Article summary

• The benefits of fish oil supplementation have been grossly overstated
• Most of the studies showing fish oil benefits are short-term, lasting less than one year
• The only fish oil study lasting more than four years showed an increase in heart disease and sudden death
• Fish oil is highly unstable and vulnerable to oxidative damage
• There’s no evidence that healthy people benefit from fish oil supplementation
• Taking several grams of fish oil per day may be hazardous to your health

A new study was recently published showing that 3g/d of fish oil in patients with metabolic syndrome increased LDL levels and insulin resistance.

Unfortunately, I don’t read Portuguese so I can’t review the full-text. But this study isn’t alone in highlighting the potential risks of high-dose fish oil supplementation. Chris Masterjohn’s latest article on essential fatty acids, Precious yet Perilous, makes a compelling argument that fish oil supplementation – especially over the long-term – is not only not beneficial, but may be harmful.

This may come as a surprise to you, with all of the current media hoopla about the benefits of fish oil supplementation. Yet the vast majority of the studies done that have shown a benefit have been short-term, lasting less than one year. The only trial lasting more than four years, the DART 2 trial, showed that fish oil capsules actually increase the risk of heart disease and sudden death.

A 2004 Cochrane meta-analysis of trials lasting longer than six months suggests that the cardiovascular benefits of fish oil have been dramatically over-stated. They analyzed 79 trials overall, and pooled data from 48 trials that met their criteria. The only effect that could be distinguished from chance was a reduced risk of heart failure. Fish oil provided no reduction in total or cardiovascular mortality.

Too much fish oil can wreak havoc in your body

Omega-3 fatty acids are highly vulnerable to oxidative damage. When fat particles oxidize, they break down into smaller compounds, like malondialdehyde (MDA), that are dangerous because they damage proteins, DNA, and other important cellular structures.

A study by Mata et al demonstrated that oxidative damage increases as intake of omega-3 fat increases. The results of this study were summarized in the Perfect Health Diet, by Paul and Shou-Ching Jaminet:

Notice the clear increase in TBARS (a measure of oxidative damage of the LDL particle) with omega-3 fat. It’s important to note that this was only a 5-week trial. If it had gone on for longer than that, it’s likely the oxidative damage caused by omega-3 fats would have been even worse. This isn’t surprising if you understand the chemical composition of fats. Polyunsaturated fats (PUFA) are highly vulnerable to oxidative damage because they’re the only fatty acids that have two or more double bonds, and it’s the carbon that lies between the double bonds that is vulnerable to oxidation (as shown in the figure below):

Another thing worth noting, if you haven’t already, is that intake of saturated and monounsaturated fats does not increase oxidative damage by a significant amount. This is illustrated in both the table and the diagram above: saturated fats have no double bonds, which means they are well protected against oxidation. MUFA is slightly more vulnerable, since it does have one double bond, but not nearly as much as PUFA which has several double-bonds.

A randomized, double blind, placebo-controlled trial likewise showed that 6 grams per day of fish oil increased lipid peroxides and MDA in healthy men, regardless of whether they were supplemented with 900 IU of vitamin E. And consumption of fresh, non-oxidized DHA and EPA has been shown to increase markers of oxidative stress in rats.

Fish oil not as beneficial as commonly believed

To be fair, at least one review suggests that fish oil supplementation is beneficial in the short and even intermediate term. A recent meta-analysis of 11 trials lasting more than one year found that fish oil reduced the relative risk of cardiovascular death by 13 percent and the relative risk of death from any cause by 8 percent.

But the effect seen in this review was mostly due to the GISSI and DART-1 trials. They found that fish oil may prevent arrhythmia in patients with chronic heart failure and patients who have recently survived a heart attack.

However, there is no evidence that people other than those with arrhythmia and chronic heart failure benefit from taking fish oil or that doses higher than one gram of omega-3 fatty acids per day provide any benefit over smaller doses. And then there’s the rather disturbing result of the DART-2 trial, the only fish oil study lasting more than four years, showing an increase in heart disease and sudden death.

It’s logical to assume the effects of oxidative damage would take a while to manifest, and would increase as time goes on. That’s likely the reason we see some benefit in short- and intermediate-term studies (as n-3 displace n-6 in the tissues), but a declining and even opposite effect in the longer-term DART-2 trial (as increased total PUFA intake causes more oxidative damage).

The danger of reductionist thinking in nutritional research

The current fish oil craze highlights the danger of isolated nutrient studies, which unfortunately is the focus of nutritional research today. Kuipers et al. eloquently described the risks of this approach in a recent paper:

The fish oil fatty acids EPA and DHA (and their derivatives), vitamin D (1,25-dihydroxyvitamin D) and vitamin A (retinoic acid) are examples of nutrients that act in concert, while each of these has multiple actions(7,8).

Consequently, the criteria for establishing optimum nutrient intakes via randomised controlled trials (RCT) with single nutrients at a given dose and with a single end point have serious limitations. They are usually based upon poorly researched dose–response relationships, and typically ignore many possible nutrient interactions and metabolic interrelationships.

For instance, the adequate intake of linoleic acid (LA) to prevent LA deficiency depends on the concurrent intakes of α-linolenic acid (ALA), γ-LA and arachidonic acid (AA). Consequently, the nutritional balance on which our genome evolved is virtually impossible to determine using the reigning paradigm of ‘evidence-based medicine’ with RCT.

Interest in fish oil supplementation started with observations that the Inuit had almost no heart disease. It was assumed their high intake of marine oils produced this benefit. While this may be true, at least in part, what was overlooked is that the Inuit don’t consume marine oils in isolation. They eat them as part of a whole-food diet that also includes other nutrients which may help prevent the oxidative damage that otherwise occurs with such a high intake of fragile, n-3 PUFA.

It’s also important to note that there are many other traditional peoples, such as the Masai, the Tokelau, and the Kitavans, that are virtually free of heart disease but do not consume high amounts of marine oils. What these diets all share in common is not a large intake of omega-3 fats, but instead a complete absence of modern, refined foods.

Eat fish, not fish oil – cod liver oil excepted

That is why the best approach is to dramatically reduce intake of omega-6 fat, found in industrial seed oils and processed and refined foods, and then eat a nutrient-dense, whole-foods based diet that includes fatty fish, shellfish and organ meats. This mimics our ancestral diet and is the safest and most sane approach to meeting our omega-3 needs – which as Chris Masterjohn points out, are much lower than commonly assumed.

Some may ask why I continue to recommend fermented cod liver oil (FCLO), in light of everything I’ve shared in this article. There are a few reasons. First, I view FCLO as primarily a source of fat-soluble vitamins (A, D, K2 and E) – not EPA and DHA. Second, in the context of a nutrient-dense diet that excludes industrial seed oils and refined sugar, and is adequate in vitamin B6, biotin, calcium, magnesium and arachidonic acid, the risk of oxidative damage that may occur with 1g/d of cod liver oils is outweighed by the benefits of the fat-soluble vitamins.

So I still recommend eating fatty fish a couple times per week, and taking cod liver oil daily, presuming your diet is as I described above. What I don’t endorse is taking several grams per day of fish oil, especially for an extended period of time. Unfortunately this advice is becoming more and more common in the nutrition world.

More is not always better, despite our tendency to believe it is.

In the last two weeks alone three articles have appeared in the scientific press about new studies reporting on vitamin D’s many crucial roles in the body. Along with promoting strong bones, a healthy immune system and protection against some types of cancer, recent studies suggest vitamin D can treat heart failure, protect against heart attacks and reduce the risk of death from both cardiovascular and overall causes.

Back in April I wrote an article called “Throw Away Your Sunscreen” about the protective effects of exposure to sunlight against melanoma. Despite conventional wisdom that tells us to avoid sun exposure at all costs, it turns out that the vitamin D our bodies synthesize when exposed to UV light is a first line of defense against developing melanoma.

In an article published on June 9 in Archives of Internal Medicine, scientists reported that low levels of vitamin D are associated with a higher risk of myocardial infarction (heart attack) in men. The study showed that rates of cardiovascular disease-related deaths are increased at higher latitudes and during the winter months, and are lower at lower altitudes.

In an article published in the July issue of the Journal of Cardiovascular Pharmacology, on June 12, researchers found that vitamin D directly contributes to cardiovascular fitness. In fact, University of Michigan pharmacologist Robert U. Simpson, Ph.D. thinks it’s apt to call vitamin D “the heart tranquilizer”. Simpson and his team discovered that treatments with activated vitamin D prevented heart muscle cells from hypertrophy, a condition in which the heart becomes enlarged and overworked in people with heart failure.

Finally, in a study published on June 23 in the Archives of Internal Medicine, a team of Austrian scientists revealed that low blood levels of vitamin D appear to have an increased risk of death overall and from cardiovascular causes. Harald Donbig, M.D. and his colleagues studied 25-hydroxyvitamin D and 1,25 dihydroxyvitamin D levels in 3,258 consecutive patients (average age 62 years) who were scheduled for coronary angiography testing at a single medical center between 1997 and 2000.

During 7.7 years of follow-up, death rates from any cause and from cardiovascular causes were higher among individuals in the lower one-half of 25-hydroxyvitamin D levels and the lowest one-fourth of 1,25-dihydroxyvitamin D levels. These associations remained when researchers controlled for other factors such as coronary artery disease, physical activity and co-occurring diseases.

So what does all this mean to you? A recent consensus panel estimated that about 50 – 60 percent of older individuals in North America and the rest of the world do not have satisfactory vitamin D status, and the situation is similar for younger individuals. Blood levels of vitamin D lower than 20 to 30 nanograms per milliliter have been associated with falls, fractures, cancer, autoimmune dysfunction, cardiovascular disease and hypertension.

To put it blankly, that means half of all people around the world are deficient in vitamin D and therefore at increased risk for serious and potentially fatal conditions.

Low 25-hydroxyvitamin D levels are also correlated with markers of inflammation such as C-reactive protein, as well as signs of oxidative damage to cells, Donbig’s study revealed. In a previous article, I explained that inflammation and oxidative damage (not cholesterol) are the primary causes of the worldwide heart disease epidemic. Inflammation and oxidative damage are also contributing factors to diabetes, metabolic syndrome, cancer and many other diseases.

So how does vitamin D work its magic? It acts as a potent hormone in more than a dozen types of tissues and cells in the body, regulating expression of essential genes and rapidly activating already expressed enzymes and proteins. In the heart, vitamin D binds to specific vitamin D receptors and produces its “calming”, protective effects.

There are essentially three ways to obtain vitamin D: exposure to UV light, food and supplements. The most effective of all of these methods is exposure to sunlight. Full-body exposure of pale skin to summer sunshine for 30 minutes without clothing or sunscreen can result in the synthesis of between 10,000 and 20,000 IU of vitamin D. At most latitudes outside of the tropics, however, there are substantial portions of the year during which vitamin D cannot be obtained from sunlight; additionally, environmental factors including pollution and the presence of buildings can reduce the availability of UVB light.

In northern latitudes or during winter months when the sun isn’t shining, I recommend taking 1 tsp./day of high-vitamin cod liver oil (Green Pasture or Radiant Life are two brands I recommend) to ensure adequate vitamin D (and vitamin A) intake. You can also eat vitamin D-rich foods such as herring, duck eggs, bluefin tuna, trout, eel, mackerel, sardines, chicken eggs, beef liver and pork. If you follow this approach further supplementation should not be necessary.

Before closing, I must mention (briefly) the issue of vitamin D toxicity. Vitamin D is widely considered to be the most toxic of all vitamins, and dire warnings are often issued to avoid excess sun exposure and vitamin D in the diet on that basis. The discussion of vitamin D toxicity has failed to take into account the interaction between vitamins A, D and K. Several lines of evidence suggest that vitamin D toxicity actually results from a relative deficiency of vitamins A and K.
So, the solution is not to avoid sun exposure or sources of vitamin D in the diet. Rather, it ensure adequate vitamin D intake (through sunlight and food) and to increase the intake (through diet and/or supplements) of vitamins A & K. Stay tuned for a future post on the interaction between vitamins A, D & K and their relevance to human health.

Suggested Links

• The Vitamin D Miracle: Is it For Real?
• From Seafood to Sunshine: A New Understanding of Vitamin D Safety
• Vitamin D Toxicity Redefined

Statins have been almost universally hailed as “wonder drugs” by medical authorities around the world. The market for statins was $26 billion in 2005, and sales for Lipitor alone reached $14 billion in 2006. Merck and Bristol Myers-Squib are actively seeking “over-the-counter” (OTC) status for their statin drugs. Statins are prescribed to men and women, children and the elderly, people with heart disease and people without heart disease.

In fact, these drugs have a reputation for being so safe and effective that one UK physician, John Reckless (I’m not kidding – that’s actually his name!) has suggested that we put statins in the water supply.

That’s a bold suggestion, of course, and it begs the question: are statins really as safe and cost effective as mainstream medical authorities claim? The unequivocal answer is no.

Statins don’t increase survival in healthy people

Statins have never been shown to be effective in reducing the risk of death in people with no history of heart disease. No study of statins on this “primary prevention population” has ever shown reduced mortality in healthy men and women with only an elevated serum cholesterol level and no known coronary heart disease. (CMAJ. 2005 Nov 8;173(10):1207; author reply 1210.) In fact, an analysis of large, controlled trials prior to 2000 found that long-term use of statins for primary prevention of CHD produced a 1% greater risk of death over 10 years compared to placebo

Statins don’t increase survival in women

Despite the fact that around half of the millions of statin prescriptions written each year are handed to female patients, these drugs show no overall mortality benefit regardless of whether they are used for primary prevention (women with no history of heart disease) or secondary prevention (women with pre-existing heart disease). In women without coronary heart disease (CHD), statins fail to lower both CHD and overall mortality, while in women with CHD, statins do lower CHD mortality but increase the risk of death from other causes, leaving overall mortality unchanged. (JAMA study)

Statins don’t increase survival in the elderly

The only statin study dealing exclusively with seniors, the PROSPER trial, found that pravastatin did reduce the incidence of coronary mortality (death from heart disease). However, this decrease was almost entirely negated by a corresponding increase in cancer deaths. As a result, overall mortality between the pravastatin and placebo groups after 3.2 years was nearly identical.

This is a highly significant finding since the rate of heart disease in 65-year old men is ten times higher than it is in 45-year old men. The vast majority of people who die from heart disease are over 65, and there is no evidence that statins are effective in this population.

Do statins work for anyone?

Among people with CHD or considered to be at high risk for CHD, the effect of statins on the incidence of CHD mortality ranges from virtually none (in the ALLHAT trial) to forty-six percent (the LIPS trial). The reduction in total mortality from all causes ranges from none (the ALLHAT trial) to twenty-nine percent (the 4S trial).

However, the use of statins in this population is not without considerable risk. Statins frequently produce muscle weakness, lethargy, liver dysfunction and cognitive disturbances ranging from confusion to transient amnesia. They have produced severe rhabdomyolysis that can lead to life-threatening kidney failure.

Aspirin just as effective as statins (and 20x cheaper!)

Perhaps the final nail in the coffin for statins is that a recent study in the British Medical Journal showed that aspirin is just as effective as statins for treating heart disease in secondary prevention populations – and 20 times more cost effective! Aspirin is also far safer than statins are, with fewer adverse effects, risks and complications.

So what if you are at risk for heart disease and you’d prefer not to take a statin? Other than aspirin, there are many clinically proven ways to prevent heart disease involving simple adjustments to diet and lifestyle. In fact, the recent INTERHEART study which looked at the incidence of heart disease in 52 countries revealed that over 90% of heart disease is preventable by diet and lifestyle modifications.

I’ll discuss these natural methods of preventing heart disease in my next post. Stay tuned!

Recommended links

• Dangers of statin drugs: what you haven’t been told about cholesterol-lowering drugs
• The effect of statins is not due to cholesterol lowering