Hormesis and its relationship with homeopathy.
(i.e., terminology, relationship to homeopathy, objective criteria to assess hormesis of the hormesis data base for pesticides and how their dose response. INTRODUCTION: Hormesis is a dose-response relationship characterized by a biphasic dose response to stressors with a low dose stimulation and a high dose . Hormesis is a description of a particular type of dose-response relationship. .. Fred vom Saal: The problem with homeopathy is you're talking about doses.
Described by Professor Charles L. The results suggest that prolonged low dose-rate radiation exposure appeared to increase risks of developing certain cancers in specific subgroups of this population in Taiwan. Breast cancer exhibited a marginally significant dose response HR mGy 1.
The results further strengthen the association between protracted low-dose radiation and cancer risks, especially for breast cancers and leukemia, in this unique cohort population. Thick lead shielding around a chemical dose experiment to rule out the effects of ionizing radiation is built and rigorously controlled for in the laboratory, and certainly not the field.
Likewise the same applies for ionizing radiation studies. Ionizing radiation is released when an unstable particle releases radiation, creating two new substances and energy in the form of an electromagnetic wave. The resulting materials are then free to interact with any environmental elements, and the energy released can also be used as a catalyst in further ionizing radiation interactions.
For example cell death is seen as a 'bad' effect but if it removes a potentially carcinogenic cell from the population of cells in a tissue it could prevent cancer starting and could be seen as 'good'. At least one peer-reviewed article accepts the idea, claiming that over substances show a U-shaped dose-response relationship.
Update on hormesis and its relation to homeopathy.
Calaberese and Baldwin wrote: This theory is called radiation hormesis. For policy making purposes, the commonly accepted model of dose response in radiobiology is the linear no-threshold model LNTwhich assumes a strictly linear dependence between the risk of radiation-induced adverse health effects and radiation dose.
A report commissioned by the French National Academy concluded that there is sufficient evidence for hormesis occurring at low doses and that LNT should be reconsidered as the methodology used to estimate risks from low level sources of radiation, like deep geological repositories for nuclear waste. In the linear model, the assumption is that there is no dosage that has no risk of causing cancer.
Past and present barriers to mainstream acceptance of hormesis Despite its relevance, applicability, and overall legitimacy as a biological phenomenon, hormesis has been plagued with systemic obstacles preventing its widespread acceptance. Chiefly, hormesis as a concept is counterintuitive and could easily be judged as misleading propaganda commissioned by big business to influence public opinion, much like the prosmoking advertisements in the mid th century American culture.
Second, the agenda of the toxicological community are largely driven by the desires of regulatory agencies, which have always been almost exclusively concerned with risk assessment.
As such, there is little monetary or professional incentive to stray from the mainstream fields of research to something more theoretical. Third, hormesis is logistically difficult to investigate; to adequately evaluate hormesis for a compound, studies must be specifically and methodically designed, including a large number of doses in a large number of trials, and include a temporal component. In a review of over 20, toxicology articles spanning from the mids to early s, only 1.
However, of those 1.
Hormesis - Wikipedia
Despite its validity, this work came at a time of heated division between homeopathy and modern medicine, and by associating hormesis with homeopathic literature, Schulz and his ideas were rejected by the medical community. Thus, it is imperative that historical paradigms on the topic be cast aside if an honest evaluation of hormesis is to be conducted.
Hormesis mechanism Current mechanistic studies on hormesis lack depth, and it seems that no single mechanism can be credited for the phenomenon. However, the mechanistic investigations that have been conducted usually produce encouraging results. Proposed mechanisms all center on the idea of homeostatic overcompensation; following homeostasis-disturbing low-dose exposure to toxins, the body has a tendency to overcompensate in its attempt to return to homeostatic set points, thereby strengthening normal homeostatic functions in preparation for further toxin exposure.
This overcompensation has been proposed as the cause of the hormetic phenomenon, and Townsend and Calabrese  have both independently cited many instances to support the excessive compensation hypothesis.
Under the umbrella of the overcompensation hypothesis, several theoretical explanations of hormesis have been put forth, including the receptor mechanism, DNA damage repair, the oxidative stress mechanism, immune function enhancement, and alteration of gene expression.
Receptor subtypes of varying affinities and effects The leading hypothesis regarding the mechanism of hormesis asserts that the observed phenomenon is due to the same agonist interacting with different receptor subtypes, each with different ligand affinities and effects.
It is plausible that higher affinity receptor subtypes stimulate one change in metabolism while lower affinity subtypes stimulate an opposite change; at low ligand concentrations, only the high affinity stimulatory receptors would be occupied, while at higher concentrations, the lower affinity inhibitory receptors would be filled as well.
This hypothesis has been confirmed experimentally; Gao et al. At low doses, the estrogen receptor played a major role in promoting lymphocyte proliferation, while at higher doses, acute toxicity mechanisms seemed to be activated that inhibit lymphocyte proliferation. In addition, a study found that steroidogenesis is stimulated in Leydig cells by low-dose administration of histamine while inhibited by higher doses.
In line with the two-receptor hypothesis, the opposing effects were mediated by subtypes of the same receptor; low-dose administration only allowed for ligand interaction with the stimulatory HRH2 receptor while high-dose administration allowed for ligand interaction with the inhibitory HRH1 receptor. A recent investigation from Zhang et al.
However, this investigation did not to investigate the role of other receptors in the observed phenomenon, which does not rule out the possibility that the two-receptor mechanism may be responsible for the given results. DNA generation DNA damage is a significant mechanism by which toxic substance damage organisms, but it seems that a reversal of this effect may be one of the mechanisms underlying hormesis.
Von Zglinicki et al. In addition, mercury is able to stimulate synthesis of metallothionein, which can clear toxic metals from the body, thereby protecting cells from free radical damage generated by normal metabolism. Under normal circumstances, the generation and removal of ROS in the body are tightly regulated, which allow them to serve beneficial roles while avoiding their deleterious effects.
However, if ROS cannot be removed quickly, they will accumulate, which can be damaging to the body. Thus, moderate levels of ROS seem to exert a stimulatory effect on the body. However, it is well-known that high levels of ROS stimulate apoptosis or necrosis in all cells. Thus, it seems that hormetic effects can be mediated by mechanisms other than the two-receptor hypothesis.
Enhancement of immune function Arinaga et al. Moreover, animal experimental data show that low-dose stimulation may enhance the body's immune function by: There are some very serious toxins that have tremendous public health impact that industries involved with their production like to see these reports, and promote them. I just want to point out the incredible double standard at work, in terms of new science around non-linear dose-response functions for carcinogens, and new science regarding a U-shaped dose-response function for non-carcinogens.
Namely, that carcinogens previously assumed to have a linear dose response function, in fact, act more like a threshold carcinogen. Thank you for that comment, David. For me, hormesis is probably the lowest dose you can be exposed to. Is that truly called hormesis? Is that what is being considered hormesis, now? What is hormetic is the shape of the curve. At the other end, you have a response in a positive direction, but it dips in the middle -- or vice-versa.
The curve can be an upside-down U. But the idea is that at some point, the curve is convex or concave. The question in your case of alcohol is that a person -- an individual -- controls their intake of alcohol.
So there is a difference, of course. We know nutrients operate on sort of a U-shaped dose-response.Top Homeopathic medicines for cure of HYPERPIGMENTATION
So, there is an issue. But the question is could you use it as a generic phenomenon in chemicals risk-assessment for environmental occupational purposes? We have examples that involve toxins, whether by choice or not by choice. Alcohol is by choice. Ozone and carbon monoxide are not by choice. We have to see those as toxins that affect huge parts of the population that behave in this way.
We have to take them case-by-case. I also think this is not trivial from an epidemiologic perspective -- but for a different reason than what has been mentioned, before.
That is, I think it just really adds to our emerging understanding of the complexity of the exposure, and the complexity of effects. I think as many of the people on the call know -- one of the biggest problems with epidemiologic studies of environmental exposure is a difficulty in measuring the exposure and not completely knowing what effect to look for. I think that actually is important from an epidemiologic point of view. So is the hormetic effect alleged to occur above or below those thresholds?
Another way to look at this is whether it has any implications beyond cancer risk-assessment? I have some data that I could use to answer that question. The presumed no-effect dose for bisphenol-A is 5 mg per kg body weight. And the no-effect or presumed reference dose used by the EPA is now 50 micrograms per kg.
The lowest dose of bisphenol-A so far to cause a really dramatic change in cell function is centigrams, or essentially 0. So you are down at a level that 20 years ago, people would have locked you up for suggesting could possibly cause an effect of what is being described as an extremely weak estrogenic chemical.
I just wanted to say that the nuclear industry has been putting out a lot of information on hormesis lately. Fred made a comment himself about tests being done based on adults. My understanding was that most tests on chemicals and other things are done on a lb male.
Well, they assume the lb man.
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- The Debate Over Low Doses: Hormesis & Human Health
This actually follows on what Marsha Marks just mentioned. Scientists at ATSDR were incorporating arguments into the reports -- the investigation that they had done for the agency, as to the health effects.
So this actually has been a problem on the radiation side of things. Yet again, federal scientists are beginning to bring these arguments in. I wonder if anybody has any comments, among the presenters, on hormesis, but on the radiation side.
So there actually is some literature now, responding to this concern. Anybody want to support the idea that perhaps in the nuclear area, hormesis is real and could have a positive benefit? Anybody want to make the nuclear industry argument in an authentic way? You have to weigh the risk and the benefit.
But there is always a risk. So it is an argument that radiation professionals use. I have a comment about definitions. The one thing that I noticed was that there seemed to be some inconsistency in how hormesis was being defined, just within our discussion.
Hormesis and its relationship with homeopathy.
So I think it is really important for this debate that we know exactly what we mean, by the word. This is actually a good point that Linda Birnbaum, who is a toxicologist at the EPA brought up on a call that Environmental Media Services put together, that I think Pete was involved in.
We should be talking about low-dose effects of chemicals, or low-dose beneficial effects.
Maybe Ed Calbrese should be arguing -- not hormesis. We need to be careful with the definition and maybe just throw it out, but respond to the fact that hormesis is generally being considered out there -- beneficial effects of low doses.
The problem is that hormesis, in that respect, is thought of as the response of a particular set of cells or a tissue or something within an organism. Calabrese also applies this concept to population data.
Then, he goes on to apply some kind of similar mechanism to events going on like survivorship curves -- as well as events going on within a specific cell. So there is an inherent problem with trying to figure out just what the heck hormesis is. But at an organism where you probably have a superimposition of various dose-response curves that represent various mechanisms.
So at relatively different doses, you see the emergence of different toxic or salutary effects -- depending on where you are in the aggregation of those dose-response curves. I want to interject a question for you, Fred.
This is outside the realm of normal science. I ask not to introduce homeopathy into CHE discourse, because it is not a scientific discipline, and should be separated out.
But it is a tradition of clinical medicine with deep roots in Europe and widely practiced in Europe.