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  • JULY 30, 2021

Metformin and its role and anti-aging
by William D. Johnson

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  • AUGUST 19, 2021

Metformin and Metabolic Flexible
by William D. Johnson

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  • MARCH 27, 2023

Allogenic Human Mesenchymal Stem Cell Infusions for Aging Frailty

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  • NOVEMBER 9, 2021

A Look into Senolytic Therapies for Longevity

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HEALTH BLOG & RESEARCH

Metformin
and its role in anti-ageing

William D. Johnson · July 30, 2021 

Metformin and its role in anti-ageing​

William D. Johnson · July 30, 2021 

Metformin, the most common drug prescribed for type II diabetes, was discovered in 1922 and first used clinically in France in 1957. It wasn’t until 1972 that it was approved in Canada, followed by the US 23 years later for the treatment of Diabetes. Over the years, millions of diabetic patients have been prescribed Metformin. Now, almost 100 years after its discovery, we have the data and understanding of all the amazing ways that Metformin can slow your ageing.

The wheels of change turn slowly in medical treatments, despite clear evidence of their effectiveness and high safety profile. The first written record of a controlled clinical trial occurred in 1747 aboard a naval ship, the HMS Salisbury. During this age of discovery, it was commonly accepted that after eight weeks at sea, ones’ mouth would begin to rot as Scurvy took hold, leading to open sores and eventual death. Scurvy killed more mariners than anything else. On the Salisbury, Dr James Lind took 12 cases and tried six different remedies. It was apparent after only six days that the two patients given citrus fruits were recovering nicely, while the other remedies were ineffective. It was almost 50 more years before the Royal Navy adopted fruit as a protocol to prevent Scurvy. After all, it was expensive.

TAME (Targeting Ageing with Metformin) 2020 was the first large-scale clinical trial where the drug was tested for its anti-ageing efficacy. The new findings helped shed light on Metformin’s apparent ability to promote healthy ageing. Although the FDA doesn’t even recognize ageing as a legitimate target for clinical trials, let alone accelerating research or development of regenerative medicines. An initiative such as TAME is inspiring and can hopefully facilitate changes within the FDA to begin addressing the core problem of ageing as a disease, rather than the chronic illness that is simply a symptom of the disease of ageing.

Some fascinating conclusions emerged from the massive amount of data collected over treating type II Diabetic patients with Metformin. Despite the fact that Diabetes shortens your life expectancy, diabetics treated with Metformin were living 15% longer than the people without Diabetes and were 30% less likely to develop cancer. Metformin reduces the incidence of almost all age-related chronic diseases, including the horrific pathologies of Alzheimer’s and early onset of dementia.

While we are well on our way to unravelling the mystery of ageing, Lopez-Otin et al. have characterized nine distinct pathways that cause ageing and are generally acknowledged by the people who study this emerging science. Metformin basically turns down the dial on all of them, reducing the speed of ageing.

We now know that Metformin has the following nine effects that are interconnected to all nine ageing pathways:

  • Improves Nutrient Sensing. Deregulated nutrient sensing is a symptom of most age-related metabolic disorders. One significant example would be the hypothalamus telling us we are hungrier than we should be… weight gain as we age is not just a product of slowing metabolism.
  • Enhances Autophagy. The process by which the body clears out damaged cells and recycles the proteins.
  • Strengthens Intracellular Communication. The ability of your cells to talk to each other diminishes as we age. Think hormones, etc.
  • Protects against Macromolecular damage. The damage to your DNA and other macromolecules like proteins and lipids.
  • Delays Stem Cell Ageing. All healing is induced by stem cells. Ageing results from stem cell exhaustion.
  • Enhances Mitochondrial Function. The Mitochondria in your cells are the energy factories for your body.
  • Regulates Transcription. This is the process by which DNA creates RNA to orchestrate gene activity. It becomes faulty with age.
  • Lowers Telomere Attrition. Telomeres protect your DNA when your cells replicate, shortening with each replication, eventually reaching the Hayflick limit (human cells stop dividing) and dying. Most cells replicate 50-70 times. Protecting the telomeres will increase the limit and extend your life.
  • Reduces Cellular Senescence. The damaged cells and those that reach the Hayflick limit are supposed to die and be recycled. Some cells remain alive even though they no longer function for their purpose, known as senescent cells. These zombie cells wreak havoc, producing toxins and inflammatory elements known as cytokines. Their buildup causes age-related chronic inflammation, which in turn causes chronic diseases.

Any one of these nine effects would make considering Metformin worth it, taken together the argument becomes seriously compelling. My goal is to introduce you to information that will slow or even reverse your ageing. Stem cell therapy, given four times a year, is the absolute gold standard for Regenerative Medicine, but it remains prohibitively expensive.

Metformin, now a generic, is inexpensive and can cost as little as a few dollars a month. Talk to your Doctor, most will prescribe off label because of its high safety profile. Hopefully, the TAME trial will usher in the era when Doctors regularly prescribe Metformin for its anti-ageing characteristics rather than just an intervention for prediabetics. We don’t know yet but imagine how many years you can add to your health span with this one intervention, especially if you don’t have Diabetes.

Western medicine has done a great job extending lifespan but not health span. Treating the symptoms of age-related chronic disease rather than its cause, the disease of ageing, we are now simply sick longer. I don’t want to live a few extra decades being ill and frail. It’s not worth it. The newest science shows that we can be vital right up until our last few months of life. A healthy death occurs over a matter of months, not years. Our health span should last almost as long as our lifespan. Metformin might be the most remarkable single intervention that we have to shorten the gap between healthspan and lifespan based on cost.

Therefore, it is my first suggestion to you because it will cost you almost nothing. I take it, and like David Sinclair, the author of “Lifespan” suggests, “I don’t leave home without it”.

The only downside to Metformin is that it can reduce your regular exercise-related muscle mass gain, yet we know now your strength increases progressively. According to Dr David Sinclair (my hero), this effect can be mitigated by not taking Metformin on days you exercise. For those of us who exercise every day, there is the one week on then off method.

Sinclair surmises with the statement that it’s vanity vs longevity. For once, I don’t entirely agree with him. I think Metformin will extend your longevity and will keep you looking younger for longer. That’s not just vanity rather longevity with vanity, and it’s smart. I work out regularly, and my muscles may not bulk as they used to, pre-Metformin. However, I like the idea of being strong and lithe, and my suits fit better.

This is the first of a series of blogs that will expose you to the leading interventions available in the industry today based on cost, effectiveness and simplicity of application. They are all safe, and the data supports it.

William D. Johnson · July 30, 2021 

HEALTH BLOG & RESEARCH

Metformin and metabolic flexibility

William D. Johnson ·  August 19, 2021

Metformin, the most common drug prescribed for type II diabetes, works wonders on slowing ageing

My last blog went into detail about how Metformin extends your lifespan and reduces the risk of most age-related diseases. I talked a great deal about the biological pathways of ageing and how Metformin can benefit each. Perhaps in too much detail. Many of you may remain unconvinced. So, I enlisted the help of Dr Aysegul Coruhlu, iconic author and anti-ageing superhero, to provide a different description of the power of Metformin and its value to our vital biological function, Metabolism, and metabolic flexibility.

Metabolic flexibility refers to your body’s ability to respond to changes in metabolic demand which means your cells should be equally adept at burning fat and glucose. Mounting evidence from clinical studies suggests that metabolic flexibility is essential to maintaining cellular energy equilibrium, decreasing with age. Metformin basically regulates the use of glucose in the energy production of your cells. The more glucose we burn, the harder it is to burn fat. Another reason why diet and intermittent fasting are important as both affect your metabolic flexibility.

Metformin reduces glucose entry in the energy-producing mitochondria of your cells. It gives your cells a hunger signal that causes them to switch to fat-burning mode. Another benefit of Metformin is to reduce sugary proteins in the body. This pathology called glycosylation increases age-accelerating residues known as AGEs. AGE production is very high in Alzheimer’s, diabetes, and rapid ageing. In particular, they cause skin ageing, sagging, wrinkling and loss of elasticity. Metformin reduces all of this while making your cells younger in their energy production.

Inexpensive with a very high safety profile, 60 years of clinical evidence proves Metformin is an effortless start in your search to close the gap between healthspan and lifespan. A concept that remains primarily unaddressed in the protocols provided by traditional reactive medical treatments. Treat the cause, not the symptoms. Mind the Gap. If you want to age slower and reduce your risk for age-related disease, talk to your doctor about Metformin. It is a cheap, safe and effective means to reduce the healthspan/lifespan gap.

William D. Johnson · July 30, 2021 

HEALTH BLOG & RESEARCH

Allogenic Human Mesenchymal Stem Cell Infusions for Aging Frailty

Journal of Gerontology · March 27, 2023 

The research paper titled “Allogenic Human Mesenchymal Stem Cell Infusions for Aging Frailty” was published in the Journal of Gerontology: Medical Sciences in 2017. The study aimed to investigate the safety and efficacy of allogenic human mesenchymal stem cell (allo-hMSC) infusions in patients with aging frailty.

Aging frailty is a common condition among older adults and is characterized by a decline in physical and cognitive functions, increased susceptibility to diseases, and a higher risk of mortality. Mesenchymal stem cells have been suggested as a potential therapy for aging frailty due to their regenerative properties and ability to modulate the immune system.

The study enrolled 15 participants aged 60 to 95 years who met the criteria for aging frailty. The participants received a single intravenous infusion of allo-hMSCs. The primary outcome was safety, and the secondary outcomes were changes in physical performance, cognitive function, quality of life, and inflammation markers. The participants were followed up for six months after the infusion.

The results of the study showed that allo-hMSC infusions were safe and well-tolerated, with no serious adverse events reported during the follow-up period. The participants showed significant improvements in physical performance, as measured by the Short Physical Performance Battery and the 6-minute walk test. The study also showed improvements in cognitive function, quality of life, and inflammation markers.

The findings of this study suggest that allo-hMSC infusions may be a safe and effective therapy for aging frailty.

This study provides evidence that allo-hMSC infusions may be a promising therapy for aging frailty. The findings of this study have significant implications for the management of aging frailty and suggest a potential new approach for improving the health and quality of life of older adults.

Journal of Gerontology · March 27, 2023 

HEALTH BLOG & RESEARCH

A Look into Senolytic Therapies for Longevity

Zuzanna Walter · November 9, 2021 

With a focus on extending and improving the human lifespan, the medical community continues to explore potential avenues in longevity. One such development has directed increased attention to the practice of senolytics – or, the process of flushing senescent cells from the body to discard harmful proteins.

Senescent cells are malfunctioning, aged cells which can trigger inflammation and dysfunction, developed in response to disease, injury, or cancerous formations.

These cells can remain in the body, contributing to the development of many diseases and features of aging, such as heart disease, dementia, osteoporosis, and lung disease. Removing senescent cells from mice was found to alleviate insulin resistance, cell dysfunction, and ameliorate other complications in cases of kidney failure and disease.

As an emerging strategy in the anti-aging sphere, senolytics still lack a sufficient body of research. Although prior animal-based studies concluded successful results of senolytic therapy, there is no direct demonstration of success in peer-reviewed human clinical trials to date. Recently, the Mayo Clinic revealed the result of an early human study aimed at confirming the effects of decreasing senescent cells in the body as found in animal-based studies.

Preliminary research reveals benefit for DKD patients

Conducted by a team of Mayo Clinic researchers, the Phase I trial tested a senolytic regimen comprised of the cancer drug dasatinib (Sprycel) and plant-derived quercetin in nine patients with diabetes-related chronic kidney disease (DKD). Patients given the medication combination for a total of three days, after which the treatment was stopped.

Despite being completely eliminated from the system within a few days, the drugs and their effects appeared to last. According to study authors, the key markers of senescent cell burden decreased in both adipose tissue and skin biopsied from subjects 11 days after treatment completion, as were key circulating SASP factors compared with pre-treatment levels. The results remained persistent across measures – including blood, skin, and fat tissue analysis of senescent cell abundance.

Implications of senolytic therapy potential

Decreasing senescent cell numbers in two human tissues brings promise of growing understanding of senolytics and credibility of animal-based senolytic study results – which may be translatable to humans. Illustrating the mechanism of action discovered in prior research, the study implicates the potential of short-term dasatinib and quercetin treatment to improve physical functioning in patients with diabetes-related chronic kidney disease.

Senolytic therapies may provide efficacious treatment opportunities for an array of age-related diseases – chronic kidney disease, cancer, and neurodegenerative disorders – which place a significant burden on the healthcare system. Current knowledge suggests that senolytics may delay, prevent, or treat Alzheimer’s and Parkinson’s disease while enhancing longevity and improving the quality of later life.

However, the field is still new. As one of the first emerging clinical trials being reported, the latest study highlights the preliminary nature of its results. Fewer than 150 subjects have been treated, knowledge of adverse effects and potential long-term health repercussions is still growing and may further influence the development of senolytic therapy. Researchers caution against implementing senolytics into the practice setting until more information is obtained from additional clinical trials. Nonetheless, the study represents the first preliminary evidence in the promising field of senolytic therapies, verifying the potential benefit of their use on the human body.

Zuzanna Walter · November 9, 2021