I would like to present to you a novel and truly unusual hypothesis about the origin of aging and aging-related medical phenomena, including Alzheimer's disease.
To get a first impression of the hypothesis, it is sufficient to read part 1, = 800 words.
TL;DR: An extremely weak, but extremely often activated self-reference mechanism in the memory system creates about 1 billion extremely weak memories of a special type in the course of life. Their combined, slowly increasing inhibitory effects on cellular repair mechanisms, meditated by so-called brain-body mechanisms, create the aging process and associated diseases.
PART 1: THE HYPOTHESIS
The hypothesis is based on the following 4 premises:
1 A memory trace, once formed in the neuronal networks of the brain, is never fully inactive. Rather it is permanently active to a tiny extent (let’s say around a micro-percent) compared to its activity during memory recall. The mechanisms causing this phenomenon are:
Existing memory traces are constantly slightly activated by both incoming and intrinsic neuronal activities that take place within memory systems (see e.g. Pubmed-Ids: 18319728 and 10980021).
In particular, aversive memories tend to lose small proportions of their inhibitory control over time, leading to their slight, permanent overactivity (more details below).
I call this tiny basic activity of a memory trace generated by the above mechanisms the “OVEREXPRESSION” of a memory.
2 The overexpression of an aversive memory, e.g. a pain memory, has an extremely weak, anti-homeostatic effect on body and brain.
This follows from research results of Brain-Body medicine, which investigates the influence of emotions on physical health.
The basic argument underlying this claim is that if a negative emotion has a proven anti-homeostatic effect, then the overexpressed memory of that emotion will have the same effect, only much weaker (see e.g. Pubmed-Id: 19524045; more follows also below).
3 Now the completely crazy part: The normal memory perception mechanisms that exist in all animals with nervous system, lead to the unconscious perception of the OVEREXPRESSED EMOTIONAL COMPONENTS of aversive memories …
… AND TO THE CONTINUOUS AND UNCONSCIOUS RE-MEMORIZATION of these overexpressed emotional components as part of the emotionality of the normal, ongoing autobiographical events … followed by their RE-OVEREXPRESSION, … and subsequent re-memorization … and so on … moment by moment, the whole life long.
Ok, that sounds really weird. Therefore again step by step:
Step 1: All memories of aversive events of your life are permanently a little bit active (i.e., „overexpressed“), thereby slightly shifting your state of mood towards negativity.
Step 2: This (consciously imperceptible) slightly negative state of mood is re-memorized as an aversive emotional memory along with the current autobiographical event. As this newly formed memory is also overexpressed, this step increases the number of aversive memories that are overexpressed.
Step 3: The now increased number of overexpressed aversive memories in turn increases to a tiny extent the negativity of your state of mood, which is again re-memorized as in step 2 … and so on, moment by moment, the whole life long.
In this way, the number of aversive memories that are overexpressed, and likewise their combined anti-homeostatic effect (remember point 2 above), increases constantly in an unstoppable manner. This is obviously a vicious cycle (hereafter just called “VC”). Vicious, because it induces a steadily increasing anti-homeostatic effect in the body, which may react with potentially dangerous health problems (see below).
Since a new autobiographical event is generated and memorized roughly every second (actually when a new visual scene occurs after an eye movement), overexpressed memories are re-memorized also roughly every second. The VC creates therefore during a human life about one BILLION of very, very, very slightly aversive memories – and every single one of them exerts a very, very, very slight anti-homeostatic effect on the body.
(Yes, you read that right, one BILLION, 10 ^ 9, 1000 MILLIONS of memories … no joke.)
A side note: It sounds a bit ridiculous, but the VC basically works like the mechanism „compound interest with contributions” in the financial sector. It starts as soon as the first aversive memory has been formed. Aversive memories, which are subsequently formed by negative life experiences, are "contributions". And like compound interest, the VC has enormous effects over a longer period of time.
Another side note: Since the future relevance of aversive memories can not be predicted, they remain memorized for a lifetime and never completely decay (proved in animal experiments; in humans, traumatic memories are an example for the long lifetime of aversive memories). Therefore, the VC really creates the postulated high number of aversive memories. But many of them lose a lot of their contextual information throughout life. For background information, google „silent engram“.
4 Now the last and decisive statement of the hypothesis:
THE COMBINED ANTI-HOMEOSTATIC EFFECTS OF THE VERY, VERY, VERY SLIGHT OVEREXPRESSION OF ALL THE MEMORIES FORMED BY THE VC, CREATE IN THE LONG RUN, MAINLY BY INHIBITING CELLULAR REPAIR AND REJUVENATION MECHANISMS, THE AGING PHENOTYPE AND RELATED DISEASES.
(To keep you on the hook, I'd like to reveal that a gene expression study indeed suggests that the most important brain area of human memory, the hippocampus, actually causes a cascade of physical aging in some tissue. In addition, there is a study showing that the skin of mice is AUTOMATICALLY REJUVENATED as soon as a particular pro-inflammatory molecule is blocked whose activity is driven by the VC. More below …)
PART 2: EXACT MECHANISMS AND IMPORTANT PROPERTIES OF THE VC
Short note: for the sake of brevity, instead of using the complicated phrase:
"the overexpression of the aversive memories created by the VC induce effect X …",
I will use in the following the phrase:
"the VC-memories induce effect X …",
or even more simply, "the VC induces effect X …".
HOW DOES THE VC INHIBIT REPAIR MECHANISMS?
Before I go into the exact mechanisms by which the VC inhibits repair mechanisms and thereby eventually creates the aging phenotype, let me first explain how the VC generally activates physiological mechanisms.
According to my hypothesis, as briefly explained in point 2, the VC-memories generate their anti-homeostatic effect by triggering a series of brain-body mechanisms.
As also briefly explained in point 2, the basic argument behind this assertion is that if a negative emotion has a proven negative physiological effect, then the overexpressed memory of that emotion has the same physiological effect, only weaker.
The following quotes from a fundamental review article of brain-body medicine support this argument:
First of all, the following quote briefly summarizes the data situation that motivates an independent brain-body medicine:
“… what this juxtaposition [of scientific papers] reveals is that there is a remarkable commonality of brain areas and brain mechanisms that appear again and again in these [brain-body neuroimaging] papers. This commonality, which exceeded our expectations, suggests that there is a coherent field of neurobiology that relates emotion, emotion regulation and stress on the one hand to systemic medical disorders and peripheral physiological processes on the other.” (Lane and Wager, 2009, p. 1135)
The next quote demonstrates the harmful physiological effects of negative emotions:
„the field of Brain–Body Medicine has … unequivocally demonstrated that negative emotional states such as depression and stress have deleterious effects on physical health“ (Lane and Wager, 2009, p. 1135)
The following decisive quote demonstrates the negative physiological effect of continuously active brain-body mechanisms triggered by negative emotions or permanent negative emotional states.
„Since these [brain-body] mechanisms related to [negative] emotion are in continuous operation, their integrated influences across months or years are likely to have clinically important effects on disease processes and outcome. Indeed, that is what the epidemiological evidence indicates …“ (Lane and Wager, 2009, p. 1135)
The important conclusion now is:
SINCE THE MEMORIES GENERATED BY THE VC ARE PERMANENTLY, 24/7, OVEREXPRESSED AND CONTINUOUSLY TRIGGER THE CORRESPONDING DELETERIOUS BRAIN-BODY MECHANISMS, THEY EXERT A SIGNIFICANT NEGATIVE PHYSIOLOGICAL EFFECT, SIMILAR TO THE EFFECT POSTULATED IN THE ABOVE QUOTE BY LANE AND WAGER FOR NEGATIVE-EMOTION RELATED BRAIN-BODY MECHANISMS THAT ARE IN CONTINUOUS OPERATION.
This, in turn, leads directly to the conclusion that the VC can trigger all diseases which, according to brain-body medicine, can be triggered by negative emotions: cardiovascular diseases, high blood pressure, chronic pain, etc.
(Please note here that the validity of this conclusion depends only on quantitative factors, since the phenomenon of overexpression of memories, as well as the resulting effects on brain-body mechanisms, certainly exists to some extent. The only question is whether the phenomenon of memory overexpression is strong enough to exert a significant activating influence on brain-body mechanisms.)
These were the explanations on how the VC generally triggers brain-body mechanisms. In order to substantiate that the VC produces the aging phenotype, it remains to be shown that among the brain-body mechanisms activated by aversive memories there are also those that inhibit repair mechanisms. In this case, the VC would generate the characteristics of the aging phenotype, such as accumulation of cell and tissue damage and molecular waste products, by inhibiting repair mechanisms.
The available literature on brain-body mechanisms shows that the VC achieves the postulated inhibitory effect on repair mechanisms mainly because overexpressed aversive memories activate brain-body mechanisms that deregulate the neuroimmunoendocrine system (i.e., ANS, immune, and endocrine systems).
The main result of this deregulation (examples follow below) is a tendential shift of cellular mechanism from anabolic to catabolic. This shift inhibits repair mechanisms, including stem cell activity necessary for tissue regeneration.
The main conclusion of my hypothesis is therefore that the inhibitory effect of the VC on repair mechanisms, acting over decades, eventually leads to the accumulation of molecular waste products and cell and tissue damage, thereby allowing the onset of the aging phenotype. This means that the VC is not directly but causally responsible for the aging process.
As an example, I would like to describe here one brain-body mechanism that is triggered by aversive memories and actually gives the VC an inhibitory effect on repair mechanisms.
According to brain-body medicine aversive experiences trigger the release of stress hormones:
—> It follows that overexpressed memories of aversive experiences lead in the same way to the release of stress hormones.
—> This also applies to the aversive memories generated by the VC.
—> Since VC-memories are continuously overexpressed, this means that the VC triggers a continuous release of stress hormones. (And, indeed, the level of stress hormones in the blood increases steadily as you get older.)
—> Since stress hormones have a catabolic effect (see e.g., PMID 6365973, or Wikipedia on „Catabolism“), it follows that the VC has a permanent catabolic effect and therefore permanently inhibits cellular repair mechanisms. Q.E.D.
Since the results of brain-body medicine are very extensive and include a variety of brain-body mechanisms, further mechanisms that give the VC inhibitory effects on repair mechanisms can easily be derived. An example of how the VC inhibits repair mechanisms by means of the autonomous nervous system follows below.
To better understand the central importance, scope, and detail of brain-body medicine, I strongly recommend reading the abstracts and introductions to the following review articles:
The new field of Brain-Body Medicine: what have we learned and where are we headed? Lane and Wager, 2009; PMID 19524045; https://canlabweb.colorado.edu/files/Lane_2009_Neuroimage.pdf
Brain-Body Pathways Linking Psychological Stress and Physical Health. Gianaros PJ, et al., 2015; PMID 26279608; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4535428/
The rebirth of neuroscience in psychosomatic medicine, Part I: historical context, methods, and relevant basic science., Lane RD, et al., 2009; PMID 19196808; https://www.researchgate.net/profile/Douglas_Drossman/publication/23983171_The_Rebirth_of_Neuroscience_in_Psychosomatic_Medicine_Part_I_Historical_Context_Methods_and_Relevant_Basic_Science/links/59f5dcc3458515547c230606/The-Rebirth-of-Neuroscience-in-Psychosomatic-Medicine-Part-I-Historical-Context-Methods-and-Relevant-Basic-Science.pdf?origin=publication_detail
The rebirth of neuroscience in psychosomatic medicine, Part II: clinical applications and implications for research., Lane RD, et al., 2009; PMID 19196806; https://www.researchgate.net/profile/Margaret_Chesney/publication/23983169_The_Rebirth_of_Neuroscience_in_Psychosomatic_Medicine_Part_II_Clinical_Applications_and_Implications_for_Research/links/5a4d0b53a6fdcc3e99d14ccc/The-Rebirth-of-Neuroscience-in-Psychosomatic-Medicine-Part-II-Clinical-Applications-and-Implications-for-Research.pdf?origin=publication_detail
What are the „unique selling points“ of the VC hypothesis?
None of the approximately 300 aging theories can explain all aspects of the aging process. The main problem of many of these theories is the lack of a clear cause-effect relationship between the aging process and its postulated origin. For example, in the free radical aging theory it is by no means clear whether the formation of free radicals leads to the aging process or is an effect of it. The same applies to all damage theories of aging (DNA damage theory, AGEs theory, protein damage theory, etc.).
In the VC hypothesis, however, the cause-effect relationship is unambiguous. The causality chain leading to the aging process begins with the formation of aversive memories and ends at the molecular endpoints of the brain-body mechanisms triggered by aversive memories.
The reason this mechanism has so far been overlooked is that among the multitude of molecular changes (ROS, AGEs, DNA damage, etc.) triggered by VC in the body, there is no unambiguous evidence that clearly points to the memory system as the origin of all these changes. The causality chains leading to these changes are simply too long, too diverse and too spatially separated to be recognized solely by the molecular changes at the endpoints of the causality chains.
Another important unique selling point of the VC hypothesis is its ability to explain, as the only one among the aging theories, certain experimental interventions leading to automatic tissue rejuvenation. This point is discussed in more detail below.
CONSEQUENCES OF AN AMPLIFIED VICIOUS CYCLE
Part 1 of this text described the VC, how it is running in its normal velocity in all animals with nervous system.
In this „normal“ velocity, the VC has after my hypothesis already a strong deleterious effect and causes or promotes in humans, mainly through its pro-inflammatory action, all the major aging-related diseases: cancer, type 2 diabetes, cardiovascular disease, etc.
This is already bad news. But unfortunately, since the VC has several intrinsic positive feedback loops, various influences are able to shift the VC into an amplified state, where it has an even stronger disease inducing effect.
In this amplified state, it creates significantly stronger aversive memories, ranging in number from dozens to hundreds of millions, depending on when in life the amplifying event took place.
The consequences of an amplified VC are disastrous in several ways:
All aging-related diseases may occur up to decades earlier.
Existing health problems of any kind, occurring at any age, are amplified by the significant anti-homeostatic effect of an amplified VC.
A whole range of new health problems specific to an amplified VC may occur (see the second part of the Introduction page on my website).
The major initiating events that lead to an amplified VC are:
The formation of traumatic memories. Its overexpression and re-memorization significantly increases the strength of memories created by the VC, and, consequently, their anti-homeostatic effects.
The induction of a chronic, subclinical brain inflammation due to various factors, like strong infections, concussion, toxic events, etc. This amplifies the VC in two, quite astonishing, ways:
A) The cytokines released during a brain inflammation induce a subclinical „sickness behavior” (see google), which entails a slightly aversive state of mood. This reinforces the VC, since from now on the memories generated by the VC are slightly more aversive.
B) Brain inflammation indirectly disinhibits aversive memories by increasing the cell-death rate among a special type of very stress-sensitive neurons that control aversive memories (the so-called „PV+ interneurons“, see more on my website, or google “Interneuron Energy Hypothesis” and PMID 24256726). This leads to an increased overexpression of the affected aversive memories, which in turn reinforces the VC.
The process B is, in my hypothesis, also to a certain extent induced by normal brain aging, and therefore represents the second general mechanism — besides the persistent neuronal activity in memory systems mentioned in premise 1 — which leads to memory overexpression.
Influences that take advantage of this second mechanism of memory overexpression are in my opinion the most important and most dangerous entry points into an amplified VC.
Furthermore, aversive memories, especially traumatic ones, most probably promote brain inflammation (as their overexpression triggers mild stress, which in turn promotes brain inflammation, see PMID 23537508). This would additionally reinforce the VC by inducing two further positive feedback loops into the VC via the two mechanisms A and B described in the preceding paragraphs.
THE VICIOUS CYCLE MUST BE DISTINGUISHED FROM CLASSICAL DISEASE MECHANISMS
The VC is basically a natural process that slowly drives many biological regulatory systems in body and brain out of their state of equilibrium. This implies several specific properties for the VC that distinguish it from classical disease mechanisms:
THE VC-INDUCED DISEASES HAVE A COMMON ORIGIN. BUT THEY NEVERTHELESS APPEAR TO BE COMPLETELY DIFFERENT MEDICAL PHENOMENA BECAUSE EVERY BIOLOGICAL REGULATORY MECHANISM DEREGULATED BY THE VC, PRODUCES ITS OWN COMPLEX OF SYMPTOMS.
IT IS DIFFICULT TO PREDICT WHICH DISEASES THE VC WILL CREATE IN AN INDIVIDUUM, BECAUSE THE WAY THE VC DEREGULATES BIOLOGICAL REGULATORY MECHANISMS DEPENDS IN AN EXTREMELY COMPLEX WAY ON GENETICS, EARLY LIFE EPIGENETIC PRIMING, LIFESTYLE, AND AUTOBIOGRAPHICAL MEMORY CONTENT.
SINCE THE VC GENERALLY DEREGULATES NOT ONE, BUT SEVERAL BIOLOGICAL REGULATORY MECHANISM, THE VC-INDUCED DISEASES HAVE A HIGH CO-MORBIDITY.
The main similarities of the VC-induced diseases are:
They are driven by chronic inflammation (since the main detrimental effect caused by the VC is chronic inflammation in brain and body, and chronic inflammation has multiple tissue-damaging effects).
Their main risk factor is aging (since in general, the VC's anti-homeostatic effects take decades to rise to a disease-inducing level).
(It is worth mentioning at this point that most of the aging-related diseases are indeed driven by chronic inflammatory processes. See e.g. https://harvardmagazine.com/2019/05/inflammation-disease-diet)
PART 3: SUPPORTING RESEARCH DATA
The hypothesis is supported by the following research findings:
GENE EXPRESSION ANALYZES SUGGEST AN IMPORTANT HUMAN MEMORY SYSTEM TO CAUSE AGING IN SOME TISSUE
A 2011 study of Huang et al. about aging-related gene expression in various tissues (https://www.ncbi.nlm.nih.gov/m/pubmed/21751870/), concludes that „the aging of hippocampus caused some kind of cascade of aging in other tissue“.
The hippocampus is the area of the brain responsible for autobiographical memory. The hippocampus is also known for its decisive role in inhibiting aversive memories. Damage to the hippocampus would, therefore, disinhibit aversive memories.
The (after my hypothesis) thereby resulting brain-wide increased level of inflammation would in turn predominantly damage the hippocampus, because it is one of the most sensitive structures of the brain. This would further disinhibit aversive memories, and so on, and so on.
This means that the hippocampus could be an area of the brain that is simultaneously the origin and target of one of the mechanisms that form and amplify the VC.
This possible role of the hippocampus as a major source and target of the VC, and therefore as a major causal source of an aging-promoting influence on the body, could be the reason why Huang et al., 2011 found the hippocampus as the causal source of the aging-related gene expression changes in some tissues of the body.
MICE SKIN AUTOMATICALLY REJUVENATES WHEN BLOCKING A MOLECULAR MECHANISM WHICH IS DRIVEN BY THE VC
My hypothesis postulates that the VC creates aging in all animals with nervous system by inhibiting repair and rejuvenation mechanisms (for exact mechanisms, see my website). Interestingly, a study shows that a molecular mechanism (the pro-inflammatory activity of the NF-κB molecule), actually exists in the skin of mice, that
a) becomes more and more active as the mice grow older, and
b) THE BLOCKING OF WHICH LEADS TO AUTOMATIC SKIN REJUVENATION.
This, in fact, suggests that aging, as postulated by my hypothesis, arises from inhibiting of repair and rejuvenation mechanisms. In this case, the inhibiting of repair and rejuvenation mechanisms is due to the overactivity of NF-κB (for details see PMID 18055696).
In addition, because the VC is highly pro-inflammatory and therefore strongly potentiates the activity of NF-κB (see e.g. PMID 19408108), the VC might be responsible for the aging-related increased activity of NF-κB and, thus, also for the resulting skin aging through the NF-κB-induced inhibition of repair mechanisms. The VC could therefore indeed represent the origin of the skin-aging process in mice.
A CAUSAL CHAIN FROM THE VC, TO THE AUTONOMOUS NERVOUS SYSTEM, TO AGING
A research line (see PMIDs (29932493 and 30303708) found, that a major source of tissue aging, the decline of stem cell proliferation during growing older, is caused (at least in vitro) by an imbalance in the activity of the two branches of the autonomous nervous system, the sympathetic (SNS) and the parasympathetic (PNS) (see e.g. https://www.fightaging.org/archives/2018/10/neurotransmitters-envisaged-as-controllers-of-stem-cell-activity/ ).
As already mentioned, one major deleterious effect of the VC is a deregulation of the ANS, i.e. a constantly increasing imbalance in SNS and PNS activity during aging. Thus, through this deregulation, the VC could be the causal source of the declining stem cell proliferation occurring during aging, and because of this property actually represent the origin of the aging process.
ALZHEIMER'S CHARACTERISTICS SUGGEST A CAUSATION BY THE VC
Now, how do I come to the conclusion that VC also causes Alzheimer's? Recently, I read this article (https://www.nytimes.com/2019/04/08/health/alzheimers-dementia-stroke.html), which states that Alzheimer's is, except for the cases caused by specific Alzheimer genes, mainly an aging-related disease.
As a mainly aging-related disease, Alzheimer's could therefore be a consequence of VC if it ran in a subject for decades in a specific "Alzheimer's generation mode". In other words, if it slowly deregulates a number of biological mechanisms so that the Alzheimer's phenotype eventually develops. The fact that VC causes chronic encephalitis and Alzheimer's is always accompanied by it supports this idea.
The article also suggests that Alzheimer's is often accompanied by hippocampal atrophy. Since the VC possibly runs predominantly in the hippocampus and damages it, it is quite possible that both hippocampal atrophy and the causally linked Alzheimer's disease are caused by the VC.
The hypothesis is described (sorry, unfortunately somewhat cumbersome) in more detail here: https://sites.google.com/site/emdhypothesis/notes
Hope, you had a little bit of fun (at least, it would decelerate the VC ;-))
Kind regards, Rudger
There is a patent pending anti-aging technology in an area that no one else is currently researching; Improvements in the uptake of nutrition.
Clinicians who actually work with the severely aged have always suspected a nutritional component of aging. Physicians routinely prescribe high calorie oral nutrition and it does not work. High caloric substance with amino acid supplementation given parentally, does work. Most physicians simply scratched their heads and said; "Go figure." The clinical pharmacist assigned to the case thought to make a note of it.
Dr. David Sinclair had earlier researched the benefit of wine with meals. His "discovery" of Resveratrol in wine served to end the further research in that area. This is likely because PhD researchers often behave like sheep and flock to where the funding is. That the projects funded also mimic the last project that was successfully funded is one reason aging research is currently on the wrong track. However, a clinical pharmacist reviewing the research noted that certain amino acids are more soluble in alcohol. This was not considered by Dr. Sinclair and his team. It could be further shown that the benefit of alcoholic beverage consumed with meals do not extend solely to wine. This was not picked up in the extensive peer review of Dr. Sinclair's work. An enhanced solubility amino acid combination was developed by the pharmacist which actually gives superior oral absorption of amino acids.
As a further test against these results, large numbers of undisputed longevity statistics were collected and weighed against the possibility that each could be caused by nutritional deficit due to malabsorption.
A small sample of the undisputed statistics involving longevity:
The connection between the possibility of a malabsorption syndrome and these seemingly random facts:
Larger species have an innately larger capacity to absorb nutrition. This is a fundamental necessity due to their much larger size.
Moderate drinking involves wine with dinner, the alcohol increasing absorption of alcohol soluble amino acids
Seven Day Adventists do not drink. but they do not eat meat (charred meat, has been associated with a lowered absorption of some amino acids)
Celibate males seem to live much longer. Gamete production appears to take nutrition away from longevity.
Females live longer …There are multiple reasons (mostly smaller meal sizes)
A lower caloric intake has been shown to have a positive effect on lifespan. The data further suggests a species specific uptake limit on the absorption of certain nutrition. Larger organisms fundamentally have a larger capacity or a greater number of receptors (as is required to support their greater bulk.) Human females benefit by generally being smaller but still sharing the same capacity to absorb nutrition as the larger male. The longevity enhancing method of Caloric Restriction extends this limited capacity over a longer period of time by lowering the daily, net intake. A lower quantity of nutrition presented to receptors, (especially diminished receptors) at any one time, of course, also increases the efficiency of absorption.
The bacteria in the gut are the beneficiaries of all of the extra unabsorbed amino acids. Randomly, bacteria begin their own bodily processes using these extra amino acids. However, The extra nutrition causes them to decline, just as the host declines from the lack of nutrition. Bacterial decline is due to bacterial processes which were begun and now cannot be finished. The affected bacteria have to compete with the host and all of the other bacteria for the remainder of the needed amino acids. Bacterial decline in the gut is another well known hallmark of aging not explained by any other theory.
Further, the colon of an older individual looks much different from the colon of a much younger individual. It is obvious that deleterious changes occur over time. Earlier researchers attributed this as a result of aging. These changes may be, in fact, the cause of aging.
A lack of absorption of specific amino acids is experimentally shown to be responsible for physical aging in humans. All 20 amino acids are needed at a precise time and in the exact sequence for the human body to make protein. Absorbing only 19 of the 20 amino acids needed for human protein is enough to trigger the aging process.
Aging and starvation are shown to be the same biological process. The lack of absorption of any essential nutrient is exactly the same to the body as not receiving any nutrition at all. Substantial proof was found that both events place the body into the metabolism mode that holds on to nutrients and expends little energy. The effect of this process in aging is the typically seen decrease in muscle mass and gain in overall body mass. In aging the unusable nutrition is stored as fat while structure is broken down for the missing nutrition. In actual starvation -just the structure is broken down for it's nutritional value.
An enhanced bioavailability formulation of the missing nutrition has been developed. As this was an entirely new product and trials of the compound were successful at multiple concentrations. We now have a safe and easy to use nutritional supplement product that is clinically proven halt the aging process. This product could likely be on the market in 2016. Followers on Reddit will not be able to ask questions of the author as his AMA request was declined. The Reddit AMA policy states that pharmacists are not legitimate researchers and are therefore ineligible to participate. Questions will, however, be taken on QUORA.com
Blake's nutritional theory of aging states aging is a two part process. The first part involves a lack of absorption while the second part involves the body replacing the unabsorbed amino acids by removing them from existing structure.
That nutrition is the initial problem leading to aging is not unexpected. Clinicians who work with the elderly have long suspected a nutritional component to aging. The lack of absorption of specific nutrition triggers the process of aging.
Acquired GI damage or a loss of receptors for specific common amino acids is the primary cause of aging. Biofilm formation blocking intestinal uptake receptors is one type of uptake flaw. The Bible warns us not to eat burnt offerings. Receptor damage from eating burnt/overcooked protein is another possibility for a lack of intestinal absorption.
As having all amino acids in protein nutrition is a biological necessary -the inability to absorb specific protein from the gut forces the lymph system to begin to "steal" needed nutrition from structure. This is the part two of the two part problem which we call aging.
There are five of the twenty amino acids comprising protein in the body with known problems of absorption. Biological aging begins with a lack of intestinal absorption of at least one, some, or all five of these amino acids. Which or all of the amino acids becomes lacking changes the observed outcome in the function or structure of the body. Often, these changes do not become readily apparent until late in the aging process.
Facial wrinkles are usually the first sign of aging to be observed. Wrinkles are caused by the loss of collagen from below the skin. The missing collagen had been "stolen" by the body for it's amino acid content. Collagen supporting the skin, capillaries and joints are the low hanging fruit from which the lymph system can most easily acquire needed amino acids.
It has been demonstrated that the lymph system has an ability to reverse structure by breaking down muscle and collagen to gain amino acids for bodily production of new peptides. This part of the aging process is identical to the orderly decline seen in starvation.
A uniquely human trait is the ability to live for up to 60 days without solid food -due to this recycling process. From which structure the amino acids are taken, becomes another factor that differentiates the process in different individuals. Congratulations on having made it to the end. Formatting on this site is not conducive to an easy read.