Fish oil could be the key to beating flu and preventing deaths

No human trials so far

The three viruses that cause flu are a major cause of sickness in the UK and are behind around 4,000 deaths a year.  However, current antiviral drugs don't protect the most seriously ill patients.

Now researchers have found a compound derived from fats found in fish oils prevents death in mice infected with influenza. It even works at advanced stages of the illness.

A flu jab is currently offered by the NHS to 'at-risk' groups including people over 65 and pregnant women.

However, because the winter flu virus mutates each year and new deadly strains develop, it only offers around 60 per cent protection.

Study author Yumiko Imai  from Akita University in Japan, said: 'Given the potential for future lethal pandemics, effective drugs are needed for the treatment of severe influenza, such as that caused by H5N1 viruses.

'We have identified a novel therapeutic target for the treatment of severe influenza that is effective under conditions where known antiviral drugs fail to protect from death.'

Flu causes a sudden high temperature, headache and general aches and pains, tiredness and sore throat. However, it can cause a bacterial chest infection and even life-threatening pneumonia in those in at-risk groups.

Current antiviral drugs are not effective when given to these patients as little as two days after infection.

In an attempt to discover more effective drug targets for influenza, the scientists studied naturally occurring lipids derived from omega-3 fatty acids found in fish oils.

They tested the lipid PD1 on human lung cells that had been infected with various flu strains.

The team found it prevented the the viruses from replicating, including bird flu (H5N1).

Further tests on influenza-infected mice revealed treatment with PD1 in combination with an approved antiviral drug improved survival rates.

It also worked even when given two days after infection.

'Our findings suggest that PD1could serve as a biomarker as well as a much needed antiviral drug for severe and lethal influenza virus infections,' Imai says.

The study was published in the journal Cell.

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Recent findings on the health effects of omega-3 fatty acids and statins, and their interactions: do statins inhibit omega-3?

The academic journal article excerpted below admits that the evidence for benefit from fish oil is very wobbly -- JR

Michel de Lorgeril et al.

Abstract

Early randomized controlled trials (RCTs) demonstrated the health benefits of omega-3 fatty acids (n-3), whereas recent RCTs were negative. We now address the issue, focusing on the temporal changes having occurred: most patients in recent RCTs are no longer n-3 deficient and the vast majority are now treated with statins. Recent RCTs testing n-3 against arrhythmias suggest that n-3 reduce the risk only in patients not taking a statin. Other recent RCTs in secondary prevention were negative although, in a post-hoc analysis separating statin users and non-users, non-significant protection of n-3 was observed among statin non-users whereas statin users had no effect. Recent RCTs testing statins - after the implementation of the New Clinical Trial Regulation in 2007 - are negative (or flawed) suggesting that the lack of effect of n-3 cannot be attributed to a parallel protection by statins. Finally, statins favor the metabolism of omega-6 fatty acids (n-6), which in turn inhibits n-3 and, contrary to n-3, they increase insulin resistance and the risk of diabetes. Thus, n-3 and statins are counteractive at several levels and statins appear to inhibit n-3.

Introduction

Until 2005, studies consistently provided clear evidence that omega-3 fatty acids (n-3) protect against cardiovascular diseases (CVD) complications [1,2]. They were thought to reduce the risk of arterial atherosclerotic and thrombotic obstruction [3,4]; to increase the myocardial resistance to ischemia-reperfusion injury [5,6]; and to prevent malignant ventricular arrhythmias [7-9]. Animal [5-7] and epidemiological studies [8,9] as well as randomized controlled trials (RCTs) [10-13] all supported that n-3 are protective. This was confirmed in meta-analyses of both prospective cohort studies and RCTs leading to the conclusion that an intake of 250 mg/day of marine n-3 (EPA+DHA (eicosapentanoic acid + docosahexanoic acid)) reduced fatal CVD by 36% when compared to no EPA+DHA [14].

Consequently, it was proposed to use blood measurements of n-3 as a predictor of CVD complications. The omega-3 index - defined as the percentage of EPA+DHA in blood red cells [15] - reflects the average dietary intake and the tissue levels of EPA+DHA, including those of the heart [16,17]. A high omega-3 index (> 8%) is thought to be associated with a low risk of CVD complications [15] whereas a low omega-3 index (< 4%) is associated with increased risk susceptible to be decreased by a preventive treatment with n-3 (fish oil) supplements. An omega-3 index between 4 and 8% indicates an intermediate risk. The effects of n-3 supplements are, therefore, expected to be different in patients with either high or low omega-3 index with large benefits for those with a low index (that is, high risk) and small or no benefits for those with a high index (that is, low risk). This concept is critical because it suggests that n-3 supplements might be potentially protective against CVD complications only in patients who are n-3 deficient and not in patients who are at high risk for reasons other than an n-3 deficiency. This underlines the fact that n-3 are nutrients and not a drug. So far this concept applies only for CVD, not for other nonvascular and non-cardiac clinical conditions.

Contrary to the expectations, the most recent RCTs - that is, those published after 2005 - did not confirm the protective action of n-3 [18-23]. In a recent meta-analysis examining the efficacy of n-3 supplements (EPA+DHA) in the secondary prevention of coronary heart disease (CHD), authors analyzed 13 RCTs involving 20,485 patients with a history of CHD and concluded that n-3 supplements did not consistently reduce CHD mortality, all-cause mortality and the risk of overall CVD complications [24].

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