Grim Age and a fundamental contradiction

 

2019 is also important for the experiments by Horovith that showed an AI computable statistic that connect methylation concentrations of cytosine in Cp blocks of the DNA, habit indices of things like smoking and predict the remaining life in years to 98% accuracy. This is called the Grim Age counting the years remaining to natural death. To the surprise of Horovith team, the damage from Smoking errored on add when the damage was already reflected in methylation alone IE habit percentages of many damage elements like drinking were already reflected in methylation levels! The number remaining in natural life were called the Grim age. Unmodified Grim age was a better number than human memory of degree of smoking!

As this reference shows, There are many question in your mind about the establishment of Grim age in DNA m Age. While the entire blog is very readable, I do believe the author believes in some programmed theory of Aging and considers the modifications from habits a perturbation in predicted age, I still cling to the minority view that aging is damage accumulation and smoking and other lifestyle habits increase damage but still reflect the summary of damage accumulation. Damages can be external and unavoidable as a consequence of passage of time. But this means that the essential amelioration theory is neither prevention (gerontology) nor dealing with consequence (geriatrics) but deal with fixing the damage however caused (SENS and Dr. Audrey de Grey). Wounds happen in a war, prevention is like bullet-proof vests help, Complex consequences will require complex studies, that is what medicine is all about, better is to save the wounded and stabilize the wounded to be processed properly. Aging is like that. Let us fix the person ready to die. In fact in a war, Enemy will likely change the bullets once the vests become common, viral enemies will evolve to those that will defeat the aging fixes and the war will continue!

The best part of a blog is to read good comments and responses.

Some anti-aging candidates seem to have no effect on methylation status-like rapamycin for example.

In addition to DNA methylation covering various stretches of DNA we also have lamin A protein (which are defective in progeria), chromatin proteins, DNA helicase subunits that attach to and differentiate stem cell DNA (defective in Werner’s Syndrome) telomeric DNA which folds over on coding DNA So I would bet we need a lot more than a DNA methylation clock to get a more accurate predictor of lifespan.

One approach is very controversial and is outside my thinking. The DNA end are called telomere and become smaller in both the daughter cells on division. Around 50-60 divisions later, the telomere reach the limiting amount and cells die thereafter. The division limit is called Hayflick limit. The enzyme telomerase fixes the shortening telomeres by extending them.

The problem is that the cells that do not obey the limit and are infinite lived are cancer cells! Telomerase might induce cancers. Some claim not. There started a trial in Columbia where the clinical trial selects had to pay million dollars first! Like all free press people, I said the trial was a sham done in Columbia to dodge USA laws. I insist the direction is fraught with dangers, but the blogger above seems to have a reference here. I will not go there, but I have no hard reason to prevent you.

 Nevertheless, the Blasco lab was able to show that the shortest telomeres in the mice were elongated, and that markers of health including insulin sensitivity were improved by short-term treatment with TA-65, designed to increase telomerase.

Blasco’s lab then worked with a more potent (though more dangerous) method of telomerase induction: infection with a retrovirus engineered to introduce telomerase into the nuclear DNA of the infected cell.  “Treatment of 1- and 2-year-old mice with an adeno associated virus (AAV) of wide tropism expressing mouse TERT had remarkable beneficial effects on health and fitness, including insulin sensitivity, osteoporosis, neuromuscular coordination and several molecular biomarkers of aging.” (Bernardes  de Jesus, Vera et al. 2012)  The mice lived 13% longer when AAV treatment began at age 2 years, and 24% longer when treatment began at 1 year.  There was no increase in cancer incidence.

Telomerase can be induced by Cycloastragenol, suspected of being the main compound in TA-65. If you get cancer, I warned you.

 

Fundamental contradiction

 Cells become senescent at some point because of errors in duplication, hitting the Hayflick limit or environmental poisoning. Another reason is ignoring apoptosis. Such cells express SASP afterwards and just stay on.  One consequence is that NAD+ causes inflammation of neighbor cells, just evolutionary multi role of this vital chemical. This is suppressed by CD38, an essential chemical but that also has a role in death of neighbors. Thus, more cells become senescent! So my initial idea of reusing own plasma in TPE after CD38 the villain is extracted won't work as it is another cancer otherwise. NAD+ goes bad in this rare case. So we have a fundamental contradiction as CD38 is both a hero(too many benefits) and villain (fixer causes aging)! Just increasing NAD+ or removing CD38 is not going to work. The only way around seems to be making cancers in most cases a gentler disease.

Cancer Response to Therapy-Induced Senescence: A Matter of Dose and Timing 

 Cancer is a consequence of many naive fixes. Another example above was adding telomerase to bypass Hayflick limit, one has possible cancer problems. Even using existing cancer victims fails as even if their cancer is subsequently fixed, who knows how many new cancers were created for whenever. It might even be caused by senolytics.

At the same time, know that cancers are thought of as terrible diseases because they are tied to devastating chemo therapy etc and not mildly painful diseases that they are and ultra modern treatment is My own sister has been afflicted twice in Boston and things were not so bad in the USA! Of course, one might just think so, psychological terror same, and the relative toleration be from early diagnosis both time. The worst thing a patient can do is avoid or delay seeking a diagnosis.

An important sidebar

 Given the state of oxygen supply, I strongly support the use of proning by doctors to know and advise their non-ventilator patients and general knowledge of you as patient yourself and helper to a sufferer. Proning is laying the patient chest down and fast large gulps of air at speed as if panting. This method is advocated by Dr. Guleria, director of AIIMS, Delhi, applied to a big-shot in government who lost his oxygen and was forced into proning. This trick was invented by US residents, interning in the USA, one year back.

According to me - the genetics break-thru for Aging

 

The latest link

The linked paper is not being heralded so, I am either presient or stupidly excitable! I EXPLAIN WHY THIS BELIEF TOO.

Dr. Sinclair has proven that all life on earth shares similar DNA which is everywhere in a nucleolus of a cell. He says that the characteristic of this DNA is that it discovered how to safely patch a break by exclusion of reproduction until repair by turning off the reproduction while the repairs were on by making the reproduction and repair genes the same and expression of repair protein causing the shut (by tight coiling) of the repair portion (the same) by coiling hard IE shut! Such a mechanism has overwhelming evolution advantages over distinct DNA and the only one which survived and is found in all life on earth! The extreme aging of the mouse with inhibiting repair is proof. Regrowth of optic nerves crushed in mice is the rejuvenation proof.

Horovith did wonderful research in totally independent manner and could train AI to predict calendar age from all kind of tissues. They being the same implies genetic aging manner and by 2021 had shown the programs applied to all species of life factored by DNA specialization! This work has been applied to eutherians and will doubtless apply to all life. The variable extract is methylation of specific Cp islands in DNA. An AI can empirically work in all tissues like blood, organ, hair, skin, and spit and predict age within 98% accuracy and predict remaining natural life too. How the methylation occurs is still a mystery and programmed life beliefs are common. I consider non programmed life in the minority, still clinging to the paradigm of damage accumulation and cite two things in my favor: One is matching is statistical, not 100% from a programmed theory; and two the fact that statistical damages can yield so good as adds of random variables; and three that human death age varies from 60 to 110 and death rates flatten after 90 to no age relative extra risk! But the short answer is that it is a programmed process. And there is no clinching experiment yet,

Now comes my orthogonal but essential expertise in formal languages. One can capture DNA derivations by L-systems of context-sensitive grammars with correct context is required for application of a rule. People have babies when the age of the boy is from 14-74 and the age of girl is 13-42. No child has ever been born aged. The DNA of the male when it fertilizes the female is striped clean of methyl marks, as is the woman's and the baby inherits two clean DNA. One can trace the process to 4-fold division after fertilization. The fertilized egg thereafter attaches itself to the womb wall. In the absence of complications, the due date can be predicted accurately within a few days, showing again a 98% accuracy. So there are grounds to believe programmed aging theory paradigm. I however, draw a different lesson from this, one the old DNA is preserved intact; and two the most important one, namely that removing the methylations have a rejuvenation effect.

That brings me the meat of my study, that is the research linked in will be considered a break-thru some day soon.

Summary

A general approach forheritably altering gene expression has the potential to enable manydiscovery and therapeutic efforts. Here, we present CRISPRoff—aprogrammable epigenetic memory writer consisting of a single deadCas9 fusion protein that establishes DNA methylation and repressivehistone modifications. Transient CRISPRoff expression initiates highly specific DNA methylation and gene repression that is maintained through cell division and differentiation of stem cells to neurons. Pairing CRISPRoff with genome-wide screens and analysis of chromatin marks establishes rules for heritable gene silencing. We identify single guide RNAs (sgRNAs) capable of silencing the large majority of genes including those lacking canonical CpG islands (CGIs) and reveal a wide targeting window extending beyond annotated CGIs. The broad ability of CRISPRoff to initiate heritable gene silencing even outside of CGIs expands the canonical model of methylation-based silencing and enables diverse applications including genome-wide screens, multiplexed cell engineering, enhancer silencing, and mechanistic exploration of epigenetic inheritance.

Here is more of my intuition. A Chinese doctor did the very unethical thing some years back - used crispr-cas9 tools of the day to genetically edit human DNA and made a Chinese women carry the result to term. Why the anger worldwide? The edit allows a contextual change in the DNA. But the change will be at all sites in the DNA, whether or not intended. The child may be born with huge unknown genetic disasters, with strange unknown diseases in life! Even most Chinese scientists were aghast, and no such experiment has been repeated.

New method referenced above will prevent unintended edits! The method is new and has applications in my specialty. It works by defining two context around the point of interest. One is the usual crisper cas9 context. Overlaid is another of some width. All genes outside are forced shut. Hence, edit cannot happen! If suitably small region is edited, bad edits cannot happen! The methylation marks can be used to bracket the context! Clearly it will work in context-sensitive grammars where the equivalent to methyl marks can be propagated and derive null at end only! Only one can derive nulls only at the end, thus context-sensitivity is kept. Whether more than 1 nonterminals can be still be nulled in the end is still context-sensitive is open!

Introduction to my specialty

Not to attract one, but just to get a feel, consider it in 2 courses. Scan rapidly if curious.

One is automata theory,  essential to becoming a theoretical computer scientist. Another is to become a compiler scientist. Before my devastation in 1990, I was working on attributed grammars, still fortunately primitive, ready for me to shine as professor emeritus, assuming that undo of my age works some, a second career as Dr. Sinclair dad! Incidentally, what makes me very excited is the backward limited understanding possibilities today of attributed grammars in programming languages (still no automatic semantics in compiler-compilers) graphics (all GUI interfaces are context-sensitive, change as you proceed in a program), pre-formatting (HTML is poor, latex too complex), compilers (context-sensitive AI applied to natural deduction like in robots), machine learning (in robot ensuring understands intended orders only) and now aging!

 

The latest link

Decay of beauty quark

The standard Model of Physics has stood for fifty years, every time standard physics is usable for all new experiments. One of the reasons LHC was built was physicist fond hope that only at 13 Tera electron volts will new physics happen. So they spent 10 billion dollar machine. It did fill one hole in the Standard model and discovered Higg's boson. But never any particles of -ino type! Either they did not exist or 100 TEV may be needed. Only china could build it! False signal reading has happened to 3 sigma levels (1000-1) chance before, science requires 5 sigmas (3 million-1) for truth. So current quark decay of electron/muon of experimental (100,80) as opposed to (100,100) predicted is (1000-1) sure. Thin but hopes, stronger in my mind because it seems to hold over 10 years of past experiments. Beyond standard model? I root for the physicists who spent entire working life to LHC, the brightest humans of all. This was their dream.

Test of lepton universality in beauty-quark decays

LHCb collaboration: R. Aaij 1000 others

The Standard Model of particle physics currently provides our best description of fundamental particles and their interactions. The theory predicts that the different charged leptons, the electron, muon and tau, have identical electroweak interaction strengths. Previous measurements have shown a wide range of particle decays are consistent with this principle of lepton universality. This article presents evidence for the breaking of lepton universality in beauty-quark decays, with a significance of 3.1 standard deviations, based on proton-proton collision data collected with the LHCb detector at CERN's Large Hadron Collider. The measurements are of processes in which a beauty meson transforms into a strange meson with the emission of either an electron and a positron, or a muon and an antimuon. If confirmed by future measurements, this violation of lepton universality would imply physics beyond the Standard Model, such as a new fundamental interaction between quarks and leptons.

Recent remarkable aging news

The latest link

Starting with 2005 parbiosis experiments of Conboy, as I have said repeatedly, the idea that young blood has any magic proteins is wrong and dangerous, says FDA and All such proponents including otherwise respected doctors of Stanford and USB are to be treated as criminal aging salesmen with snake oil, say I.

The following is a touching example about aging, "Will Future Humans be Forever Young?". Regardless of the answer that you have, it has many good aging ideas.

Next is a long but prescient view of direction by Drs. Conboys in this interview "Irina & Michael Conboy – Resetting Aged Blood to Restore Youth". This deals with many things, including launch of their company IMYu. It is too important to not add my comments and abbreviate some.

Answer to aging skeptics

You stated that aging is not just progression of time; it seems to be a highly regulated process with a great deal of plasticity, and by understanding that regulation, it means aging is something we might slow or reverse. Despite this evidence, why do you think the world, and even academia, have been slow to accept that aging is not a one-way process?

Irina: I think that lack of cure goes hand in hand with inability to accept that this is disease. For example, there was some resistance to accept tuberculosis as the actual disease. When there were no antibiotics or cure for it, people tended to discard it and said, oh, it’s just nerves, you need to go to a sanatorium and relax. Perhaps it’s a subjective human feeling; if we cannot cure it, let’s just say it just happens, you cannot deal with that. That is my kind of feeling about it. Instead, it goes hand in hand that as human beings, you just want to say okay, I am going to die from old age, but it’s okay, it’s just a normal process.

Do you think we can reverse it at this point; we have visibility enough to know we will be able to reverse it?

Irina: At some point. Right now, we cannot, clearly, still, but we are making great strides over the situation where we can reverse it, like for example tuberculosis, or meningitis, bacterial meningitis. It used to be that, please do not diagnose that there’s bacterial meningitis, because there is no cure. Whatever else you can come up with, do it first. Now, diagnose it as fast as possible, so we can put patients on antibiotics immediately. My prediction is that the same will happen to aging; right now, we say it’s no disease. Then, okay, just take this thing or do these things, and then you will stop deterioration; of course, we will say, yeah, it’s bad, and this is good. Why not?

Arun: Within 3 years, for 50 years, younger by doctors by 2030.

England's politics: We are likely years or even decades from gaining wide societal support for the defeat of aging itself, but initiatives like this serve as useful ways to nudge society in the right direction. If more people can be convinced that health and longevity are desirable, it will not be so hard to convince them that increased longevity or perhaps even indefinite lifespans free from age-related diseases are also a good thing. This may be a small start in that direction, but at least it is a start.

STEM cells don't vanish, but sleep all over, forever, from chemical signal

Your work suggests that stem cells do not suffer the ravages of time that somatic cells do, as even older cells utilize telomerase to maintain telomeres. They don’t appear to accumulate DNA and other forms of damage as fast if at all, and activated stem cells produce young, healthy tissue, even in an aged body, so what is preventing stem cells from working properly as we age?

Michael: We and others have demonstrated that you can, from the outside, either by some signal or blood therapy, parabiosis, something like that, some intervention, jump-start the aged resident stem cells in the tissue and get them to behave as, by whatever means you’re measuring it, young or a lot closer to young than they would normally be. The intrinsic capacity of them to act that way is there.

Arun: magic growth like teen years can happen even in old age by turning off sleep signals!

Brain neurons do not replace themselves

Happens because otherwise human memory will have strong forget periods! So DNA repair is critical for them. Five times more frequent than neurons are astrocytes in the brain which have so far believed to be helpers to neurons. Someone recently figured out how they could be converted to neurons, in vivo! Brain repair is crucial part of extending age to 500 years or longer!

Medical Tourism for reduction of Aging in India

 

No one previously has undertaken the systemic study of the immunomodulatory benefits of TPE for the broad class of age-associated disorders, which medical data suggests share deficiencies similar to autoimmune disorders. There are independent other methods using intravenous methods on NMN, NR, direct NAD, direct NaDH, SKQ1, MIB-626 and Mitoq, all that can be infused in a doctor presence. Collectively, these methods are specific to aging, based on chemistry and genetics and not a new specialty of medicine.

That is medical doctor as a class too cautious and unfit to be an advisor to Aging benefits in persistent slow diseases like heart troubles, diabetes, cancers, Alzheimer, Parkinson etc that do not have a germ cause, are distinct from germ caused diseases, and can not be handled by germ theory of diseases that underlies the victory of allopathy over ALL OTHER MEDICAL SYSTEMS. PREVIOUSLY MENTIONED DISEASES AND OTHERS ARE ALL AGING BASED. Age is the wrong type of subject to entrust to FDA and will negatively impact their mission or aging!

Therefore, I believe strongly that better benefits of aging undo are best done by Medical Tourism in developing or semi-developed countries with strong administration that can effectively control the market and has dedicated Aging consultants who can guide the patients to secure TPE procedures ordered by them from medical establishments with particular design of replacement plasma. The replacement design is crucial for filtering the evil proteins if the same plasma is reused after filtration, or fresh albumen is used in a saline solution but also having patient-centric compounds added.

If FDA is removed, how will quality control be done? I suggest the use of improvements not by FDA, anecdotal evidence but by family use! There is no reason why FSSAI mandate is not extended to supplements and aging procedures. It gives India a huge opportunity for development, once the belief in Medical improvements in aging undo in India is established! What is more, the higher order medical methods based on artificial thymus and Yamanaka factors are still done best in developed countries. Of course, even they can be competed for!

Albumin is a protein naturally synthesized by our liver on a daily basis.  Replacing plasma with Albumin cleans the blood.  Albumin also acts as a carrier protein for many substances around the body that are protein bound, and it helps maintain the correct amount of intravascular volume circulating in the body.

The entire process is best viewed as an exercise in genetics and effecting the whole body through blood that reaches everywhere but not brain which can be shown by AMBAR like project to lose some chemicals to be trapped by Albumen and excreted!

Similar to American Society for Apheresis (ASFA) , an Indian Society for Aging (ISA) be set up and be responsible for all aging methods, not just TPE, many referenced here, some very medical and two not, Dr. Sinclair (not MD but PhD) based and TPE based. No doctor can know about differences between NMN, NR and MIB-626

Sinclair anticipates that improved blood flow could be important in helping not just aging tissues and organs, but speeding healing of wounds, particularly for people with diabetes who often lose fingers and toes as their circulation falters.

One way in which the body disposes of harmful reactive oxygen species is their conversion by the enzyme thioredoxin-1 (TRX-1). TRX-1 has been proven to play a role in protecting DNA from oxidative stress and slowing down aging processes. Its antagonist TXNIP inhibits thioredoxin-1 and thus ensures that the reactive oxygen molecules are retained. TXNIP increases proportionally with AGE, similarly, in flies to humans! Don't see the relevance of this German research to doctors or how they will make sense of it!

The Best history of aging TPE.

One approach to undo aging is to focus on mitochondria and control the reactive oxide syndrome ROS which can be very destructive past a point, but toothless against viral infections if removed. One way is SKQ1, the Russian chemical with FDA certification at level 2 for the ophthalmic applications as drops. But that project has 11yr history!

Reduced Nicotinamide Mononucleotide (NMNH)

 

The latest link

The issue till today was understood and solve conflict between NMN, NR, or direct NAD+ etc. A non-natural predecessor to NAD+ has been reported tb better than NMN.

Reduced Nicotinamide Mono-nucleotide (NMNH) Potently Enhances NAD⁺ and Suppresses Glycolysis, the TCA Cycle, and Cell Growth.

First read the abstract, Then a check - no bias to grind etc. The answer seems to be NMNH alter long analysis of empirical data on use, particularly data on intravenous route and Dr. Sinclair speeches and use on self and family. The molecule proved to be highly efficient and fast in increasing cellular NAD+, largely surpassing the effect of NMN in every cell line tested. In fact, while NMN was only able to double cellular NAD+ at its maximum concentration (1mM), NMNH led to a 3- fold NAD + increase even at 50µM. The response to NMNH was also faster, as 15minutes were enough for NMNH to almost double basal NAD+, with maximal effects after 6 hours, which remained stable even 24hours after supplementation.

All methods for increasing NAD+ bad?

There are critical voices, particularly this doctor. He believes, as I do, in programmed theories of aging which hold that all chemical processes in the human body had useful purposes before mating and became bad with advancing age as that effect is not evolutionary and hence has no evolution purpose. But not all natural processes are good or inevitable. Some chemicals as CD38 are BAD.

What is behind empirical loss in NAD+ that has been documented? It turns out CD38 concentration increases in step and CD38 and NAD+ are enemies! What is the role of CD38? It is produced by senescent cells and destroys NAD+ in nearby cells. CD38 is a marker that attract immune cells that kill the nearby cells from the fact they marked foreign objects. Sounds good, except that NAD+ was inflaming them and CD38 put off that fire. Explains the empirical finding that NAD+ declines with age and CD38 levels increase.

What happens if NAD+ levels are somehow boosted, NAD+ driven fireworks increase, so more CD38 is needed and that worsens the aging. Instead of improving aging, the NAD+ increase increases aging.

I happen to disagree but publicize a well argued other side and point out that I will add anti-CD38 agents to my TPE. I do not think that NAD+ becomes bad as one ages, hence growing CD38 is a curse, not a heroic act by senescent cells.

No age fix in my time?

Most people are certain that there is no singularity in their lifetime, even if they live past 2030. This is not the conclusion of those who read the stuff related to this issue but of all the others! And I think that till 2040, people will be bombarded with information on how to benefit from possibilities of cure, including reconstitute of new inspector-raj in India and no sane way of distinguishing between sane and insane sellers! This is the calm before the storm. Already in the USA, emfubar marketeers draw 95% of people to useless brands by glowing anecdotal reports. Slow or not, only FDA can shield from free markets! But that slowness is wrong for aging. What is more, advertiser goons have discovered ways of politicians and courts to delay and kill FDA regulators. And all these shark attacks have some abused truth! Like all advertising using anecdotes, selective bias is persistent. People using selection bias are not advertising professionals, politicians and other professionals, but severe criminals.

There has also been a lot of excitement over the work of Drs. Irina and Michael Conboy who have spent over a decade exploring factors in young and old blood which spur or prevent regeneration respectively. They have conducted a number of animal studies suggesting that there are a handful of factors in aged blood which prevent tissue regeneration in older individuals and most importantly, when these factors are blocked or removed, tissue regeneration resumes as it did during youth. This suggests it may be possible to “reset” the signature of aged blood and restore it to a more youthful state. The technology to filter pro-aging factors from our blood already exists too, which means this could reach humans fairly soon.

A second very big reason is the rise of a very important side effect - rejuvenation biotechnology. BEYOND ARRESTING THE EFFECTS OF adverse medical events IN PERSISTENT DISEASES, time is ripe for aging based attack on persistent diseases like diabetes by tools different from usual doctors by chasing doctors conversant with benefits of these, certainly not non-allopathic medicine, but new aging medicine and its rejuvenation biotechnology.

Senolytics

This word was invented by Dr. Aubrey de Grey, used in 2001 to describe one of 7 ways he would attack aging. Cellular senescence is a response to damage or stress in which cells stop dividing and undergo a range of other changes. Senescent cells also secrete a cocktail known as the senescence-associated secretory phenotype (SASP), which includes inflammatory factors such as cytokines as well as growth hormones, protease, and other molecules. The SASP has a variety of local and systemic effects, and it is involved in both wound healing and chronic inflammation. It is known to maintain senescence in senescent cells and to signal for senescent cell clearance by the immune system. The fact that senescent cells become more common with age led researchers to begin developing drugs to target them; these drugs are known as senolytics.

SRF’s Chief Science Officer, Dr. Aubrey de Grey, recently estimated a 50% chance that aging could be brought under medical control in as little as 15 years’ time. In a new interview with NextBigFuture, Dr. de Grey explains how recent development.

Making senolysis a science?

The concept of senolysis was not based o0n any science existing in 2001. Slowly researchers began to describe their research products as senolytic. Today there exist many senolytic in FDA clinical testing. The Newest problem is that any drug, peripheral to senescence-associated secretory phenotype (SASP) can suggest that insignificant changes are senolytic. Not possible if senolysis can be measured! That makes senolysis a science. This will do it! It has found a lipid whose concentration varies with blood carried senescence cell inflaming markers. Routine lipid profile candidate. Henceforth, senolysis is no more a future science but a science. It is like Horovith clock! I want to know my senolytic age today and after an aging procedure.

 

Predictions?

 

Three now predict singularity by 2035

Very big, Dr. kurzweil at google     2029

me                                                    2030

Very big, Dr. de Graey at SENS      2035

 

Doctor consult assumptions

 

Disclaimer        The latest link

I realize medicine is not my specialty, but I (keep getting inputs), often serious, like friends say that they benefitted from x, but never why, or some weak or known wrong reason. Never argue, consult a real responsible doctor as "why not x advertised?". If the doctor says "Never heard of it" or "advances a weak reason", then time to change the doctor! Question must apply to doctor specialty! Never proceed without responsible doctor gave permission.

Surprising nonmedical things have science established aging utility over adequate threshold. These include fasting and exercise, both can be justified by evolution beneficial reasons. More important is empirical benefits making these procedures scientific. It is however very wrong to believe in them for logic reasons and not empirical facts justified later!

I have some expertise in this subject as an unfortunate victim of a divorce from a generalist lady MD, both as husband (good) and divorcee (critical). I am not used to statements for cliché reasons, which are assumed to be known to my readers, I only bother with rationally understood reasons of non-cliche kind! Neither of I, reader, or doctor is right, every one must apply skeptic reasons. Science is RS, any other meaning is forbidden.

A doctor is a human responsible for a practice and incapable of simple niceties of remembering facts so important and obvious to you. Like your name, disease, details of diagnoses visit, course of treatment etc. This problem applies to all humans dealing with many people, like government servants and salespeople. Even routine people about guests as names, marital status, life goals, relatives etc. Smart people keep files on all important things ventured and consult prior to meet. Doctors do maintain a file per patient, but there is proverbial meeting a patent while grocery shopping! My mother is superb filing information in her head, not me. Even my system has degraded with problems in writing. A voice recording filing computerized system is needed and know not if one can be bought.

All doctors are human, capable of falling for simple scams, have no idea of their success in a very scientific field IE RS, humor bizarre by non-doctor standards, admirable talents different from profession (like loveliness, strength, automobile knowledge, niceness etc) But they are shy too, like Normal not of the same profession.  Untimely memory loss is never RS!