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Considering the normal function of adipose tissue in sequestering 'persistent organic pollutants [POPs]', is there any evidence that the existence of such POPs within fat cells interferes with the function of leptin; more particularly in the normal suppression of appetite in the hypothalamus. Were there in fact such evidence, might it then be supposed that such derangement in leptin function might account for tendencies to obesity in populations exposed to POPs?

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  • $\begingroup$ The normal function of adipose tissue is to stare triglycerides. Please quote a source for your statement about organic pollutants (and for goodness sake don't abbreviate them as POPs). $\endgroup$ – David Apr 29 '18 at 17:54
  • $\begingroup$ It seems fairly well accepted that part of the function of AT is to store fat soluble toxins such as OPs. [e.g. Env.Health Perspectives 121(2) La Merrill]. There is a Korean study citing numerous references and discussing the relation of OPs to obesity [Obesity Reviews 18(2) Y-M Lee]. However, I could find no study which proposes an underlying mechanism according to which, presuming that the accumulation of fat serves an entirely necessary--rather than erroneous--function in all cases, dysfunction in the leptin-mediated circuit induced by OPs in AT is implicated. If so, it would explain a lot. $\endgroup$ – jeremiah May 1 '18 at 9:16
  • $\begingroup$ How do you differentiate between "function" and "they happen to accumulate there because they are fat-soluble? I thought it was the P450 system that had the function of dealing with toxic compounds, the endpoint being elimination (not sequestering). Whatever the connection between modern organic pollutants and obesity, you should remove the assertion that the normal function of adipose tissue is to sequester these compounds. $\endgroup$ – David May 1 '18 at 10:17
  • $\begingroup$ Perhaps it is more pertinent to ask to what extent fat cells discriminate between lipophilic organic compounds; the point being that because in the general case they do not, it is not unreasonable to argue--without quibbling over semantics or even raising the philosophical issue of intention--that this capacity for AT to dissolve, thus temporarily sequester organic pollutants within the process of their eventual detoxification--if this is indeed possible--, therefore protecting vital organs from the harmful action of these compounds. I will elaborate a little in answer to the question. $\endgroup$ – jeremiah May 4 '18 at 8:03
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It seems that the answer to this question is at present no--and might remain so until or unless researchers dedicated to elucidating any such relation between leptin and obesity are prepared to subject some population of poor leptin-producing creatures to given organic pollutants, with the aim of determining any measurable effect on leptin capability--a difficult assignment to say the least.

Various studies seeking to confirm the so-called 'obesogen hypothesis' have not unreasonably argued a mechanism of 'endocrine disruption' by certain common organic pollutants, but these are neither comprehensive nor capable of resolving certain paradoxes in the relation between leptin and obesity: notably that leptin levels are routinely observed to be raised in cases of severe obesity. The idea of some derangement in leptin function induced by a local cause therefore becomes attractive in explaining such 'leptin resistance'.

At the same time, it is probably negligent to blame rising levels of obesity merely upon the delinquent appetites and profligacy of affluent people, particularly when certain benefits of fat accumulation, apart from the sheer simple joy of being fed, have been observed: putatively there are diminished rates of neuro-degenerative disorders such as Alzheimer's disease in the mildly obese. (There are various studies drawing such conclusions). Possibly such effects also pertain to the capacity for adipose tissue (AT) to sequester organic pollutants.

Now the respondee to this question has objected to the characterisation of this latter effect as a 'function' of AT when it is clear that this capacity for fat cells to accommodate fat-soluble substances without the necessity for their elaborate discrimination is indeed inherently and innately part of the broader function of AT. The inference of the question itself is in fact that the proliferation of fat cells and fat mass in obese individuals may serve precisely this purpose or function.

Such an assertion requires no incursion into philosophical dispute--regarding the argument that nothing 'just happens' to be the way it is, having merely settled into place as dust from some ancient 'big bang' (according to the paradigm of 'chaotic erroneous nature' groping its way aimlessly in the eternal darkness or some such ugly intellectual nihilism)--nor great excesses of the imagination--that we are creatures not only essentially organic but increasingly immersed in the products of oil and other hydrocarbons themselves loosed from the ancient abeyance of that essential nature--, only the understanding that part of the actual mundane function of fat stores is to hold in continuing abeyance those organic compounds, in particular those which are broadly derivatives of hydrocarbons, which the organism generally is unable to accommodate elsewhere in its metabolism: as if effectively indigestible food for example.

The aim of any such inquiry into the relation between organic pollutants and obesity--possibly mediated by a derangement in leptin function--is not of itself to redress any such local cause determined empirically; since realistically such would come only with the inevitable obsolescence of oil and the derivatives of hydrocarbons generally: petroleum, plastics, organic pollutants etc. The aim is to elucidate the nature of this phenomenon of modern obesity, that at least it might be understood as part of universal necessity, that indeed it must in principle serve some eventual 'evolutionary advantage', not of a family of reproducing organisms--although this is an aspect of it--, but of the universal entirety itself in eternity: of the 'Soul' if you will.

I might add here that there has developed an obsession in the biological sciences with a theory of evolution based not only on the philosophically repugnant idea of 'chance'--which despite the fervour with which such a paradigm is defended cannot of course be quantified in any meaningful way: this of itself requires that the entire notion be removed from orthodox thinking--, but on the necessity to impute to some detail of formal reality an 'evolutionary advantage' conferred by it upon some limited context of which it is merely an aspect; when the ultimate parameters of such advantage are essentially unknowable.

This is not to dispute the absolute preeminence of an 'evolutionary principle' within universal reality; only to argue that this principle is entirely singular and simply inherent within the fact of existence itself; and most importantly that the ultimate parameters of such a principle can never be objectively discriminated or 'known' by those such as we mere humans entirely within and comprised of the unitary fabric of an inviolate universal unity in eternity imbued necessarily with a unitary cause, process and intention. And for those who would object that such 'a priori' postulate is improperly metaphysical in character, it would be well for them to remember that the existing scientific and cultural ethos of blind aimless nature, and the preeminence of 'happenstance' as its primary impetus, the denial of universal purpose for want of the capacity to discern it, is only the expression of a passing alternative school of philosophy.

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