Beginning at three months she began to improve functionally in a slow linear fashion and by early June attended a family reunion and actually water skied, cooked, cleaned and walked daily for the first time in years. She noted to her husband that she was 95% recovered. In the two months after the reunion, she had a mild relapse attributed in part to her over-extension during the reunion. In the last month she has rebounded and now cooks, shops, engages in some limited hobbies and goes out socially with friends. She does feel limited in choice of activities, in part, because she fears a relapse. I estimate her KPS at 65 as she notes she could live alone and engage in regular hobbies. She could not work a regular part-time job, however.

I though she looked great with glowing, pink skin and seemed alert and very relaxed and rested compared to her gray, haggard look in February. Her exam was largely unremarkable except for slightly increased ankle jerks at 3-4+ and a positive augmented Tandem Stance as in her May visit. She failed to desaturate on breath-old. Her B/P was up to 120/82 c/w 90/60 in January.

On echo she demonstrated continued pseudonormal diastolic dysfunction but with a pretty good cardiac output for her size and a normal IVRT for age at 88 msec. Her ETM was spectacularly improved and is the first CFS case with a normalized pLiver and Fructose backflash. The amplitudes of her only two remaining significant backflashes were 40% improved over May and at low, single digits (3%). Of the seven backflashes the typical CFS ETM shows, she only has three left and one of the three is only 2% while the other two are at 3% which is significantly better than any other patient in the practice by far. Her ETM is both quantitatively and qualitatively improved over May and even better c/w January suggesting the stem cells remain active at nine months out.

She was XMRV antigen negative in May. Antibody status is unknown. TGF Beta 1 was significantly improved in February as were many other tests but we are awaiting a whole list of tests from this visit. MSQ and SF-36 SF are pending but should be significantly improved. She takes Artesunate and Wormwood 5-days per week as part of her protocol. Her favorite medicine is Inosine for its punch and not an uncommon statement in my practice.

Dan Peterson MD, a long time resident of Incline Village, NV (Lake Tahoe) and I worked for over eight years (1984-1992) to link CFS to a retrovirus. Dan first sent five patient samples to Specialty Labs in 1985 to test for HTLV-1 and 4 of 5 were positive. We did this due to incredible disturbances on flow cytometry of peripheral mononuclear cells producing elevated CD4/CD8 ratios due to CD8 depletion as well as scatter patterns (debris patterns) that the laboratory flow cytometrist said she had only seen in HIV infections. A radiologist at UC San Diego, on review, said our MRI brain scans done on CFS cases showing UBO’s (1988), looked exactly likes AIDS cases. Repeat testing was negative for HTLV-1 and Dr. James Peters of Specialty Labs suggested these CFS patients might have a cross reacting and novel retrovirus that looks like HTLV-1. In 1986, I called the NCI and Robert Gallo MD, head of the foremost retrovirology laboratory in the world at the time, accepted Lake Tahoe samples for a year resulting in the association of an HHV-6A strain with Lake Tahoe CFS cases (1992), only previously linked to HIV infection.

While practicing in Charlotte, NC and based on continued evidence of unusual immune disturbances by flow cytometry including CD4 depletion (ICL) in 15% of CFS patients which was investigated in my clinic and dismissed by the CDC as clinically irrelevant and continued high RNAse-L activity (1994), I contacted Elaine DeFreitas PhD at the Wistar Institute who ultimately found HTLV-II-like genes associated with CFS (1991). Her work was unfortunately assaulted by the CDC that claimed either an endogenous RV sequence that lighted up in cases and controls using her primers (per Dr. J.W. Gow) or null responses to cases and controls (per CDC scientist). Elaine argued that these two scientists with diametrically opposing results manipulated the primer stringency conditions and got whatever result they wanted, to make their opposite claims. Her proposal to physically run the assays side by side with the CDC scientists to see if these results could be replicated was dismissed by the CDC. Dr. Gow would later publish his opinion (1992). Left unfunded by senior administrators at the NIH and the CDC, the search for a retroviral link in CFS dissipated and was lost until Judy Mikovits PhD, operating out of the independent Whittemore-Peterson Institutes, revived the long search. I congratulate her and the Whittemore-Peterson Institute.

The finding of antibody or active virus in 95% of CFS and 4% of controls is a result that argues for causality, in my opinion, especially with the associated RNAse-L corruption and NK functional impairment that might predict such an infection. This novel retrovirus could easily shift the redox state just like HIV as published in (2001) and (1995) and induce all manner of associated pathogens as seen in CFS. A redox shift could ultimately corrupt the gut ecology and create P450 decoupling based on NADPH depletion observed in CFS and lead to environmental illness as well. Time will tell but I think Dr. Mikovits is right to suspect causality. I also think this virus is infectious with at least ten million Americans infected who appear healthy and perhaps another four million Americans or more with CFS as recently estimated by the CDC (2007). However, disease expression may be more limited causing the illusion that it is not infectious. Furthermore, there may be other diseases that are similar and dissimilar to CFS that are associated with if not caused by XMRV.

In this post, we explore the incredible finding that different ratios of omega-3 to omega-6 EFA’s appear to produce dramatically different effects on the echocardiographically derived ETM, both positive and negative.  Surprisingly, the use of omega-3 EFA’s and especially fish oil is uniformly negative (N=10) in CFS but not in controls (N=3).  This is not terribly surprising since omega-3 oils are far more easily oxidized and is possibly explained by the more redox impaired status of CFS.  However, we are also finding that omega-6 alone, while better than omega-3 alone in an oxidizing state such as CFS, is not nearly as positive as a mixture of the omega-3, omega-6 and omega-9 EFA’s.  In particular, a ratio of omega-6 to omega-3 of 3:1 appears ideal and generates the most positive ETM response.  Such a ratio is found in high grade olive oil but not lower grades of olive oil which are as high as 13:1, omega-6 over omega-3.  The use of fish oil as an omega-3 source is inferior to the use of a plant source of omega-3 such as flaxseed oil or possibly a cyanobacteria derived source such as spirulina.  As the ratios of six to three approach 1:1, the ETM response becomes more variable in each patient but the 3:1 ratio of omega-six over omega-three is always a good choice if it excludes fish oil.

This important finding of large EFA ratio variances in ETM response could be used to great advantage as the regulation of the eicosanoids are very dependent on a proper EFA ratio and this appears especially so for CFS.  This means that the entire paracrine and autocrine hormone system involved in eiconasoid regulation can be favorably influenced with the right EFA ratio and this could have profound and positive effects in CFS.  Conversely, the wrong EFA ratios could have significant and negative consequences in CFS.