fatty acids than to the increase in HDL levels.

The Mediterranean diet increases HDL levels. But the decrease in heart disease outcomes is more likely due to the diet than to the increase in HDL levels.

And if you want to go the drug route:

Statins and some other heart drugs increase HDL levels, but the reduction in heart disease outcomes is probably due to their effect on LDL levels rather than their effect on HDL levels.

On the other hand:

Saturated fats increase HDL levels. But saturated fats increase heart disease risk and create pro-inflammatory HDL particles. So, in this case the increase in HDL levels is not a good omen for your heart.

Drugs have been discovered that selectively increase HDL levels. However, there is nothing of value behind this increase in HDL levels, so the drugs have no effect on heart disease outcomes.

The Bottom Line

In this article I discuss several studies that have challenged the HDL/heart health paradigm – the belief that HDL is good for your heart.

For example, one group of investigators analyzed the studies underlying the HDL/heart health paradigm. They hypothesized that these studies were inaccurate because they failed to account for the effects of LDL levels on heart disease outcomes.

After correcting for the effect of decreased LDL levels on heart disease outcomes in the previous studies, the authors showed that increases in HDL levels had no significant effect on any heart disease outcome.

In other words, this study:

Supports the author’s hypothesis that LDL levels were a confounding variable that biased the studies supporting the HDL/heart health paradigm.

Concludes that increasing HDL levels has no effect on heart disease outcomes, thus invalidating the HDL/heart health paradigm.

Does that mean that everything you knew about HDL is wrong? Not exactly. It just means that you need to change your perspective. Don’t focus on HDL levels. Focus on what’s behind the HDL levels. For more information on that, read the article above.

For more information on this study, and what it means for you, read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease.

____________________________________________________________________________

For more detail about FTC regulations for health claims, see this link.

https://www.ftc.gov/business-guidance/resources/health-products-compliance-guidance

Can Healthy Eating Help You Lose Weight?

September 27, 2022 by Dr. Steve Chaney

Who Benefits Most From A Healthy Diet?

Author: Dr. Stephen Chaney

Fad diets abound. High protein, low carb, low fat, vegan, keto, paleo – the list is endless. They all claim to be backed by scientific studies showing that you lose weight, lower your cholesterol and triglycerides, lower your blood pressure, and smooth out your blood sugar swings.

They all claim to be the best. But any reasonable person knows they can’t all be the best. Someone must be lying.

My take on this is that fad diet proponents are relying on “smoke and mirrors” to make their diet look like the best. I have written about this before, but here is a brief synopsis:

They compare their diet with the typical American diet.

- Anything looks good compared to the typical American diet.

- Instead, they should be comparing their diet with other weight loss diets. That is the only way we can learn which diet is best.

They are all restrictive diets.

- Any restrictive diet will cause you to eat fewer calories and to lose weight.

- As little as 5% weight loss results in lower cholesterol & triglycerides, lower blood pressure, and better control of blood sugar levels.

Simply put, any restrictive diet will give you short-term weight loss and improvement in blood parameters linked to heart disease, stroke, and diabetes. But are these diets healthy long term? For some of them, the answer is a clear no. Others are unlikely to be healthy but have not been studied long term. So, we don’t know whether they are healthy or not.

What if you started from the opposite perspective? Instead of asking, “Is a diet that helps you lose weight healthy long term?”, what if you asked, “Can healthy eating help you lose weight?” The study (S Schutte et al, American Journal of Clinical Nutrition, 115: 1-18, 2022) I will review this week asked that question.

More importantly, it was an excellent study. It compared a healthy diet to an unhealthy diet with exactly the same degree of caloric restriction. And it compared both diets to the habitual diet of people in that area. This study was performed in the Netherlands, so both weight loss diets were compared to the habitual Dutch diet.

How Was The Study Done?

This was a randomized controlled trial, the gold standard of clinical studies. The investigators recruited 100 healthy, abdominally obese men and women aged 40-70. At the time of entry into the study none of the participants:

Had diabetes.
Smoked
Had a diagnosed medical condition.
Were on a medication that interfered with blood sugar control.
Were on a vegetarian diet.

The participants were randomly assigned to:

A high-nutrient quality diet that restricted calories by 25%.
A low-nutrient-quality diet that restricted calories by 25%.
Continue with their habitual diet.

The study lasted 12 weeks. The participants met with a dietitian on a weekly basis. The dietitian gave them the foods for the next week and monitored their adherence to their assigned diet. They were advised not to change their exercise regimen during the study.

At the beginning and end of the study the participants were weighed, and cholesterol, triglycerides, and blood pressure were measured.

Can Healthy Eating Help You Lose Weight?

To put this study into context, these were not healthy and unhealthy diets in the traditional sense.

Both were whole food diets.
Both included fruits, vegetables, low-fat dairy, and lean meats.
Both restricted calories by 25%.

The diets were designed so that the “high-nutrient quality” diet had significantly more plant protein (in the form of soy protein), fiber, healthy fats (monounsaturated and omega-3 fats), and significantly less fructose and other simple sugars than the “low-nutrient-quality” diet.

At the end of 12 weeks:

Participants lost significant weight on both calorie-restricted diets compared to the group that continued to eat their habitual diet.

- That is not surprising. Any diet that successfully restricts calories will result in weight loss.

Participants on the high-nutrient quality diet lost 33% more weight than participants on the low-nutrient-quality diet (18.5 pounds compared to 13.9 pounds).

Participants on the high-nutrient quality diet lost 50% more inches in waist circumference than participants on the low-nutrient-quality diet (1.8 inches compared to 1.2 inches).

- This is a direct measure of abdominal obesity.

When the investigators measured blood pressure, fasting total cholesterol levels, and triglyceride levels:

These cardiovascular risk factors were significantly improved on both diets.

- Again, this would be expected. Any diet that causes weight loss results in an improvement in these parameters.

The reduction in total serum cholesterol was 2.5-fold greater and the reduction in triglycerides was 2-fold greater in the high-nutrient quality diet group than in the low-nutrient-quality diet group.

The reduction in systolic blood pressure was 2-fold greater and the reduction in diastolic blood pressure was 1.67-fold greater in the high-nutrient quality diet group than in the low-nutrient-quality diet group.

The authors concluded, “Our results demonstrate that the nutrient composition of an energy-restricted diet is of great importance for improvements of metabolic health in an overweight, middle-aged population. A high-nutrient quality energy-restricted diet enriched with soy protein, fiber, monounsaturated fats, omega-3 fats, and reduced in fructose provided additional health benefits over a low-nutrient quality energy-restricted diet, resulting in greater weight loss…and promoting an antiatherogenic blood lipid profile.”

In short, participants in this study lost more weight and had a better improvement in risk factors for heart disease on a high-nutrient-quality diet than on a low-nutrient-quality diet. Put another way, healthy eating helped them lose weight and improved their health.

Who Benefits Most From A Healthy Diet?

None of the participants in this study had been diagnosed with diabetes when the study began. However, all of them were middle-aged, overweight, and had abdominal obesity. That means many of them likely had some degree of insulin resistance.

Because of some complex metabolic studies that I did not describe, the investigators suspected that insulin resistance might influence the relative effectiveness of the two energy-restricted diets.

To test this hypothesis, they used an assay called HOMA-IR (homeostatic model assessment of insulin resistance). Simply put, this assay measures how much insulin is required to keep your blood sugar under control.

They used a HOMA-IR score of 2.5 to categorize insulin resistance among the participants.

Participants with a HOMA-IR score >2.5 were categorized as insulin-resistant. This was 55% of the participants.

Participants with a HOMA-IR score ≤2.5 were categorized as insulin-sensitive. This was 45% of the participants.

When they used this method to categorize participants they found:

Insulin-resistant individual lost about the same amount of weight on both diets.

Insulin-sensitive individuals lost 66% more weight on the high-nutrient-quality diet than the low-nutrient-quality diet (21.6 pounds compared to 13.0 pounds).

The investigators concluded, “Overweight, insulin-sensitive subjects may benefit more from a high- than a low-nutrient-quality energy-restricted diet with respect to weight loss…”

What Does This Study Mean For You?

Simply put this study confirms that:

Caloric restriction leads to weight loss, and…

Weight loss leads to improvement in cardiovascular risk factors like total cholesterol, triglycerides, and blood pressure.

- This is not new.

- This is true for any diet that results in caloric restriction.

This study breaks new ground in that a high-nutrient quality diet results in significantly better:

Weight loss and…

Reduction in cardiovascular risk factors…

…than a low-nutrient quality diet. As I said above, the distinction between a “high-nutrient-quality” diet and a “low-nutrient-quality” diet may not be what you might have expected.

Both diets were whole food diets. Neither diet allowed sodas, sweets, and highly processed foods.

Both included fruits, vegetables, grains, and lean meats.
Both reduced caloric intake by 25%.

- If you want to get the most out of your weight loss diet, this is a good place to start.

In this study the investigators designed their “high-nutrient-quality” diet so that it contained:

More plant protein in the form of soy protein.

- In this study they did not reduce the amount of animal protein in the “high-nutrient-quality” diet. They simply added soy protein foods to the diet. I would recommend substituting soy protein for some of the animal protein in the diet.

More fiber.

- The additional fiber came from substituting whole grain breads and brown rice for refined grain breads and white rice, adding soy protein foods, and adding an additional serving of fruit.

More healthy fats (monounsaturated and omega-3 fats).

- The additional omega-3s came from adding a fish oil capsule providing 700mg of EPA and DHA.

Less simple sugars. While this study focused on fructose, their high-nutrient-quality diet was lower in all simple sugars.

All these changes make great sense if you are trying to lose weight. I would distill them into these 7 recommendations.

Follow a whole food diet. Avoid sodas, sweets, and highly processed foods.

Include all 5 food groups in your weight loss diet. Fruits, vegetables, whole grains, dairy, and lean proteins all play an important role in your long-term health.

Eat a primarily plant-based diet. My recommendation is to substitute plant proteins for at least half of your high-fat animal proteins. And this study reminds us that soy protein foods are a convenient and effective way to achieve this goal.

Eat a diet high in natural fibers. Including fruits, vegetables, whole grains, beans, nuts, seeds, and soy foods in your diet is the best way to achieve this goal.

Substitute healthy fats (monounsaturated and omega-3 fats) for unhealthy fats (saturated and trans fats) in your diet. And this study reminds us that it is hard to get enough omega-3s in your diet without an omega-3 supplement.

Reduce the amount of added sugar, especially fructose, from your diet. That is best achieved by eliminating sodas, sweets, and highly processed foods from the diet. I should add that fructose in fruits and some healthy foods is not a problem. For more information on that topic, I refer you to a previous “Health Tips” article .

Finally, I would like to remind you of the obvious. No diet, no matter how healthy, will help you lose weight unless you cut back on calories. Fad diets achieve that by restricting the foods you can eat. In the case of a healthy diet, the best way to do it is to cut back on portion sizes and choose foods with low caloric density.

I should touch briefly on the third major conclusion of this study, namely that the “high-nutrient quality diet” was not more effective than the “low-nutrient-quality” diet for people who were insulin resistant. In one sense, this was not news. Previous studies have suggested that insulin-resistant individuals have more difficulty losing weight. That’s the bad news.

However, there was a silver lining to this finding as well:

Only around half of the overweight, abdominally obese adults in this study were highly insulin resistant.

- That means there is a ~50% chance that you will lose more weight on a healthy diet.

Because both diets restricted calories by 25%, insulin-resistant individuals lost weight on both diets.

- That means you can lose weight on any diet that successfully reduces your caloric intake. That’s the good news.

- However, my recommendation would still be to choose a high-nutrient quality diet that is designed to reduce caloric intake, because that diet is more likely to be healthy long term.

The Bottom Line

A recent study asked, “Can healthy eating help you lose weight?” This study was a randomized controlled study, the gold standard of clinical studies. The participants were randomly assigned to:

A high-nutrient quality diet that restricted calories by 25%.
A low-nutrient-quality diet that restricted calories by 25%.
Continue with their habitual diet.

These were not healthy and unhealthy diets in the traditional sense.

Both were whole food diets.
Both included fruits, vegetables, low-fat dairy, and lean meats.
Both restricted calories by 25%.

At the end of 12 weeks:

Participants on the high-nutrient quality diet lost 33% more weight than participants on the low-nutrient-quality diet (18.5 pounds compared to 13.9 pounds).

When the investigators measured cardiovascular risk factors at the end of 12 weeks:

The reduction in total serum cholesterol was 2.5-fold greater and the reduction in triglycerides was 2-fold greater in the high-nutrient quality diet group than in the low-nutrient-quality diet group.

The reduction in systolic blood pressure was 2-fold greater and the reduction in diastolic blood pressure was 1.67-fold greater in the high-nutrient quality diet group than in the low-nutrient-quality diet group.

For more details on this study, what this study means for you, and my 7 recommendations for a healthy weight loss diet, read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease.

Omega-3s Reduce Preterm Births

August 9, 2022 by Dr. Steve Chaney

Do Omega-3s Make For A Healthy Pregnancy?

Author: Dr. Stephen Chaney

The role of omega-3s on a healthy pregnancy has been in the news for some time. Claims have been made that omega-3s reduce preterm births, postnatal depression, and improve cognition, IQ, vision, mental focus, language, and behavior in the newborn as they grow.

The problem is that almost all these claims have been called into question by other studies. If you are pregnant or thinking of becoming pregnant, you don’t know what to believe.

Should you eat more fish?
Should you take omega-3 supplements?
Or should you just ignore the claims about omega-3s and a healthy pregnancy?

These are not trivial questions. Let’s consider preterm births as an example. The medical profession has made enormous advances in keeping premature babies alive. However, premature babies are still at higher risk of several health conditions including:

Visual impairment.
Developmental Delay.
Learning difficulties.

Plus, it is expensive to keep premature babies alive. One recent study estimated that increasing omega-3 intake during pregnancy could reduce health care costs by around $6 billion in the United Stated alone.

Unfortunately, it’s not just omega-3s and pregnancy. The same is true for almost all nutritional health claims. One day a study comes out claiming that nutrient “X” cures some disease or has some miraculous benefit. The bloggers and news media hype that study. Suddenly you see that health claim everywhere. It becomes so omnipresent that you are tempted to believe it must be true.

But wait. A few months later another study comes to opposite conclusion. Now the media is telling you that health claim is false. The months come and go, and new studies keep coming out. Some support the health claim. Others refute it.

Pretty soon the nutrition headlines just become “noise”. You don’t know what to believe. If you want the truth, “Who ya gonna call?”

Who Ya Gonna Call?

It’s not Ghostbusters. It not Dr. Strangelove’s health blog. It’s a group called the Cochrane Collaboration.

The Cochrane Collaboration consists of 30,000 volunteer scientific experts from across the globe whose sole mission is to analyze the scientific literature and publish reviews of health claims so that health professionals, patients, and policy makers can make evidence-based choices about health interventions.

The Cochrane Collaboration reviews all the relevant studies on a topic, exclude those that are biased or weak, and make their recommendations based on only the strongest studies. Their reviews are considered the gold standard of evidence-based medicine.

If you are of a certain age, you may remember that TV commercial “When EF Hutton talks, people listen.” It is the same with the Cochrane Collaboration. When they talk, health professionals listen.

This week we will examine the Cochrane Collaboration’s review titled “Omega-3 Fatty Acid Addition During Pregnancy”.

How Was The Study Done?

For this analysis the Cochrane Collaboration reviewed 70 randomized controlled trials which compared the effect of added omega-3s on pregnancy outcomes with either a placebo or a diet no added omega-3s. These trials included almost 19,927 pregnant women.

In one sense, Cochrane reviews are what is called a “meta-analysis”, in which data from numerous studies are grouped together so that a statistically significant conclusion can be reached. However, Cochrane Collaboration reviews differ from most meta-analyses found in the scientific literature in a very significant way.

Many published meta-analyses simply report “statistically significant” conclusions. However, statistics can be misleading. As Mark Twain said: “There are lies. There are damn lies. And then there are statistics”.

The problem is that the authors of most meta-analyses group studies together without considering the quality of studies included in their analysis. This creates a “Garbage In – Garbage Out” effect. If the quality of individual studies is low, the quality of the meta-analysis will also be low. Simply put, the conclusions from some published meta-analyses are not worth the paper they are written on.

The Cochrane Collaboration also reports statistically significant conclusions from their meta-analyses. However, they also carefully consider the quality of each individual study in their analysis. They look at possible sources of bias. They look at the design and size of the studies. Finally, they ask whether the conclusions are consistent from one study to the next. They clearly define the quality of evidence that backs up each of their conclusions as follows:

High-quality evidence. Further research is unlikely to change their conclusion. This is generally reserved for conclusions backed by multiple high-quality studies that have all come to the same conclusion. These are the recommendations that are most often adopted into medical practice.

Moderate-quality evidence. This conclusion is likely to be true, but further research could have an impact on it.

Low-quality evidence. Further research is needed and could alter the conclusion. They are not judging whether the conclusion is true or false. They are simply saying more research is needed to reach a definite conclusion.

Omega-3s Reduce Preterm Births

Here are the conclusions that the Cochrane Collaboration said were supported by high-quality evidence:

Omega-3s reduce the risk of preterm births.

Omega-3s reduce the risk of low-birth-weight infants.

The authors concluded: “Omega-3 supplementation during pregnancy is an effective strategy for reducing the risk of preterm birth…More studies comparing omega-3s and placebo are not needed at this point.”

In other words, they are saying this conclusion is definite. Omega-3 supplementation should become part of the standard of medical care for pregnant women.

However, they did say that further studies were needed “…to establish if, and how, outcomes vary by different types of omega-3s, timing [stage of pregnancy], doses [of omega-3s], or by characteristics of women.”

That’s because these variables were not analyzed in the Cochrane study. Their review and meta-analysis included clinical trials:

Of women at low, moderate, and high risk of poor pregnancy outcomes.

With DHA alone, with EPA alone, and with a mixture of both.

Omega-3 doses that were low (˂ 500 mg/day), moderate (500-1,000 mg/day), and high (> 1,000 mg/day).

Do Omega-3s Make For A Healthy Pregnancy?

What about the effect of omega-3s on other pregnancy outcomes?

The conclusions the Cochrane Collaboration said were supported by moderate quality evidence included reductions in:

Perinatal death.

Admissions to the neonatal intensive care unit.

There was not enough high or moderate quality data to determine the effect of omega-3s on other pregnancy outcomes such as postnatal depression. More research is still needed in those areas. However, if you do receive any of these benefits from omega-3 supplementation, you can just consider them as side benefits.

What Does This Report Mean For You?

1) The proven effect of omega-3 supplementation on preterm births is significant because preterm births increase the risk of:

Visual impairment.
Developmental Delay.
Learning difficulties.

2) The likely effect of omega-3s on admission to neonatal intensive care units is significant because those units are very expensive.

3) The Cochrane study did not determine whether omega-3 supplementation was equally important for women at low, moderate, and high likelihood of poor pregnancy outcomes.

Therefore, omega-3 supplementation should be considered for all pregnant women.

4) The Cochrane study did not determine whether omega-3 supplementation was equally important during the first, second, or third trimester.

Therefore, omega-3 supplementation should be considered by all women of childbearing age who might become pregnant and throughout pregnancy.

5) The Cochrane study did not determine whether DHA, EPA, or a mixture of the two was most effective.

Therefore, your omega-3 supplement should probably contain both DHA and EPA. A group of experts recently recommended that adults consume at least 650 mg/day of omega-3s with ≥ 220 mg of that coming from DHA and ≥ 220 mg/day coming from EPA.

Since most pregnant women in this country consume around 89 mg/day of DHA + EPA, omega-3 supplementation is warranted.

The Bottom Line

The effect of omega-3s on pregnancy outcomes have been confusing. Some studies conclude that omega-3s are important for a healthy pregnancy. Other studies suggest they are ineffective. What are you to believe?

Fortunately, a group called the Cochrane Collaboration recently conducted a comprehensive review of this topic. This is significant because Cochrane Reviews are internationally recognized as the highest standard in evidence-based health care. They influence the treatment protocols recommended by the medical community.

This Cochrane Review concluded that omega-3 supplementation during pregnancy:

Reduces preterm births and low birth weight infants.

Likely reduces perinatal death and admissions to the neonatal intensive care unit.

The authors of the review said: “Omega-3 supplementation during pregnancy is an effective strategy for reducing the risk of preterm birth…More studies comparing omega-3s and placebo are not needed at this point.”

In other words, they are saying this conclusion is definite. Omega-3 supplementation should become part of the standard of medical care for pregnant women.

For more details on the study and what it means for you, read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

Omega-3s And Congestive Heart Failure

May 3, 2022 by Dr. Steve Chaney

We Have Been Asking The Wrong Questions

Author: Dr. Stephen Chaney

Today’s Health Tip is a follow-up to the article I published last month on omega-3s and heart disease risk. In that article I pointed out the reasons why studies of the effect of omega-3s and heart disease risk have been so confusing.

One of the reasons is that many of the studies have been asking the wrong questions.

They were asking whether omega-3s reduced the risk of heart disease for everyone. Instead, they should have been asking who benefited from omega-3 supplementation.

They were asking whether omega-3s reduced the risk of all forms of heart disease combined. Instead, they should have been asking whether omega-3s reduced the risk of specific kinds of heart disease.

I also discussed a large clinical trial, the VITAL study, that was designed to answer those two questions.

The study I will describe today (L Djoussé et al, JACC Heart Failure, 10: 227-234, 2022) mined the data from the VITAL study to evaluate the effect of omega-3 supplementation on congestive heart failure, a form of heart disease that was not discussed in the VITAL study.

Everything You Need To Know About Congestive Heart Failure

Congestive heart failure is a killer. The term congestive heart failure simply means that your heart no longer pumps blood well. The initial symptoms are relatively non-specific and include things like.

Shortness of breath.
Fatigue and weakness.
Reduced ability to exercise.
Rapid or irregular heartbeat.
Persistent cough or wheezing.

However, as it progresses, the symptoms get much worse. Fluid builds up in your tissues.

Fluid buildup in your legs, ankles, and feet can make it difficult to walk.

Fluid buildup in your lungs makes it difficult to breathe. In advanced stages it can feel like you are drowning in a room full of air.

According to the CDC:

4 million Americans have congestive heart failure (CHF).

- It leads to ~380,000 deaths/year.

83% of patients diagnosed with CHF will be hospitalized at least once.

- 67% will be hospitalized two or more times.

CHF costs >$30 billion per year in health care costs and lost wages.

The risk of congestive heart failure is not spread evenly across the American population. Black Americans and Americans with type 2 diabetes are at increased risk.

According to the Framingham Heart Study:

Type 2 diabetes increases the risk of CHF 2-fold in men and 5-fold in women. The reasons are not entirely clear. However:

- High blood sugar is thought to either damage cells in heart muscle, weakening it, or damage small blood vessels within the heart, making it more difficult for the heart to pump blood.

- Some diabetes drugs that lower blood sugar also appear to increase the risk of congestive heart failure.

According to the CDC:

Black Americans are 2-fold more likely to develop CHF than White Americans. Again, the reasons are not clear. However:

- Some experts feel it could be due to the higher incidence of untreated high blood pressure in Black Americans.

In summary:

Congestive heart failure is a serious disease. Its symptoms affect your quality of life, and it can lead to hospitalizations and death.

Black Americans and Americans with type 2 diabetes are at higher risk of developing congestive heart failure.

How Was The Study Done?

The VITAL study, from which these data were extracted, was a placebo-controlled clinical trial designed to measure the effects of 1,000 mg omega-3 supplementation on the risk of developing heart disease. It enrolled 25,871 Americans aged 55 years or older and followed them for an average of 5.3 years.

The participants enrolled in the VITAL study represented a cross-section of the American population. Most were at low risk of heart disease, but there were subsets of the study group who were at higher risk of heart disease. A strength of the VITAL study was that it was designed so the high-risk subgroups could be evaluated separately.

The current study utilized data from the VITAL study to look at the effect of omega-3 supplementation on hospitalizations due to congestive heart failure. It also evaluated the effect of type 2 diabetes and race on the risk of hospitalizations.

Omega-3s And Congestive Heart Failure

When the investigators looked at the whole population, most of whom were at low-risk of congestive heart failure, they did not see any effect of omega-3 supplementation on the risk of hospitalizations due to congestive heart failure.

However, when they looked at high risk groups, the story was much different.

In patients with type-2 diabetes:

Omega-3 supplementation reduced the risk of the initial hospitalization for congestive heart failure by 31%

Omega-3 supplementation reduced the risk of multiple hospitalizations due to congestive heart failure by 47%.

The effect of omega-3 supplementation on hospitalizations was greatest for the Black participants in the study.

In the words of the authors, “Our data show beneficial effects of omega-3 fatty acid supplements on the incidence of heart failure hospitalizations in participants with type 2 diabetes but not in those without type 2 diabetes, and such benefit appeared to be stronger in Black participants with type 2 diabetes.”

We Are Asking The Wrong Questions

As I said above, there is so much confusion about the effect of omega-3s on heart disease because we scientists have been asking the wrong questions:

We have been asking whether omega-3s reduce the risk of heart disease for everyone. Instead, we should have been asking who benefits from omega-3 supplementation.

We have been asking whether omega-3s reduced the risk of all forms of heart disease combined. Instead, we should have been asking whether omega-3s reduced the risk of specific kinds of heart disease.

In my “Health Tip” last month I discussed a large clinical study, the VITAL study, that was specifically designed to answer the right questions. Like so many other studies it found that omega-3 supplementation did not significantly reduce the risk of all kinds of heart disease for everyone.

However, what it did find was more important than what it did not find:

When they looked at the effect of omega-3s on heart disease risk in high-risk groups, they found that major cardiovascular events were reduced by:

- 26% in African Americans.

- 26% in patients with type 2 diabetes.

- 17% in patients with a family history of heart disease.

- 19% in patients with two or more risk factors of heart disease.

When they looked at the effect of omega-3s on heart disease risk in people with low omega-3 intake, they found that omega-3 supplementation reduced major cardiovascular events by:

- 19% in patients with low fish intake.

When they looked at the effect of omega-3s on the risk of different forms of heart disease, they found that omega-3 supplementation reduced:

- Heart attacks by 28% in the general population and by 70% for African Americans.

- Deaths from heart attacks by 50%.

- Deaths from coronary heart disease (primarily heart attacks and ischemic strokes (strokes caused by blood clots)) by 24%.

In other words, when they asked the wrong questions, they got the wrong answer. If they had just looked at the effect of omega-3 supplementation on all forms of heart disease for everyone (like most other omega-3 studies), they would have concluded that omega-3s are worthless.

However, when they asked the right questions, they found that omega-3s were very beneficial for high-risk populations and for certain types of heart disease.

The current study utilized the same data to analyze the effect of omega-3 supplementation on hospitalizations due to congestive heart failure. And the results were similar.

If they had asked the wrong question, “Does omega-3 supplementation reduce congestive heart failure hospitalizations for everyone?”, they would have concluded that omega-3 supplementation was worthless.

However, instead they asked, “Does omega-3 supplementation reduce congestive heart failure hospitalizations for certain high-risk groups” and were able to show that omega-3 supplementation significantly reduced congestive heart failure hospitalizations for people with type 2 diabetes and for Blacks.

We need to change the paradigm for clinical studies of supplements. The old paradigm asks the wrong questions. If we really want to know the role of supplementation for our health, we need to start asking the right questions.

The Bottom Line

There is perhaps nothing more confusing to the average person than the “truth” about omega-3 supplementation and heart disease risk. Much of the confusion is because we have been asking the wrong questions:

We have been asking whether omega-3 supplementation reduces the risk of heart disease for everyone. Instead, we should have been asking who benefits from omega-3 supplementation.

We have been asking whether omega-3 supplementation reduces the risk of all forms of heart disease combined. Instead, we should have been asking whether omega-3 supplementation reduces the risk of specific kinds of heart disease.

A recent study on the effect of omega-3 supplementation on hospitalizations due to heart disease is a perfect example.

For more details read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.