A substance can produce the harmful effect associated with its toxic properties only if it reaches a susceptible biological system within your body in a sufficient concentration (a high enough dose). The toxic effect of a substance increases as the exposure (or dose) to the susceptible biological system increases. For all chemicals there is a dose response curve, or a range of doses that result in a graded effect between the extremes of no effect and 100% response (toxic effect). All chemical substances will exhibit a toxic effect given a large enough dose. If the dose is low enough even a highly toxic substance will cease to cause a harmful effect. The toxic potency of a chemical is thus ultimately defined by the dose (the amount) of the chemical that will produce a specific response in a specific biological system.
They Claim Every Individual Will Respond The Same
The statement "dose makes the poison" is not appropriate when taking in wide variable populations with different genetic makeups. Forcing patients to take medications that will throw them into anaphylactic shock because you are fine with the dose is not acceptable. Even Yale stated "a specific response in a specific biological system". The dose is specific to the specific biological system based on the individuals genetic makeup.
Now let us review some science...
"Certain individuals with a mild mitochondrial defect may be highly susceptible to mitochondrial specific toxins like the vaccine preservative thimerosal" (Sharpe et al., 2013). And, "These findings suggest that the epidemiological link between environmental mercury exposure and an increased risk of developing autism may be mediated through mitochondrial dysfunction and support the notion that a subset of individuals with autism may be vulnerable to environmental influences with detrimental effects on development through mitochondrial dysfunction" (Rose et al., 2014).
Here there is an identified sub-population that the dose/poison might not correlate with mito-typical peers. In one study "44% of autistic children showed higher copy numbers of all three mitochondrial genes examined. Furthermore, ND4 and Cyt B deletions were observed in 44% and 33% of autistic children, respectively. This study indicates that autism is associated with mitochondrial dysfunction in the brain" (Gu et al., 2013).
In another study the researchers looked at children's susceptibility to environmental toxicants, which correlate separately from adults stating; "Critical to their development is the need to understand mechanisms underlying children's sensitivity to environmental toxicants... putting these considerations of children's susceptibility into an overall framework for ascertaining relevancy for human risk assessment" (Faustman et al., 2000).
Further, Lawler et al among other researchers show that specifically with autism there are polymorphism (SNPs) in genes that detoxify coined 'environmental response genes' (Lawler et al., 2004). These gene alterations are believed to increase a child's risk of adverse effects to environmental toxicants (Livingston et al., 2004).
Not all children are created equal and as Yale stated specific dose is specific to the individual. This argument is used to deny accountability regarding atypical adverse events following vaccination. Just because I can eat peanuts does not mean my neighbor who is allergic can.
This post is dedicated to the pro-vaccine injury supporter Trevor Lowe.
History Of Infantile Acrodynia Or "Pink Disease"
Further, those children who were adversely affected by mercurial ointments/powders (1:500 exposed) also had a higher incidence of autism in their offspring, which leads to the growing suggestion that exposure to mercury may be a strong causal factor for an autism outcome (Shandley, K., Austin, D., 2011). This points to a genetically vulnerable population that should be pre-screened prior to exposure to thimerosal containing vaccines. These are very important factors when thinking about "the dose makes the poison" argument.
Two core patterns in this emerging research violate simplistic uses of "the dose makes the poison."
One arises because sensitivity to contamination is not the same at all stages of the life of an individual. The same low dose that may pose no risk to an adult can cause drastic effects in a developing fetus.
The second involve dose-response curves in which low levels of a contaminant actually cause greater effects than higher levels, at the same stage of development. These dose-response curves, shaped like inverted-U's, are called "non-monotonic dose-response curves."
Both of these patterns require a more sophisticated view of what it means for "the dose makes the poison" (Colborn, T., Dumanoski, D., Peterson, M., n.d.).
The Dose Makes the Poison--Or Does It?
Counterargument: It’s not that simple
The idea that “the dose makes the poison” relies on the assumption that the higher the dose of any particular chemical, the greater its toxic effect on living organisms. However, this assumption is not always correct. The more we learn about the complex ways in which organisms interact with the chemicals to which they are exposed, the more difficult it seems to be to establish understandings that can be generalized across different types of organisms and chemical substances (American Institute of Biological Sciences, 2014).