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What may be a driving force for both clinical benefits as well as relative risk of using antioxidants as well as omega-3 fish oil is the redox stability of the patient being treated. In the case of CFS, that redox stability or redox buffer capacity is very poor and demonstrable by ETM in all cases of CFS so far tested. The point is that antioxidants are all potentially pro-oxidants and possibly harmful if used to excess in an overly oxidizing state such as CFS as they cannot be maintained in their reduced state. If fully oxidized, antioxidants are pro-oxidants if they cannot be re-reduced. Published meta-analysis studies of anti-oxidant use show both increased mortality and morbidity in populations of both healthy and non-healthy patients. It is likely that if those studies could separate the redox stable vs. the redox unstable sub-sets of patients under study, the data might be much more compelling concerning the risk vs. benefit of pharmacologic doses of antioxidants.

Three family members, mother, son and daughter, all with CFS, were evaluated recently in my clinic. They all became sick in Prague, the Czech Republic, on the mothers sabbatical LOA from her college teaching position after all had a chicken-pox like illness. They are all seven months out from stem cell therapy in Panama. They all have improved significantly following stem cell therapy with the daughter claiming a complete cure after 17 years of illness at the age of 29. She is the second stem cell patient claiming a complete cure and includes an unrelated 23 year old male patient, also 7 months out from stem cells. Both cures took at least 90 days to become manifest with the first thirty days exhibiting significant hypersomnolence and with little energy to do much and typical for all the CFS stem cell patients (N=13).

Two published studies show that diastolic heart failure (DHF) in the elderly and low birth weights at term in infants have occurred during the same time frame from 1990-2000. No one has an explanation for these anomalies at the ends of the age spectrum in humans but suspect an environmental factor or factors. We have a rising case load of diastolic dysfunction seen in 97% of our CFS cases (ave. age 49) and some appear to have what I would call compensated diastolic heart failure. I would define compensated DHF in CFS as an extremely low cardiac output with a cardiac index (CI) below 2.0 and very poor functional capacity combined with the inability to stand which is the corollary in DHF to the inability to lay down flat in systolic heart failure (SHF). Heart failure patients are typically below 2.0 in CI. I have several CFS patients below that number and they cannot stand still for more than 15-30 seconds without having to sit down or fall down. Walking or moving helps which makes sense as that would increase filling pressures and equivalent to laying down. They might be diagnosed as having orthostatic intolerance by others. These patients are also typically thin or near ideal body weight and have a high catabolic to anabolic ratio on 24 hour urine hormone analysis when I have measured it.

Vitamin D3 is regulated by P450 enzyme systems that are in turn decoupled due to low NADPH levels in CFS. This raises important questions regarding the reasons that may underlie low D3 levels typical for most CFS cases. The finding of increased intracellular calcium by UK investigators may also play into the reasons for finding low D3 in CFS. Given these deeper issues that may underlie D3 levels suggests that aggressive D3 therapy may not be the best course of action in CFS. D3 is a highly regulated pro-hormone and there could be good reasons for it to be down-regulated in CFS.

It appears vaccine contamination risk will be a rising threat as we approach over 50 different vaccinations now recommended in children and now including the increased microbial contamination risk of cell associated vaccine manufacturing. In such vaccination decisions, one has to weigh the risk to benefit ratio of each vaccination including the multi-vaccine vaccinations in a particular individual at one moment in time. The longer view risk to the population of such aggressive vaccination programs is even murkier.

Curcumin is a member of a class of complex biochemicals known as curcuminoids and the principal constituent of the spice known as turmeric and responsible for its yellow color. In turn, turmeric is the principal spice in common yellow curry powder which can contain many spices that vary widely among popular cuisines. Curcumin contains polyphenols that have significant medicinal properties and used historically in southeastern Asia and India and commonly used in Ayurvedic medicine. Turmeric is a perennial herb and member of the ginger family and native to tropical southeast Asia. Heavy curcumin use in India is thought to explain, in part, the low incidence of Alzheimers disease as it is anti-inflammatory and an antioxidant and promotes neurogenesis. It is also anti-bacterial and anti-viral as well as having anti-cancer properties and heavy metal chelation properties, especially iron.

Before we learned that Artesunate might inhibit XMRV via NF Kappa B inhibition in August of 2009, we were aware that Artesunate was a known inhibitor of all known human herpes viruses against which it has been tested as well as HIV. I was first introduced to Artesunate by a prominent Autism expert at a medical conference who finds it helpful in Autism. We were also impressed that Artesunate and its relative Wormwood, using SL administration on the echo table, produced the most powerful ablation of oxygen toxicity as well as the ablation of other echo terrain map (ETM) backflashes than any other therapy we have ever used. Both Artesunate and Wormwood will do this in 30 seconds.

To explain this case report, one of my colleagues notes that alcohol inhibits cysteine entry into the brain and therefore could evoke a rebound induction of methylation cycle block in the brain that later improves CNS glutathione production and possibly improve CNS function. The immediate effect of methylation cycle block would cause CNS depression but then CNS functional rebound later which is what she reports. Initially she feels poorly and even sick after alcohol ingestion but sleeps better with the alcohol and then does better cognitively for the next several days. She calls this a love-hate relationship with alcohol. Another colleague thinks that certain gut pathogens and especially helminth infections can be inhibited and killed by alcohol. On the negative side, alcohol increases gut permeability and puts severe pressure on liver detoxification mechanisms. A CT scan of this patient’s liver shows fatty metamorphosis and in line with this negative view of alcohol on the liver-gut system. Like all other drugs and alcohol is a drug, the good they do must be weighed against the bad they do and this can vary from person to person and is dose dependent in each person.

I placed three cell phones on his chest wall as he lay on the echocardiograph table and called my office number and left the phones on his mid-sternum for one minute while they rang that number. I then measured the IVRT response every minute after turning the phones off. He “experienced” the documented free energy decline by IVRT criteria as feeling heaviness in his chest. Below is the powerpoint slide of the resulting IVRT decline at each minute after the cell phones were turned off.

Below is an interesting link to a thorough discussion on gammaretroviruses and the related human endogenous retroviruses ERV’s of which there are 2,000 ERV genes located on a single human chromosome. There are thousands of ERV’s spread across the entire human DNA grouped into 24 families. XMRV has 95% homology with human ERV’s. What is very interesting about ERV’s and likely true for XMRV is that they are TH1 immunosuppressive which is believed to be critical in the ability to get pregnant as the mother needs to be Th1 immunosuppressed to avoid rejection of the implanted fetus. The hormones of pregnancy and especially progesterone are in part responsible for activating env proteins of ERV’s which apparently are largely responsible for this immunosuppression. It is likely that progesterone activates XMRV env protein and may explain why we see women with more CFS at 4 to 1 over men and the apparent vulnerability of adolescent girls to CFS onset and the relative reduction of the point prevalence of CFS in the elderly and in children compared to the young to middle ages. I have also observed a reduction in severity of CFS symptoms in post-menopausal women though perhaps modulated by their use of HRT. The related hormones to progesterone are pregnenolone and cortisol. I have seen both devastate a handful of CFS cases.