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mune responses and tolerance, and play a role in determining bacterial composition.33


Their


inappropriate activation and their expression mediated by IL-1β and IL-18 leads to altered innate immune receptor hyper- responsiveness and may con- tribute to immune-mediated inflammatory diseases as well as fatigue via inflammasomes that induce dysbiosis.34


Thus it’s likely that mitochon- drial damage creates fatigue not only directly by impairing mi- tochondrial function, but also indirectly through pro-inflam- matory promotion of cytokines and inflammasomes, the conse- quences of which include local inflammation, loss of mucosal barrier integrity, dysbiosis and fatigue.35, 36


A cautiously opti-


mistic idea is now taking hold that invokes using mitochon- drial-induced symbiosis of the gut microbiota to track, target and treat a plethora of diseases, even ones beyond the confines of the gastrointestinal tract.37


This sequence of events places mitochondria at the cross roads of bioenergetics, cell death sig- naling, microbial ecology and the innate and adaptive im- mune system, and associated inflammation.


Inflammation is, of course, an essential immune response that enables survival during infection or injury and main- tains tissue homeostasis under


a variety of noxious conditions. Inflammation comes at the cost of a transient decline in local tissue function, which in turn contributes to the pathogenesis of diseases and loss of function related to altered homeostasis. Inflammation, at least at the molecular level, has been de- scribed as the ‘common soil’ of altered health and function.38


Lipid Replacement: An Ideal Approach?


Pro-inflammatory cytokines are capable of inducing many if not all the cardinal symp- toms of CFS in humans.39, 40 The use of LRT® is attractive, since it can restore mitochon- drial membranes and the gut milieu, including its delicate lining at the same time. The resolution of inflammasome- induced dysbiosis makes a considerable contribution to- wards improving mitochon- drial fitness; just as mitochon- drial fitness contributes to the management of healthy, gut- mediated immune reactivity and associated symbiosis.


The results of using LRT® and the subsequent recovery from fatigue provided by LRT® are


consistent and profound.25, 26, 27, 28, 30


This health altering intersection of immunity, inflammasome activation, oxidative stress and dysbiosis, can be found in the membranes of the mitochon- dria residing in our cells - not


only of the gastrointestinal tract but all other tissues as well.


The clinical use of LRT® has the potential to decrease the adverse effects of aging on mi- tochondria and improve mi- tochondrial function in vari- ous chronic diseases, diminish fatigue and improve altered states of mucosal immuni- ty and associated microbial ecology through the partici- patory resolution of inflam- masome-mediated dysbiosis. The improvement in terms of restitution of mucosal and im- munological tolerance has po- tential health benefits that ex- tend systemically.41


In summary, LRT® is not just the dietary substitution of lip- ids with proposed health bene- fits; it is the actual replacement of damaged cellular lipids with undamaged lipids to ensure proper structure and function of cellular structures, mainly cellular and organelle mem- branes that contribute to im- portant functional support of good health.25,30


References:


1. Lewis G, Wessely S: The epidemiology of fatigue: more questions than answers. J Ep- idemiol Community Health 1992; 46(2):92- 97.


2. Cloninger CR. A systematic method for clinical description and classification of personality variants. A proposal. Arch Gen Psychiatry. 1987;44(6):573-588.


3. Nelson E, Kirk J, McHugo G, Douglass R, Ohler J, Wasson J, Zubkoff M. Chief com- plaint fatigue: a longitudinal study from the patient's perspective. Fam Pract Res J. 1987;6(4):175-188.


4. Nijrolder I, van der Windt DA, van der


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