Fish oil dramatically boosts metabolism?

toxikon

I just stumbled upon this article, and I'm wondering if anyone has an opinion on this!

The article states:
"EPA and DHA, the omega-3 fatty acids found only in fish oil, may have the power to dramatically boost your metabolism -- by about 400 calories per day, researchers from the University of Western Ontario report. Fish oil increases levels of fat-burning enzymes and decreases levels of fat-storage enzymes in your body. For the best metabolism boosting benefit, choose capsules containing at least 300 milligrams of EPA and DHA total."

Thoughts?

Link: http://www.webmd.com/diet/features/increase-your-metabolism-start-losing-fat?page=3

psych0kitty

Either way, fish oil is super good for you.

med2017

fish oil is very good

Silver_Star

Fish oil is a great supplement...but I'm not sure that it can zoom through your body by itself and cause your metabolism to gallop without added exercise.

Timshel_

I just eat lots of fish. Great protein and low cal. If the oil is good, so be it.

ApexLeader

I just eat lots of fish. Great protein and low cal. If the oil is good, so be it.

i eat fish AND i take a fish oil supplement

Cr01502

Fish or Krill oil. Both are just as effective.

" A significant increase in plasma EPA, DHA, and DPA was observed in the subjects supplemented with n-3 PUFAs as compared with the controls, but there were no significant differences in the changes in any of the n-3 PUFAs between the fish oil and the krill oil groups. No statistically significant differences in changes in any of the serum lipids or the markers of oxidative stress and inflammation between the study groups were observed. Krill oil and fish oil thus represent comparable dietary sources of n-3 PUFAs, even if the EPA + DHA dose in the krill oil was 62.8% of that in the fish oil."



Metabolic effects of krill oil are essentially similar to those of fish oil but at lower dose of EPA and DHA, in healthy volunteers.

http://www.ncbi.nlm.nih.gov/pubmed/21042875

moustache_flavored_lube

Fish Oil = good skeptical on dramatic metabolism boost

chrisdavey

typical western diet is high in Omega 6. Fish oil can help bring the ratio of 6:3 back to a better level.

All the studies, I've seen haven't shown any great fat reduction benefit from fish oil supplementation but the other benefits are worth it IMO.

etoiles_argentees

No.
http://raypeat.com/articles/articles/fishoil.shtml



A R T I C L E

The Great Fish Oil Experiment

Reading medical journals and following the mass media, it's easy to get the idea that fish oil is something any sensible person should use. It's rare to see anything suggesting that it could be dangerous.

During the recent years in which the U.S. government has gone from warning against the consumption of too much of these omega-3 oils ("to assure that the combined daily intake of two fatty acids that are components" "(i.e., eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) would not exceed 3 grams per person per day (g/p/d)") to sponsoring biased industry claims, there has been considerable accumulation of information about the dangers of fish oils and omega-3 fatty acids. But there has been an even greater increase in the industry's promotional activities.

The US government and the mass media selectively promote research that is favorable to the fish oil industry. The editorial boards of oil research journals often include industry representatives, and their editorial decisions favor research conclusions that promote the industry, in the way that editorial decisions in previous decades favored articles that denied the dangers of radiation and reported that estrogen cures almost everything. Marcia Angell, former editor of the NEJM, has observed that the "significant results" reported in published studies can be properly interpreted only by knowing how many studies reporting opposite results were rejected by the editors.

One way to evaluate published studies is to see whether they tell you everything you would need to know to replicate the experiment, and whether the information they provide is adequate for drawing the conclusions they draw, for example whether they compared the experimental subjects to proper control subjects. With just a few minimal critical principles of this sort, most "scientific" publications on nutrition, endocrinology, cancer and other degenerative diseases are seen to be unscientific. In nutritional experiments with fish oil, controls must receive similar amounts of vitamins A, D, E, and K, and should include fat free or "EFA" deficient diets for comparison.

In declaring EPA and DHA to be safe, the FDA neglected to evaluate their antithyroid, immunosuppressive, lipid peroxidative (Song et al., 2000), light sensitizing, and antimitochondrial effects, their depression of glucose oxidation (Delarue et al., 2003), and their contribution to metastatic cancer (Klieveri, et al., 2000), lipofuscinosis and liver damage, among other problems.

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"Houston-based Omega Protein Inc.'s bottom line may get a little fatter.

The publicly traded company, which produces an Omega-3 fatty acid product called OmegaPure, has signed an agreement to provide its fish oil in school lunches in 38 school districts in South Texas beginning this month.

The 500-person company, which has ties to former President George Bush's Zapata Corp., will distribute the product through an agreement with Mercedes-based H&H Foods.

Although the dollar amount of the contract between Omega Protein and H&H Foods hinges on future sales, the company is poised to cash in as school administrators and parents refocus their attention on the nutritional content of student diets.

Omega Protein President and CEO Joseph von Rosenberg says the company's recent investment of $16.5 million for a fish oil refinery in Reedville, Va., scheduled for completion in May, and an increased awareness of the benefits of Omega-3 in human food, positions Omega to capitalize on predicted demand."

Jenna Colley
Houston Business Journal

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Andrew Weil was on the radio recently recommending DHA (usually found in fish oil*) to treat depression, and I think that means that a lot of people are buying it and eating it. A few years ago the government declared that it was "generally regarded as safe" and approved its use in baby formula, and a few months ago Texas school districts contracted with Omega Protein (which grew out of the Bush family's Zapata Corporation) to provide menhaden fish oil for school lunches. Between the 1950s and the 1970s, people were assured that eating polyunsaturated seed oils would protect them against heart disease. There's no evidence that the bad outcome of that campaign decreased the gullibility of the public. They are happily joining in the latest public health experiment.

*Weil recommends eating "oily fish"--"wild Alaskan salmon, mackerel, sardines, or herring"--. "If you do take supplements, fish oil is a better source of DHA than algae"

When a group of people in government and industry decide on a policy, they can use carrots (good jobs, grants, and prestige) and sticks (loss of jobs and grants, organized slander, and worse) to make their guidelines clear, and most people will choose to follow those cues, even if they know that the policy is wrong. Historically, policy makers have told the public that "radiation is good for you," "estrogen will make you fertile (or safely infertile) and feminine and strong and intelligent," "starchy foods will prevent diabetes and obesity," "using diuretics and avoiding salt will make pregnancy safer," and that the polyunsaturated fatty acids are "nutritionally essential, and will prevent heart disease."

The original "essential fatty acids" were linoleic, linolenic, and arachidonic acids. Now that the toxic effects of those are coming to be recognized, new "essential fatty acids," the omega-3 fatty acids, including those with long chains, found in fish oils, are said to make babies more intelligent, to be necessary for good vision, and to prevent cancer, heart disease, obesity, arthritis, depression, epilepsy, psychosis, dementia, ulcers, eczema and dry skin.
With just a normal amount of vitamin E in the diet, cod liver oil is certain to be highly oxidized in the tissues of a mammal that eats a lot of it, and an experiment with dogs showed that it could increase their cancer mortality from the normal 5% to 100%. Although fish oils rapidly destroy vitamin E in the body, some of them, especially the liver oils, can provide useful vitamins, A and D. In studies comparing fish oil diets with standard diets, these nutrients, as well as any toxins besides fatty acids (Huang, et al., 1997; Miyazaki, et al., 1998) in either type of oil, should be taken into account, but they seldom are.


Despite the nutritional value of those vitamins, fish oils are generally much more immunosuppressive than the seed oils, and the early effects of fish oil on the "immune system" include the suppression of prostaglandin synthesis, because the more highly unsaturated long chain fats interfere with the conversion of linoleic acid into arachidonic acid and prostaglandins. The prostaglandins are so problematic that their suppression is helpful, whether the inhibition is caused by aspirin or vitamin E, or by fish oil.


Some of the important antiinflammatory effects of fish oil result from the oxidized oils, rather than the unchanged oils (Sethi, 2002; Chaudhary, et al., 2004). These oils are so unstable that they begin to spontaneously oxidize even before they reach the bloodstream.


In experiments that last just a few weeks or months, there may not be time for cancers to develop, and on that time scale, the immunosuppressive and antiinflammatory effects of oxidized fish oil might seem beneficial. For a few decades, x-ray treatments were used to relieve inflammatory conditions, and most of the doctors who promoted the treatment were able to retire before their patients began suffering the fatal effects of atrophy, fibrosis, and cancer. (But a few people are still advocating x-ray therapy for inflammatory diseases, e.g., Hildebrandt, et al., 2003.) The fish oil fad is now just as old as the x-ray fad was at its peak of popularity, and if its antiinflammatory actions involve the same mechanisms as the antiinflammatory immunosuppressive x-ray treatments, then we can expect to see another epidemic of fibrotic conditions and cancer in about 15 to 20 years.

Around 1970 researchers reported that animals given fish oil in their food lived longer than animals on the standard diet. Alex Comfort, who was familiar with the research showing that simple reduction of food intake increased longevity, observed that the animals were very reluctant to eat the food containing smelly fish oil, and were eating so little food that their longevity could be accounted for by their reduced caloric intake. Even when "fresh" deodorized fish oil is added to the diet, its spontaneous oxidation before it reaches the animal's tissues reduces its caloric value. Without antioxidants, fish oil is massively degraded within 48 hours, and even with a huge amount of antioxidant there is still considerable degradation (Gonzalez, 1988; Klein, et al., 1990).

Fish oil has been used for hundreds of years as varnish or for fuel in lamps, and the fatty fish have been used as fertilizer and animal feed, and later the hydrogenated solid form of the oil, which is more stable, has been used in Europe as a food substitute for people. When whale hunting was reduced around 1950, fish oil was substituted for whale oil in margarine production. Like the seed oils, such as linseed oil, the fish oils were mostly replaced by petroleum derivatives in the paint industry after the 1960s.


Although by 1980 many animal diseases were known to be caused by eating oily fish, and the unsaturated oils were known to accelerate the formation of the "age pigment," lipofuscin, many "beneficial effects" of dietary fish oil started appearing in research journals around that time, and the mass media, responding to the industry's public relations campaign, began ignoring studies that showed harmful effects from eating fish oil.


When reviewers in professional journals begin to ignore valid research whose conclusions are harmful to the fish oil industry, we can see that the policy guidelines set by the industry and its agents in government have become clear. Around the end of the century, we begin to see a strange literary device appearing, in which research reports on the toxic effects of omega-3 oils are prefaced by remarks to the effect that "we all know how great these oils are for good health." I think I detect groveling and shuffling of the feet by authors who want to get their work published. If you are willing to say that your work probably doesn't mean what it seems to mean, maybe they will publish it.


For more than 50 years, the great majority of the medical publications on estrogen were part of the drug industry's campaign to fraudulently gain billions of dollars, and anyone who cared to analyze them could see that the authors and editors were part of a cult, rather than seekers of useful knowledge. Likewise, the doctrine of the harmlessness of x-rays and radioactive fallout was kept alive for several decades by demonizing all who challenged it. It now looks as though we are in danger of entering another period of medical-industrial-governmental cultism, this time to promote the universal use of polyunsaturated fats as both drugs and foods.
In 2004, a study of 29,133 men reported that the use of omega-3 oil or consumption of fish didn't decrease depression or suicide, and in 2001, a study of 42,612 men and women reported that after more than 9 years the use of cod liver oil showed no protective effect against coronary heart disease (Hakkarainen, et al., 2004; Egeland, et al., 2001).


The most popular way of arguing that fish oil will prevent heart disease is to show that it lowers blood lipids, continuing the old approach of the American Heart Association's "heart protective diet." Unfortunately for that argument, it's now known that the triglycerides in the blood are decreased because of the fish oil's toxic effects on the liver (Hagve and Christophersen, 1988; Ritskes-Hoitinga, et al., 1998). In experiments with rats, EPA and DHA lowered blood lipids only when given to rats that had been fed, in which case the fats were incorporated into tissues, and suppressed mitochondrial respiration (Osmundsen, et al., 1998).


The belief that eating cholesterol causes heart disease was based mainly on old experiments with rabbits, and subsequent experiments have made it clear that it is oxidized cholesterol that damages the arteries (Stapran, et al., 1997). Since both fish oil and oxidized cholesterol damage rabbits' arteries, and since the lipid peroxides associated with fish oil attack a great variety of biological materials, including the LDL lipoproteins carrying cholesterol, the implications of the rabbit experiments now seem very different.


Another way of arguing for the use of fish oil or other omega-3 fats is to show a correlation between disease and a decreased amount of EPA, DHA, or arachidonic acid in the tissues, and to say "these oils are deficient, the disease is caused by a deficiency of essential fatty acids." Those oils are extremely susceptible to oxidation, so they tend to spontaneously disappear in response to tissue injury, cellular excitation, the increased energy demands of stress, exposure to toxins or ionizing radiation, or even exposure to light. That spontaneous oxidation is what made them useful as varnish or paint medium. But it is what makes them sensitize the tissues to injury. Their "deficiency" in the tissues frequently corresponds to the intensity of oxidative stress and lipid peroxidation; it is usually their presence, rather than their deficiency, that created the disposition for the disease.


One of the earliest harmful effects of polyunsaturated fatty acids, PUFA, to be observed was their acceleration of the formation of lipofuscin or ceroid, the "age pigment," during oxidative stress or vitamin E deficiency. Associated with the formation of lipofuscin, the PUFA were discovered to cause degeneration of the gonads and brain, and the fact that vitamin E could prevent some of their toxic effects led to the idea that vitamin E was essentially an antioxidant. Unfortunately, the protective effect of vitamin E against the PUFA is only partial (Allard, et al., 1997).


The degenerative diseases are all associated with disturbances involving fat metabolism and lipid peroxidation. Alzheimer's disease, alcoholic and nonalcoholic liver disease, retinal degeneration, epilepsy, AIDS, diabetes, and a variety of circulatory problems involve breakdown products of the PUFA. The products of PUFA decomposition include acrolein, malondialdehyde, hydroxynonenal, crotonaldehyde, ethane, pentane, and the neuroprostanes, which are prostaglandin-like molecules formed from DHA by free radical lipid peroxidation products, especially in the brain and at a higher level in Alzheimer's disease.


The reactions of three types of cell--vascular endothelium, nerve cells, and thymus cells--to the PUFA will illustrate some of the important processes involved in their toxicity.


When the body doesn't have enough glucose, free fatty acids are released from the tissues, and their oxidation blocks the oxidation of glucose even when it becomes available from the breakdown of protein caused by cortisol, which is released during glucose deprivation. Cells of the thymus are sensitive to glucose deprivation, and even in the presence of glucose, cortisol prevents them from using glucose, causing them to take up fatty acids. The thymic cells die easily when exposed either to excess cortisol, or deficient glucose. The polyunsaturated fatty acids linoleate, arachidonate, and eicosapentaenoic, are especially toxic to thymic cells by preventing their inactivation of cortisol, increasing its action. (Klein, et al., 1987, 1989, 1990). Lymphocytes from people with AIDS and leukemia are less able to metabolize cortisol. An extract of serum from AIDS patients caused lymphocytes exposed to cortisol to die 7 times faster than cells from healthy people. AIDS patients have high levels of both cortisol and free polyunsaturated fatty acids (Christeff, et al., 1988).

The cytotoxicity caused by EPA and its metabolites (15 mg. of EPA per liter killed over 90% of a certain type of macrophage) isn't inhibited by vitamin E (Fyfe and Abbey, 2000). Immunological activation tends to kill T cells that contain PUFA (Switzer, et al., 2003).


When animals are fed fish oil and then exposed to bacteria, their immunosuppressed thymic (T) cells cause them to succumb to the infection more easily than animals fed coconut oil or a fat free diet. Natural killer cells, which eliminate cancer cells and virus infected cells, are decreased after eating fish oil, and T suppressor cells are often increased. More subtle interference with immunity is produced by the actions of PUFA on the "immune synapse," a contact between cells that permits the transmission of immunological information. The immunosuppressive effect of fish oil is recognized as a useful aid in preventing the rejection of transplanted organs, but some studies are showing that survival a year after transplantation isn't improved.


Polyunsaturated fatty acids, especially those that can be turned into prostaglandins, are widely involved in causing inflammation and vascular leakiness. EPA and DHA don't form ordinary prostaglandins, though the isoprostanes and neuroprostanes they produce during lipid peroxidation behave in many ways like the more common prostaglandins, and their enzymically formed eicosanoids have some functions similar to those of the common prostaglandins. The brain contains a very high concentration of these unstable fatty acids, and they are released in synapses by ordinary excitatory process.


Chan, et al., 1983, found that polyunsaturated fats caused brain swelling and increased blood vessel permeability. In 1988, Chan's group found that DHA and other polyunsaturated fatty acids added to cultured cells from the cerebral cortex produced free radicals and stimulated production of malondialdehyde and lactate, and inhibited the uptake of glutamic acid, which suggests that they would contribute to prolonged excitation of the nerves (Yu, et al., 1986). In brain slices, the polyunsaturated fatty acids caused the production of free radicals and swelling of the tissue, and the saturated fatty acids didn't (Chan and Fishman, 1980). The PUFA inhibited the respiration of mitochondria in brain cells (Hillered and Chan, 1988), and at a higher concentration, caused them to swell (Hillered and Chan, 1989), but saturated fatty acids didn't produce edema. Free radical activity was shown to cause the liberation of free fatty acids from the cellular structure (Chan, et al., 1982, 1984). The activation of lipases by free radicals and lipid peroxides, with the loss of potassium from the cells, suggests that excitation can become a self-stimulating process, leading to cellular destruction.


DHA itself, rather than its decomposition products, facilitates excitatory (glutamate) nerve transmission (Nishikawa, et al., 1994), and that excitatory action causes the release of arachidonic acid (Pellerin and Wolfe, 1991).


Considering just one of the products of fish oil peroxidation, acrolein, and a few of its effects in cells, we can get an idea of the types of damage that could result from increasing the amount of omega-3 fats in our tissues.
The "barrier" between the brain and blood stream is one of the most effective vascular barriers in the body, but it is very permeable to oils, and lipid peroxidation disrupts it, damaging the ATPase that regulates sodium and potassium (Stanimirovic, et al., 1995). Apparently, anything that depletes the cell's energy, lowering ATP, allows an excess of calcium to enter cells, contributing to their death (Ray, et al., 1994). Increasing intracellular calcium activates phospholipases, releasing more polyunsaturated fats (Sweetman, et al., 1995) The acrolein which is released during lipid peroxidation inhibits mitochondrial function by poisoning the crucial respiratory enzyme, cytochrome oxidase, resulting in a decreased ability to produce energy (Picklo and Montine, 2001). (In the retina, the PUFA contribute to light-induced damage of the energy producing ability of the cells [King, 2004], by damaging the same crucial enzyme.) Besides inhibiting the ability of nerve cells to produce energy from the oxidation of glucose, acrolein inhibits the ability of cells to regulate the excitatory amino acid glutamate (Lovell, et al., 2000), contributing to the excitatory process. High levels of acrolein (and other products of PUFA degradation) are found in the brain in Alzheimer's disease (Lovell, et al., 2001).


The "prion" diseases, CJD and TSE/BSE (mad cow disease) have many features in common with Alzheimer's disease, and several studies have shown that the "prion" protein produces its damage by activating the lipases that release polyunsaturated fatty acids and produce lipid peroxides (Bate, et al., 2004, Stewart, et al., 2001).
Acrolein reacts with DNA, causing "genetic" damage, and also reacts with the lysine in proteins, for example contributing to the toxicity of oxidized low density lipoproteins (LDL), the proteins that carry cholesterol and that became famous because of their involvement in the development of atherosclerosis that was supposedly caused by eating saturated fats.


My newsletter on mad cow disease discussed the evidence incriminating the use of fish meal in animal feed, as a cause of the degenerative brain diseases, and earlier newsletters (glycemia, and glycation) discussed the reasons for thinking that inappropriate glycation of lysine groups in proteins, as a result of a lack of protective carbon dioxide/carbamino groups, produces the amyloid (or "prion") proteins that characterize the dementias. Acrolein, produced from the decomposing "fish oils" in the brain, is probably the most reactive product of lipid peroxidation in the brain, and so would be likely to cause the glycation of lysine in the plaque-forming proteins.
These toxic effects of acrolein in the brain are analogous to the multitude of toxic effects of the omega-3 fatty acids and their breakdown products in all of the other organs and tissues of the body. Cancer cells are unusual in their degree of resistance to the lethal actions of the lipid peroxides, but the inflammatory effects of the highly unsaturated fatty acids are now widely recognized to be essentially involved in the process of cancerization (my newsletters on cancer and leakiness discuss some of the ways the fats are involved in tumor development).
The fats that we synthesize from sugar, or coconut oil, or oleic acid, the omega-9 series, are protective against the inflammatory PUFA, in some cases more effective even than vitamin E.


In Woody Allen's 1973 movie, Sleeper, the protagonist woke up after being frozen for 200 years, to find that saturated fats were health foods. At the time the movie was made, that had already been established (e.g., Hartroft and Porta, 1968 edition of Present Knowledge in Nutrition, who showed that adequate saturated fat in the diet helped to protect against the formation of lipofuscin).

PS:
Royal Society for the Protection of Birds says 2004 has been the most catastrophic breeding season on record for seabirds along UK coasts. It says industrial fishing to supply fish meal and oil is barely sustainable and imperils the whole marine food web.
"The UK has suffered serious seabird disasters this year already. In Shetland and Orkney, entire colonies of birds failed to produce any young because of severe food shortages. "On top of that, hundreds of seabirds have been washing ashore having perished at sea. Again, lack of food is thought to be one of the reasons." The report, Assessment Of The Sustainability Of Industrial Fisheries Producing Fish Meal And Fish Oil, was compiled for the RSPB by Poseidon Aquatic Resource Management Ltd and the University of Newcastle-upon-Tyne.

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© Ray Peat Ph.D. 2007. All Rights Reserved. www.RayPeat.com

taso42

no

fish oil is an excellent supplement, for Omega 3. but it does not dramatically boost metabolism. sorry.

Contrarian

It dramatically boosts the fishiness of your burps.

etoiles_argentees

HOME » FOOD & NUTRITION » WHEN IT COMES TO FISH OIL, MORE IS NOT BETTER

By Chris Kresser on October 25, 2010 in Food & Nutrition, Heart Disease | 136 comments


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.

cbferriss

I take flax seed oil instead. I can't stand the fishy burps.

coffee_rocks

Depends on which study you read..maybe not so good for you

http://www.vancouversun.com/health/Fish+supplements+more+harm+than+good+researcher+finds/7857942/story.html

toxikon

I appreciate everyone's opinion!

I've never taken fish oil myself. Burning an extra 400 cals just by taking a fish oil pill seemed kinda too good to be true so I just thought I'd get some opinions on it.

carrieous

no

etoiles_argentees

http://www.westonaprice.org/know-your-fats/precious-yet-perilous

Read, or don't, it's your body.

Lrdoflamancha

I have taken fish oil supps for several years. My Dr is a big fan of them. They are good for several things... Weight Loss is NOT one of them. I wish they were.

deanabailey

I take fish oil because they say it's good for you. I work out everyday and eat healthy, I have lost some weight but don't really attribute that to the fish oil.

ndj1979

fish oil is good for you ..but there are no magic metabolism boosters out there...no matter what you read on MFP threads or see on Dr Oz...

Cr01502

I stand corrected. After reading the previous article I posted both fish and krill oil are effective supplements if you're looking to include more EFAsinto your diet. However they do not appear to boost your metabolism.

Metabolic Data

No significant differences between groups were observed over time for resting metabolic rate (SO = -62 ± 184 kcal, FO = 17 ± 260 kcal; p = 0.40), or for the respiratory exchange ratio (SO = 0.023 ± 0.54; FO = -0.019 ± 0.85, p = 0.16).

But if you look at the rest of this study it still makes alot of compelling reasons to include fish oil in your diet.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2958879/

"
The results of this study showed that 6 weeks of supplemental fish oil significantly increased lean mass, and significantly reduced fat mass in healthy adults. This is in agreement with Couet et al. [21], who observed a significant 0.88 kg reduction in fat mass, and a non-significant 0.20 kg increase in lean mass following 3 weeks of an increased consumption of fish oil. In their study, they added fish oil to the diet, but kept total fat and energy constant between the treatments. In the present study, the fish oil was added on top of an ad libitum diet, with instructions given to the subjects to maintain their normal dietary patterns throughout the study. Similarly, Hill et al [22] found a significant reduction in fat mass following 12 weeks of supplementation with fish oil in overweight subjects. They also observed an increase in lean mass in the fish oil group, however, like the data reported by Couet et al. [21], it did not reach significance. Thorsdottir et al. [23] recently found that supplementation with fish oil, or inclusion of fish in an energy-restricted diet resulted in significantly greater weight loss in young men. Additionally, they found that young men taking the fish oil supplements had a significantly greater reduction in waist circumference compared to the control group, or the group that increased their dietary intake of fish.

Unlike the Couet et al. study [21], we did not observe an increase in RMR, or a decrease in RER following fish oil treatment. The failure to find an increase in RMR following fish oil treatment is hard to explain given the significant increase in lean mass observed in the present study. Several studies have shown that lean mass is the largest determinant of RMR [28-30], and decreasing lean mass decreases RMR [31], while increasing lean mass increases RMR [32]. Therefore, it would be expected that the increase in lean mass would correspond to an increased RMR following fish oil treatment. In the Couet et al. study [21], metabolic data were measured for 45 min following a 90 min rest period. This is a longer time period than the 40 min used in the present study. However, it is doubtful that this methodological difference between the studies contributed to the differing effects observed for RMR and RER values since recent studies have shown that very short rest periods (as little as 5 min) produce reproducible results that correlate extremely well with RMR measures made over much longer time periods [33,34]. It is also unlikely that the use of a subset (n = 24) of the total subject population can explain the failure to observe any metabolic changes since analysis of the 24 subjects found that they responded similar to the entire group in regards to body composition changes. It remains unclear why the increased lean mass observed following fish oil treatment did not correspond to an increase in RMR.

Intuitively it would make sense that if fat mass was reduced, but resting metabolic rate did not change following fish oil treatment, then the amount of calories coming from the oxidation of fatty acids should be increased. However, this was not the case in the present study. Although there was an absolute reduction in the RER following fish oil treatment (which would indicate an increased oxidation of fatty acids), the difference was not statistically significant. While it is possible that a type II error was committed and the reduction in RER was a real effect, it is also possible that the fish oil treatment increased fat oxidation at other times during the day such as during exercise [35], or during the post-prandial period [36].

A potential shortcoming of the present study was not using dietary records to monitor the subjects' intake during the study. Although there are several potential problems with the use of dietary records (for a review of inaccuracies with self-recorded diet records see [37]), they would have provided us with some insight into the dietary habits of the subjects during the study. It therefore remains a possibility that the fish oil supplements resulted in the subjects changing their normal dietary habits. Although increasing dietary fat does not generally cause a decrease in voluntary fat intake [38], it has been shown that fish oil may reduce appetite [39], which could have led to the subjects consuming less total calories during the study. While a reduction in volitional food intake would explain the observed reduction in fat mass following fish oil treatment, it does not explain the increase in lean mass we observed.

Although other studies have observed a significant [3,5], or insignificant [21,22], increase in lean mass following fish oil treatment, to date no study has determined the mechanism by which dietary fish oil causes an increased accretion of lean mass. One possibility lies in the well-documented ability of dietary omega 3 fatty acids to reduce inflammatory cytokines [40], since inflammatory cytokines have the ability to increase protein degradation mainly by activating the ATP-ubiquitin-dependent pathway [41-45]. It is possible then, that dietary fish oil is simply decreasing the breakdown of protein tissue caused by inflammatory cytokines, and this results in an increased accretion of protein over time.

An alternative possibility is that fish oil supplementation was able to increase lean mass by reducing cortisol levels since it is well established that cortisol increases protein catabolism [46-49]. The significant negative correlation (r = -0.504, p = 0.02) observed in the fish oil group between the change in lean mass and the change in salivary cortisol concentrations would support this hypothesis. Although other studies have observed a decrease in cortisol levels following fish oil consumption [20], the exact mechanism(s) responsible are currently unknown. However, it is possible that the reduction of IL-6 as a result of fish oil consumption [50] is causing a reduction in cortisol production since it has been shown that IL-6 induces increases in cortisol levels [51,52]. It is unclear whether it is the well-documented ability of fish oil to reduce inflammatory cytokines, the reduction in cortisol, or a combination of both, that resulted in the increased lean mass observed in the present study following fish oil treatment. More work is needed to determine the mechanism(s) responsible for the accretion of lean mass following fish oil consumption.

The role of cortisol in obesity is poorly understood. Excessive cortisol levels, such as those observed in patients with Cushing's disease, results in substantial fat mass gains - especially in the abdominal region [17,19]. However, there is disagreement between studies about the relationship between values of cortisol that are within a normal physiological range, and obesity [18]. Nevertheless, several studies have shown an association with higher levels of cortisol and fat mass [53-58]. In the present study, there was a significant correlation between the change in salivary cortisol and the change in fat mass following fish oil treatment (r = 0.661, p = 0.001). Recent work by Purnell et al. [59] has shown that a reduction in fat mass as a result of dieting does not lower cortisol production, which would suggest that the relationship observed in the present study between salivary cortisol and fat mass was not simply a result of the reduction in fat mass. However, further work is needed to determine exactly how the reduction in cortisol levels may have influenced fat loss observed in the FO group.

In conclusion, 6 weeks of supplemental fish oil significantly increased lean mass, and significantly reduced fat mass in healthy adults. Given the short duration of this study, it is unclear how these changes would impact long-term body composition changes and more research is needed to determine the impact of chronic fish oil supplementation on long-term body composition. The reduction in salivary cortisol following fish oil treatment was significantly correlated with the increased fat free mass and the decreased fat mass observed. To the best of our knowledge, this is the first time that this association has been described in the literature. Since higher salivary cortisol levels are associated with higher mortality rates [60], the reduction in salivary cortisol levels observed in the present study following fish oil supplementation likely has significant implications beyond positive changes in body composition."

ShariTho1

I just stumbled upon this article, and I'm wondering if anyone has an opinion on this!

The article states:
"EPA and DHA, the omega-3 fatty acids found only in fish oil, may have the power to dramatically boost your metabolism -- by about 400 calories per day, researchers from the University of Western Ontario report. Fish oil increases levels of fat-burning enzymes and decreases levels of fat-storage enzymes in your body. For the best metabolism boosting benefit, choose capsules containing at least 300 milligrams of EPA and DHA total."

Thoughts?

Link: http://www.webmd.com/diet/features/increase-your-metabolism-start-losing-fat?page=3

I just read the same thing on WebMD website. Surely you can believe WebMD, can't you?
My husband is picking some up today!! :-)

jjking54

It dramatically boosts the fishiness of your burps.

Truth.

Anonycatgirl

If that were true, I wouldn't need to be here.

IVMarkIV

Let's see FDA approved indication based on Randomized Clinical Trial(s) (key word) remains only hypertriglyceridemia...that is for Omega-3-acid ethyl esters (LOVAZA) whereas fish oils have a laundry list of reported/observational/anecdotal etc. uses for everything ranging from Alzhiemer's to cancer to respiratory diseases to ulcerative colitis (man, many more). It's the same deal with Melatonin.

CodeMonkey78

fish oil is good for you ..but there are no magic metabolism boosters out there...no matter what you read on MFP threads or see on Dr Oz...

^^ This. I do take a fish oil supplement daily for its' health/nutrition benefits, but pertaining to boosting your metabolism, I'm sorry -- but no.

mufamuscles

Fish oil is great for you, but boosting metabolism by 400 cal/day is probably too good to be true for the vast majority of people
Regardless, it probably can't hurt to take it for the other benefits unless you're on blood thinners or have clotting problems or are having surgery soon. Check with your doctor first!

ndj1979

IF that was the case you could eat at maintenance, take fish oil, and lose almost a pound per week….which I think you would have about 0.0% chance of happening...

YorriaRaine

I take a flaxseed oil supplement in the morning and a fish oil supplement in the evening so I can get various forms of omega-3. Mostly just because it helps with Dry Eyes and also because I absolutely hate seafood.

cwolfman13

Pretty skeptical on it bumping the metabolism significantly but in general, fish oil or krill oil are one of the few supplements that I legitimately think most people should be taking, especially if they cannot afford or otherwise do not eat much in the way of fish.

I take one daily that is 657 Mg of EPA and 253 Mg DHA. I also eat salmon at least once per week and usually MahiMahi another time during the week...the Mahi isn't as great a source as the salmon, but I like MahiMahi and it's still a reasonably good source of Omega 3 fatty acids.