Dear Future Centenarian,

This warning is not to discourage you from necessary surgery. Rather, it is a sobering reminder to avoid any underlying conditions or diseases that make surgery necessary in the first place.

Use your own discretion regarding optional surgery such as any cosmetic surgery that may require general anesthesia.

If you are not aware of my condition, I am a paraplegic from a spinal cord injury in 1978. Neuropathic pain (some call it fathom pain) was part of the package I inherited.

It was troublesome since my injury and was partially controlled by drugs. But their effectiveness wore off and even opioids didn’t help.

The past few years, pain got really bad, and the past six months have been torture.

After an MRI, CT Scan and numerous X-Rays, my doctors collaborated and determined a spinal decompression surgery was necessary and that it should relieve my pain to the degree that I can function again as a human being… but no guarantee due to the length of time since my injury.

I exhausted all the other options I could find over the years so far, so I enthusiastically agreed to get it done asap.

Surgery took a couple of hours and the neurosurgeon said it was successful. Then a long drawn out recovery period where the doctor said I could resume light exercise in about two weeks.

General anesthesia carries potential side effects with it. Although the anesthesiologist agreed to use as light a dose as possible, I got almost every side effect in the book… and then some.

Everywhere I searched, the “data” stated they are temporary and typically disappear in two days maximum. Mine were at their peak after 48 hours and most are pretty much the same now, almost five days post-op. Here’s a list of most of them:

Chills – My chills were so bad that for the first two days, I shivered and shook so badly that I could barely write. Signing my name was a lesson in futility. Now, on day 5, I still have a bad case of the chills but am barely shivering.

Sweating – This magnified the negative effects of chills. I could bring the chills down fairly well with a sweatshirt, climbing under heavy covers, and keeping the heat turned on, but then I would sweat profusely. So, I had cold sweats with the sweats magnified as I warmed up. I still have cold sweats, but they are subsiding.

Persistent dry cough – I had a very slight dry cough the past couple of months, but since surgery, it has become a major issue. It’s about 4 times worse now.

Gas – My abdomen swelled up so much that I had enough gas to launch a blimp. It’s slightly better after a couple of days on an OTC chewable tablets but is still an issue.

Nausea – I never quite threw up, but it still lingers.

Appetite – I have none. The thought of eating was, and is repulsive. I know I have to eat and need nourishment, especially protein to move along the healing process, so I force feed myself. Even so, I’m only getting about half of the calories I need.

Hiccups – I would never have anticipated this, but they are a constant nuisance and magnify the effects of burping from gas and from nausea.

Sore throat – That was a real problem the first 2 days or so but has improved a lot.

Cramping – I couldn’t find this listed as a side effect, but my hands cramp up from time-to-time.

Constipation – This was an issue the first few days, now it’s…

… Diarrhea – probably caused by stool softeners and laxatives to treat constipation.

Brain fog – This issue still persists but is improving.

Pain – Of course, this is the problem I wanted to resolve with the surgery. So far, no luck. In fact, it’s just as bad… and maybe worse. I still have hope in this department and realize it would probably take weeks or much longer to improve.

So, that has been my experience so far from the surgery and general anesthesia. Any one of these side effects could be managed or at least coped with. However, taken as a whole, they have disabled me more than I can describe.

I don’t want any of this to affect you. The purpose of this letter is to encourage you to adopt the 7 lifestyle habits I covered in just completed 7 e-books. You can find them at https://www.amazon.com/s?k=kekich&i=stripbooks&ref=nb_sb_noss_1.

You don’t have to pay for them though. Simply email me at hanno2033@mail.com. I do ask that you give them good reviews which will allow me to reach more readers.

Virtually every killer disease is aging-related, and most can result in major surgery… which is often too much too late. The first signs of heart disease are often death. If a stroke doesn’t kill you, you could end up paralyzed and unable to speak.

And of course, any one of these diseases could condemn you to living out your time agonizing and dying much before your time in a nursing home. Especially if you get Alzheimer’s or another dementia.

The sad fact is, the vast majority of these diseases could, and should be prevented.

And as a bonus, you may live an extra 10-20 years in vibrant good health. With that awareness, wouldn’t be insane to not adopt preventative strategies?

Then, surgery side effects should not be an issue in the first place.

More Life,
David Kekich

d7d2d43a2c5a494eae8587476e739abff79fa41e847447e98867cda9d5fb566b02048748677348adb8c3dfc285546915

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Weekly News

Finding the Limits of Amyloid Clearance as a Treatment for Alzheimer’s Disease

Alzheimer’s disease is associated with a slow buildup of amyloid-? aggregates in the brain over the years of later life. The amyloid cascade hypothesis puts this process as the first step in the development of Alzheimer’s disease, setting the stage for later neuroinflammation, tau aggregation, and cell death in the brain.

This view of the condition has yet to lead to meaningful therapies, however. Several immunotherapy approaches have succeeded in clearing a meaningful degree of amyloid-? in human trials. Clinical improvement in those patients was very limited at best, even given a generous interpretation of the data.

Read More https://www.fightaging.org/archives/2021/03/finding-the-limits-of-amyloid-clearance-as-a-treatment-for-alzheimers-disease/

James Peyer of Cambrian Biopharma on Defining Aging as a Disease

James Peyer was involved in the aging-focused fund Apollo Ventures before he moved on to the more recent venture industry initiative that evolved into Cambrian Biopharma.

Cambrian is arguably even more focused on creating new biotech startups to treat aging, rather than investing in existing companies, than is the case for Apollo.

Many venture capitalists are coming to the conclusion that the pace at which new biotech companies in this space are arising is too slow to provide sufficient opportunities for the capital that could be harnessed to produced progress. That pace must thus be accelerated.

Read More https://www.fightaging.org/archives/2021/03/james-peyer-of-cambrian-biopharma-on-defining-aging-as-a-disease/

Supplementation with Glutathione Precursors Improves Mitochondrial Function, Reduces Oxidative Stress and Inflammation

Mitochondria are the power plants of the cell, turning out the chemical energy store molecule ATP that is needed to power cellular processes. Mitochondrial function declines with age, and this faltering of energy production is an important contribution to degenerative aging.

A broad range of proximate causes have been identified, changes in gene expression that directly or indirectly disrupt the supply of rate-limiting molecules necessary for mitochondria to carry out their work.

Read More https://www.fightaging.org/archives/2021/03/supplementation-with-glutathione-precursors-improves-mitochondrial-function-reduces-oxidative-stress-and-inflammation/

Naked Mole Rats Employ Cholesterol Metabolism to Enable Cells to Resist the Senescent State

Naked mole-rats exhibit an unusually longevity, with a life span something like nine times as long as that of equivalently sized mammals. They are also highly resistant to cancer.

This makes them an attractive subject for research into ways to treat aging and age-related disease. No one mechanism will be the exclusive source of these traits in the naked mole-rat, but it is interesting to look at the way in which cellular senescence is different in this species.

Read More https://www.fightaging.org/archives/2021/04/naked-mole-rats-employ-cholesterol-metabolism-to-enable-cells-to-resist-the-senescent-state/

Chronic Infection Contributes to Age-Related Hematopoietic Stem Cell Dysfunction

Hematopoietic stem cells (HSCs), resident in the bone marrow, are at the base of a complicated tree of descendant progenitor cells that collectively produce immune cells and red blood cells.

With age, the HSC population becomes damaged and dysfunctional. The number of competent stem cells diminishes, while mutational damage followed by clonal expansion causes issues such as myeloid skew in the hematopoietic populations, in which too many myeloid cells are produced at the expense of needed lymphoid cells. This all contributes to an age-related decline in immune system function.

Read More https://www.fightaging.org/archives/2021/04/chronic-infection-contributes-to-age-related-hematopoietic-stem-cell-dysfunction/

Unsurprisingly, Different Age-Related Conditions Share Overlapping Metabolic Signatures

The enormous variety of degenerative aging, the many forms of declining function and organ failure, derives from a simpler array of underlying cell and tissue damage.

One might look at the SENS research proposals for an overview of that damage. Given this, it isn’t surprising to see that many age-related conditions share metabolic signatures. One might suppose these signatures to be reactions to specific forms of damage or consequences of specific forms of damage.

Read More https://www.fightaging.org/archives/2021/03/unsurprisingly-different-age-related-conditions-share-overlapping-metabolic-signatures/

A Role for Cellular Senescence in Brain Aging, and for Senolytics in the Reversal of Brain Aging

Senescent cells accumulate throughout the body with age, the result of an increased pace of creation and slowed pace of clearance. Senescent cells secrete a mix of inflammatory signals that disrupt tissue maintenance and function, and this contributes to the progression of degenerative aging.

Clearing senescent cells with senolytic therapies has been shown to produce rejuvenation in mice, robust reversal of many different age-related conditions.

Read More https://www.fightaging.org/archives/2021/03/a-role-for-cellular-senescence-in-brain-aging-and-for-senolytics-in-the-reversal-of-brain-aging/

Exercise Programs Boost Blood Flow to the Aging Brain

Some fraction of aging in the brain is due to a reduced blood flow to brain tissue, and thus a reduced delivery of nutrients and oxygen to brain cells.

Vascular aging reduces the density of capillary networks in tissue, and increases stiffness of blood vessels. Equally, a sedentary lifestyle – and, later, heart failure – reduces the ability of the heart to pump blood uphill to the brain.

Structured exercise programs consistent demonstrate health benefits in older individuals, likely because near everyone in later life fails to undertake sufficient exercise. Here, researchers show that one of those benefits is an increased flow of blood to the brain, an outcome that should slow the progression of neurodegeneration to some degree.

Read More https://www.fightaging.org/archives/2021/03/exercise-programs-boost-blood-flow-to-the-aging-brain/

Gene Therapy to Reduce Tau Expression in Mouse Models of Tauopathy

Tau is one of the few proteins in the body capable of becoming altered in ways that form harmful aggregates, capable of disrupting cell function or killing cells. Tau aggregation occurs in the aging brain, and particularly in the class of neurodegenerative conditions known as tauopathies.

Read More
https://www.fightaging.org/archives/2021/03/gene-therapy-to-reduce-tau-expression-in-mouse-models-of-tauopathy/

Engineered Cells Drive Blood Vessel Formation Following Stroke to Restore Lost Function in Mice

Researchers have recently demonstrated a cell therapy approach that drives greater blood vessel formation in the brain.

In mice this treatment restores most of the loss of motor function that occurs following a stroke, a surprisingly large restoration given that the brain is notoriously lacking in regenerative capacity.

Read More https://www.fightaging.org/archives/2021/03/engineered-cells-drive-blood-vessel-formation-following-stroke-to-restore-lost-function-in-mice/

PPAR? Slows Atherosclerosis by Inhibiting Vascular Cellular Senescence

It may turn out to be the case that many mechanisms of cellular regulation that slow aspects of aging function, at least in part, by slowing the pace at which senescent cells accumulate.

Senescent cells induce tissue dysfunction via inflammatory signaling. Studies in which senescent cells are selectively destroyed in old tissues via senolytic drugs have resulted in rejuvenation, showing that the accumulation of these errant cells has a sizable role in the progression of degenerative aging.

Read More https://www.fightaging.org/archives/2021/03/ppar%ce%b1-slows-atherosclerosis-by-inhibiting-vascular-cellular-senescence/

Cholesterol Metabolism in Alzheimer’s Disease and Other Age-Related Conditions

Cholesterol metabolism is interesting in that humans (a) do not break down cholesterol to any great degree, and (b) cholesterol is only created in a limited number of locations in the body.

Thus intricate mechanisms shuffle cholesterol from place to place via the circulatory system. LDL particles carry cholesterol from the liver to the body, APOE aids in cellular update of cholesterol, ABCA1 enables cells to hand off cholesterol to HDL particles, and those HDL particles carry cholesterol to the liver.

Read More https://www.fightaging.org/archives/2021/04/cholesterol-metabolism-in-alzheimers-disease-and-other-age-related-conditions/

Age-Related Upregulation of Autophagy as a Possible Contribution to Bat Longevity

Bat species include many that are long-lived for their size. Flying species in general are long lived; one can find many similarities in metabolism between bats and birds.

It may be the case that the much higher metabolic rate of flying species requires improved mechanisms of cell resilience and cell maintenance that have the side-effect of better resisting the damage of aging.

Read More https://www.fightaging.org/archives/2021/04/age-related-upregulation-of-autophagy-as-a-possible-contribution-to-bat-longevity/

Long Term Consequences of Brain Ischemia in the Development of Alzheimer’s Disease

Transient ischemia is the loss of blood supply to tissue followed by its restoration, leading to cell death, tissue damage, and harmful cell signaling.

While the paper here is focused on connecting the significant ischemia of stroke with the later development of Alzheimer’s disease, it is also the case that aging brains undergo many unnoticed, tiny ischemic events over the years.

Read More https://www.fightaging.org/archives/2021/04/long-term-consequences-of-brain-ischemia-in-the-development-of-alzheimers-disease/

Tau Knockout in Normal Mice Improves Mitochondrial Function and Slows Cognitive Decline

Tau is involved in Alzheimer’s disease and other tauopathies; it is one of the few proteins in the body capable of becoming naturally altered in ways that encourage aggregation of the protein into solid deposits that are toxic to cells.

Tau is highly expressed in nerve cells, and helps in the function of the microtubule network of the cell. It also has roles in other processes peculiar to nerve cells, such as synaptic transmission.

Read More https://www.fightaging.org/archives/2021/04/tau-knockout-in-normal-mice-improves-mitochondrial-function-and-slows-cognitive-decline/