Chronic Fatigue Syndrome is not Psychosomatic, Probably Epigenetic

in #health3 years ago

Molecular biologist Warren Tate, Otago University Emeritus Professor, has recently published two papers that shed some light on the condition known as Myalgic Encephalamyelitis (ME), also known as Chronic Fatigue Syndrome (the preferred term is now ME/CFS).

His daughter developed ME at the age of 14 and, as in so many so-called auto-immune or psychosomatic conditions, when professor Tate did a search of the medical literature he found precious little in the way of solid information.

There are other conditions where the collective signal from the medical cartels seems to be, "We don't know and we don't care!" So, if you suffer from such a condition, then I will show you how to find out as much as you can so that you can either heal yourself or have a solid foundation to request further medical investigations. OK, let's move on.

A SWATH-MS analysis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome peripheral blood mononuclear cell proteomes reveals mitochondrial dysfunction.

Of particular relevance to the core symptoms of fatigue and post-exertional malaise experienced in ME/CFS, a proportion of the identified proteins in the ME/CFS groups were involved in mitochondrial function, oxidative phosphorylation, electron transport chain complexes, and redox regulation. A significant number were also involved in previously implicated disturbances in ME/CFS, such as the immune inflammatory response, DNA methylation, apoptosis and proteasome activation.

Sounds to me like a reaction to "medication". Always, always, think back to when your own symptoms started and recall any medications taken within, say, 3 months previously.

The Conclusions in the Abstract go on to say:

The results from this study support a model of deficient ATP production in ME/CFS, compensated for by upregulation of immediate pathways upstream of Complex V [ATP synthase] that would suggest an elevation of oxidative stress.

Further on:

Flu-like and respiratory symptoms are common, and for a large subset of sufferers, the onset of the illness is sudden and is preceded by an acute viral-like infectious period.

No mention of the "medication" taken during such an illness. Never blame the drugs. This is a guided tour of a devastating landscape of chronic illnesses. This will take many articles to pick through the rubble.

As always, medical researchers are taught to look for a "pathogen" - even an invented one - rather than look at the most obvious and causal trigger. The word "pathogen" means a "creator of disease", combining the Greek pathos amd genesis; indeed "pathos" also means "suffering" or, in literature and rhetoric, the more general meaning of "eliciting emotions". Note that in the Wikipedia entry for Pathogen the causative agent is always some organism - other causes such as toxins (like drugs) are not included. This means that the "hunt for a pathogen" is invariably a search for some nefarious organism - while the real culprit is often left unmolested.

Don't get me wrong, this is nothing against Warren Tate, as his research is interesting, else I wouldn't bother writing about it, but is an observation on the intellectual culture of medicine whereby research is hemmed in by very real ideological boxes. I shall go into more details in another post as medspeak is an interesting mixture of precision and obfuscation.

Tate's observations about DNA methylation lead into his second paper: Changes in DNA methylation profiles of myalgic encephalomyelitis/chronic fatigue syndrome patients reflect systemic dysfunctions.

Major differences were identified in the DNA methylation patterns of ME/CFS patients that clearly distinguished them from the healthy controls. [...] Within the enriched functional immune, metabolic and neurological pathways, a number of enriched neurotransmitter and neuropeptide reactome pathways highlighted a disturbed neurological pathophysiology within the patient group.

So, what is DNA methylation? The article says:

DNA methylation is the best understood epigenetic modification where the addition of a methyl group to the cytosine base of DNA is associated with changes in gene expression without altering the genomic code itself. This biological interface between an individual’s environment and the regulation of their genome can provide insights into an individual’s disease activity.

Read that last sentence again... slowly. Your environment can regulate your gene expression!

Your environment includes everything that interacts with your body - air, food, drugs, water - including those molecules that can effect an epigenetic change. Such changes do not affect your DNA directly but they can switch some genes on and off. Think of a computer code where you can "comment out" certain lines so that they are still within the code but they are not processed - that's an epi(genetic)code change. Such genes are the instruction-sets to create certain proteins, so that switching them on when they should be off, or switching them off when they should be on, can create a wealth of problems, from mild to catastrophic, depending on the gene.

You may now be wondering what DNA methylation and epigenetics have to do with prescribed drugs? Take a look at this website: The Human Epigenetic Drug Database (HEDD).

The Human Epigenetic Drug Database (HEDD) is a comprehensive web-based database for epigenetic drugs, which focuses on the storage and integration of epigenetic drug datasets that were obtained from laboratory experiments that is essential for understanding the mechanism of action of these epigenetic drugs at a systematic level.

The site includes data on clinical trials and also novel uses for some existing drugs, which means... some existing drugs already cause epigenetic changes!

In theory:

Epigenetic enzymes ‘write’ the DNA methylation and histone code and ‘erase’ the histone code. The recognition of these changes by adaptor proteins ‘read’ the histone code. Working in concert, three classes of epigenetic proteins (‘writers’, ‘erasers’ and ‘readers’) function to determine whether genes are turned on or off, and the deregulation of these processes plays a central part in several diseases. [source]

However, if researchers will never admit that existing prescription drugs may well be causing epigenetic changes, then that "reverse step" will never be developed because it isn't even an option on the table. Remember that drugs are not considered pathogens, hence cannot be the cause of so much misery around the world.

Think again.

Coin Marketplace

STEEM 0.30
TRX 0.12
JST 0.033
BTC 63527.41
ETH 3109.34
USDT 1.00
SBD 3.86