ALS Part 2: The “roll” of body fat, serum lipids, and environmental toxins (organic solvents, for example) as viewed through a health model lens
by H.L. Sam Queen
While our modern human culture associates health with being physically fit, shapely, and having low % body fat, a recent case-controlled interview of people with ALS showed that the majority of those at disease onset were likewise in step with the norm, not fat and somewhat physically active. 1 In a second, somewhat related study, ALS researchers found that a higher BMI, not the lower one preferred by our culture, was the most reliable of several independent predictors of a longer survival time. 2 Toxic, environmental exposure could very well explain the contradiction, but to gain a good grasp of that reality requires a review of our body makeup and how the body responds to protect itself from such exposure.
The healthy human brain and nerves is comprised of more than 60% fat. Couple this with the reality that most environmental toxins are fat soluble (and that every person on earth is today carrying some mixture of these toxins) and you begin to see why surviving in such a toxic environment depends upon our body learning to identify and respond to each category of the many toxic intruders. Included in the body’s protective response is a strategy not only for capturing, transporting, storing, and detoxing a single type of toxin, but also multiple types of toxins.
When viewing the intentional handling of toxins from the human health model perspective what immediately becomes apparent is the highest priority assigned to protecting the brain and nerves, even at the expense of the heart. In viewing the chemistry in this manner you begin seeing an intentional dance taking place among chemistry parameters, which is where the practice of health and medicine begin to diverge. In response to organic solvent exposure, for instance, the health model-trained practitioner will see a protective rise in serum triglyceride, requiring a need to confirm organic solvent exposure, followed by detoxification support (where appropriate); Whereas, the disease model-trained practitioner will traditionally see dyslipidemia, requiring treatment to prevent thrombosis and other downstream events that this might foretell. Both approaches have proven useful, and the two certainly can be combined. Yet, training is needed to do so, which is intended to start here. NOTE: Throughout the remainder of this discussion, organic solvents will be the focus of discussion. Pesticides, Herbicides, heavy metals, latex, and other petrochemicals will be covered later. 3
Medicine is well acquainted with the effects of industrial solvent poisoning, which readily crosses the blood/barrier to cause a wide range of brain and neurological effects, ranging from migraine headaches to encephalopathy, gastroparesis, and a mix of nerve related dysfunction. Where ALS is concerned, there are two downstream events of interest. The first of these has to do with people who fail to get a triglyceride response to their exposure. These people tend to experience the greatest toxicity from their exposure, requiring a high fat diet just to mobilize and keep the toxin away from the affected nerves. The second downstream event is the effect of chronic, low level exposure on the liver’s ability to synthesize correctly the iron-binding protein, transferrin. Each transferrin protein has two pH-controlled sites for binding onto iron, and solvent exposure tends to cause the binding sites to be made incorrectly, resulting in free, unbound iron. The finding of free iron in the person with neuropathy of any kind, and who has a low reading for serum triglyceride helps to complete an organic solvent exposure profile in someone who is not a triglyceride responder.
Free iron and iron overload (has been noted in the serum of people with many diseases, ranging from diabetes to stroke, and is well known to be toxic to the blood brain barrier and choroid plexus (where spinal fluid is made).4 One of the key notations made in the cerebral spinal fluid (CSF) of people experiencing ALS onset has been the appearance of free, unbound iron, which is highly toxic to the glial cells that are known to play a central role in motor neurons degeneration in ALS.5 Too, a study of cell cultures showed that neurons that overexpress the SOD1 mutant (G93A) had a much higher iron level compared to controls,6 likely due to free radicals stimulated by the unbound iron. Finally, 7 in a recent study out of France, it was concluded by the researchers reporting on the French Cohort of people with ALS that “perturbations of iron metabolism found in this study may be suggestive of a new pathophysiological pathway for ALS”. And, while free, unbound iron may be arrived at by a variety of mechanisms, one of the more commonly-occurring means is through chronic, low level exposure to organic solvents, but which has largely gone unrecognized due to failure to see the tell-tale expressions of chemistry through the human health model lens.
Click here to read Part 1: ALS: the Search for an Underlying Cause, by H.L. Sam Queen
1 Gallo, V., et al., “Prediagnostic body fat and risk of death from amyotrophic lateral sclerosis”, Neurology 80(9): 829-838, February 26, 2013.
2 Paganoni, S, et al., “Body mass index, not dyslipidemia, is an independent predictor of survival in amyotrophic lateral sclerosis”, Muscle Nerve 44(1): 20-24, July 2011.
3 In response to an organophosphate pesticide or herbicide (which account for 50% of the pesticides in use today) the body will protectively raise the HDL “good cholesterol”, due to stimulation of PON1 enzyme. In response to heavy metals the body may raise the total serum cholesterol and LDL as part of a larger chemistry response…what I refer to as “The Toxic Footprints of Chemistry”
4 Shetty, J K., Prakash, M., and Ibrahim, M., “Relationship between free iron and glycated hemoglobin in uncontrolled type 2 diabetes patients associated with complications”, Indian j Clin Biochem 23(1): 67-70, January 2008.
5 Shaw, P.J., “Molecular and cellular pathways of neurodegeneration in motor neuron disease”, J Neurol, Neurosurg, and Pscychiatry 76(8): 1046-1057, 2005.
6 Hadzhieva, M., Kirches, E., and Wilisch-Neumann, A., “Dysregulation of iron protein expression in the G93A model of amyotrophic lateral sclerosis”,
Neuroscience 230: 94-101, 2013
7 Veyrat-Durebex, Charlotte, et al., “Iron Metabolism Disturbance in a French Cohort of ALS Patients”, BioMed Research International, Volume 2014 (2014).
Iron Metabolism Disturbance in a French Cohort of ALS Patients