Monday, November 3, 2014

Medical Marijuana

Tomorrow is Election Day here in Pennsylvania, and I’ll be doing my part to oust current Republican Pennsylvania Governor Tom Corbett out of office for, among other things, his not-over-my-dead-body’s approach to the legalization of medical marijuana.  After pressure was applied on Corbett last spring—80 percent of Pennsylvanians support legalized medical marijuana—he grudgingly partially reversed his opinion on the subject—but only for severe childhood epilepsy.

A friend of mine’s 16-year-old is daughter is plagued with severe epilepsy—and anticonvulsant meds and the Johns Hopkins high-fat ketogenic diet haven’t worked: The young woman has tried multiple drugs and multiple combinations, and still she experiences multiple seizures daily.  Whether pot can reduce her seizures is anybody’s guess, but she should have the right to try it now and not wait for the grindingly slow wheels of Pennsylvania politics to make it possible.  How many more seizures will she have before medical marijuana is approved here?  

The marijuana that’s effective for seizures has little to no THC, the chemical that makes you high. Instead, marijuana with anti-seizure activity is high in another chemical called CBD, which doesn’t make you high but can control or eliminate seizures. Marijuana high in CBD can be taken orally as an oil. 

CBD is also great at reducing pain and helping sleep, so it’s not surprising that CBD also helps fibromyalgia, ME and Lyme patients.  Several ME patients have reported that marijuana helps diminish nerve, muscle and joint pain and improves sleep. Shouldn’t fibro, Lyme and ME patients, and other patient with other diseases have the right to medical marijuana as well, Governor Corbett?

The good news is he probably won’t be governor for long. Democratic candidate Tom Wolf, still leading in the polls, supports medical marijuana.  In a recent debate with Corbett, Wolf said:  “We need to legalize medical marijuana immediately. We need to work quickly on that. We need to decriminalize small amounts of marijuana. We put too many people in prison. We break up families and destroy too many lives.”

Amen to that. 


Tuesday, August 26, 2014

Autism Study Redux

In a TV interview, Dr. Brian Hooker explains other problematic autism findings CDC tried to bury, according to CDC whistleblower Dr. William Thompson, and that includes thimerosal, at about 13:38.  He also mentions class-action suits.

What Lies Beneath

Age of Autism’s Dan Olmstead and Kent Heckenlively, among others, have been covering the developing story of a CDC autism study whose findings were allegedly altered. They reported that Dr. William W. Thompsonone of the authors of the 2004 CDC study that found no link between how early the MMR shot was administered and the development of autismdisclosed that he and others buried evidence about that study. In fact, according to a new study just published by Dr. Brian Hooker that was based on a reanalysis of the original data of the 2004 study, giving the MMR shot before 36 months increased the rate of autism in African American boys by a whopping 340 percent.

Provided the findings of Hooker’s study are correct, who at CDC and elsewhere in the government knew the authentic autism statistics in that study? Did the researcher or researchers act on their own, or were they ordered to change the findings? Were findings in other autism studies altered? Did Dr. Julie Gerberding, the head of CDC at the time (who now serves as the president of Merck’s vaccine division) know about the alleged tampering with the statistical analysis? Have any of the scientists who participated in the alleged tampering perjured themselves before Congress?

The story has yet to break on major networks and newspapers. CNN weighed in for about a minute, summoning, Dan Olmsted wrote, attorney Dorit Reiss to comment that even if the claims about the CDC study were correct, “which is doubtful, it would show that for most of the population MMR does not cause autism.” In what universe is that reassuring? Not surprisingly, CNN quickly yanked the clip from its lineup.

Add to the mix Congressman Bill Posey’s (R/Florida) disgust with what he calls CDC’s “incestuous” relationship with the vaccine makers. Will he help get to the bottom of this?

There’s a video hosted by Dr. Andrew Wakefield about the 2004 study and a petition to retract the study; click here to see both.


Monday, July 7, 2014

Is CDC Out to Bury PEM?

CDC's head of CFS research Dr. Beth Unger said at last month's Chronic Fatigue Syndrome Advisory Committee meeting that she couldn't figure out how to measure post-exertional malaise (PEM)--the hallmark of ME--and thus believes problems would ensue if PEM is a mandatory symptom. 

"My concern about making post-exertional malaise an absolute criteria for diagnosis is if you don't have a consistent, validated way of measuring it that clinicians can use easily, it's big barrier," Unger explained at the meeting. A few minutes later, when committee member Donna Pearson asked again about PEM being included in the criteria, Unger replied, "I think everybody agrees that it's very characteristic and a very important symptom, and clinicians will tell you that they can recognize it, they can elicit this information from patients, but to make that quantifiable and to make it easily implementable is another question...."

What? Several researchers have shown how to measure PEM.  Cardiac pulmonary testing used by Dr. Chris Snell is one way, gene expression testing devised by Drs. Alan and Kathleen Light is another, comprehensive patient history is yet another, and using a pedometer like the Fitbit would also work. Dr. Jose Montoya conducted VO2 max studies with patients on the antiviral Valcyte to determine if their exercise tolerance improved on the antiviral. Unger's familiar with all of this. In fact, Unger is one of the authors of a 2012 paper, "Minimum data elements for research reports on CFS," in which the authors discuss how to measure PEM:  


"As post-exertional malaise is a key symptom of all CFS case definitions, it would be appropriate to measure the extent of activity and how such activity might result in symptoms of fatigue and malaise. Light et al. (2009) found patients with CFS demonstrated increases after exercise that reliably exceeded responses of control subjects in mRNA for genes receptors that can detect muscle produced metabolites, genes that are essential for sympathetic nervous system processes, and immune function genes. The researchers concluded that CFS patients might have enhanced sensory signal for fatigue that is increased after exercise. Activity, or in work performed is generally quantified in terms of energy used, i.e., caloric expenditure. Because this is difficult to measure during activity, total oxygen consumption which increases in a similar fashion, is typically used in its place. 

"Sometimes represented as METs or metabolic equivalents, oxygen consumption may be assessed directly using cardiopulmonary exercise testing with measured gas exchange (Milani et al., 2006), or estimated from heart rate or other indicators of effort such as time and/or distance travelled. Assessment of effort is critical when exercise is used as a physiological stressor to elicit symptoms in CFS patients or for assessments of functional capacity as part of clinical trials. Heart rate as a percentage of age-predicted maximum is the most recognized indicator of subject effort for both maximal and submaximal exercise protocols. However, the maximal heart rate response to exercise varies widely in the general population (Balady et al., 2010) and has been shown to be blunted in some subjects with CFS (e.g., VanNess et al., 2003) and also in fibromyalgia (Ribeiro et al., 2011). 

"As an alternative to heart rate, the peak respiratory exchange ratio (RER) is acknowledged as the most valid and reliable gauge of subject effort (Balady et al., 2010). Because it can only be obtained from ventilatory expired gas analysis, RER may not be available in all exercise studies. Similarly, submaximal exercise protocols do not provide for the measurement of peak RER. In such instances selecting alternative measures that can accurately assess effort both within and across subjects is particularly important."

In addition, in Table 2 in the paper, the authors cite actigraphy and pedometers for activity assessments. 


Thus, Unger knows how to measure PEM. So why is CDC trying to bury PEM? After all, PEM is the most important symptom of the disease--and PEM distinguishes ME patients from people diagnosed with CFS who in reality are just depressed. But maybe that's the point. To lump bona fide ME patients in with the depressed.  That way you don't get meaningful data or treatment, and the band plays on. Every time I think CDC can't get more devious, the agency surprises me. First, Unger nixed a two-day exercise test in favor of a one-day test, even though Dr. Chris Snell has shown PEM isn't apparent until the second day of testing. And now Unger can't figure how to measure PEM. If Unger is hung up a "consistent, validated way" of measuring PEM, she only has herself to blame for not having done a two-day exercise test after all these years. Leaving off PEM in the definition is like omitting elevated blood sugar in diabetes or a depressed CD4 count in AIDS. It's insanity.