Lifeboat Foundation

Having multiple conditions that affect the heart are linked to a greater risk of dementia than having high genetic risk, according to a largescale new study.

Led by Oxford University and the University of Exeter, the study is among the largest ever to examine the link between several heart-related conditions and dementia, and one of the few to look at the complex issue of multiple health conditions.

Published in The Lancet Healthy Longevity, the paper looked at data from more than 200,000 people, aged 60 or above, and of European ancestry in UK Biobank. The international research team identified those who had been diagnosed with the cardiometabolic conditions diabetes, stroke, or a heart attack, or any combination of the three, and those who went on to develop dementia.

Osaka University researchers discovered that adjusting lifestyle behaviors can have a significant impact on lifespan, even in those with chronic health issues.

Ever since the beginning of civilization, humans have wanted to live longer. Whether it be the Fountain of Youth, Gilgamesh’s secret plant of immortality, or the elixir of life, the idea of immortality is incredibly prevalent in humanity’s oldest and most well-known stories.

Unfortunately, immortality is only a myth. The average lifespan in the United States is nearly 79 years and it is unlikely to increase dramatically in the next few years. Still, scientists have been researching how to increase our longevity and have found promising results.

The Saudi royal family is determined to slow down and even reverse aging and is set to invest $1 billion a year to do so.

New research has uncovered how genetic changes that accumulate slowly in blood stem cells throughout life are likely to be responsible for the dramatic change in blood production after the age of 70.

The study, by scientists at the Wellcome Sanger Institute, the Wellcome-MRC Cambridge Stem Cell Institute and collaborators, has been published in the journal Nature.

Longevity. Technology: Has our understanding of one of the mechanisms of aging taken a quantum leap? Molecular damage accumulates throughout our lives, gradually increasing year-on-year as we suffer telomere attrition, mutation, epigenetic change and oxidative and replicative stress. It’s a double whammy as our ability to repair this damage also declines as we age, but given the gradual nature of these processes, why, as the paper authors themselves put it, “Is there an abrupt increase in mortality after 70 years of age? [1]”.

As people across the globe look forward to longer life expectancies, malignant cancers continue to pose threats to human health. The exploration and development of immunotherapy aims to seek new breakthroughs for the treatment of solid tumors.

The successful establishment of anti-tumor immunity requires the activation, expansion and differentiation of antigen-specific lymphocytes. This process largely depends on specific interactions between various T cells and antigen-presenting cells (APCs) in the body. However, existing tumor vaccines, such as neoantigen vaccines and various vector vaccines, all rely on random interactions with APCs in the body. Furthermore, inappropriate interactions may lead to the silencing of other immune responses.

Although immune checkpoint-based immunotherapy has been shown to have great potential, only a small proportion of patients fully respond to this therapy, and the relevant molecular mechanisms need to be further explored. This delivery method is however complex and inefficient.

Methylation clocks are taking the longevity community by storm, but why are they so useful?

Do you know how old you really are? I am not doubting your ability to remember your birthday or questioning the honesty of your parents. Do you, on a fundamental level, know how ‘old’ your body truly is? Now surely that is just the same as the number of years you have been around, which would be your chronological age? Well in reality the answer to how ‘old’ your body is comes down to much more than simply how long you have been around for.

Allow me to explain by falling back to the commonly used automobile analogy. Let’s imagine I bought two identical Ford Escorts in 1982, and then proceeded to place one of them inside a time capsule, where it would be kept at a constant temperature in a non-reactive atmosphere. I then proceeded to drive the second car for the next 40 years. Over that 40 years, this car is going to experience wear and tear, and will most likely break down several times which will require mechanical intervention (analogous to medical intervention). Now, after this 40-year period I am going to take the first car out of storage and compare the two cars side by side. Which car is in the better condition? Well, the car that was preserved, obviously. Which car is likely to last the longest from that point onward? Well, the car which has been preserved, obviously.

“Functional mutations in the growth hormone pathway” meaning it is not active. What’s good for you as a youngster might not be good for you when you’re old.

Dr Nir Barzilai reveals what the longevity genes project found on why Centenarians live longer, not the longevity genes, not healthy lifestyles in this clip.

Continue reading “NOT The Longevity Genes!? Surprising Facts WHY Centenarians LIVE LONGER | Dr Nir Barzilai Clips” »

The oil kingdom fears that its population is aging at an accelerated rate and hopes to test drugs to reverse the problem. First up might be the diabetes drug metformin.

Circa 2021 Immortality of the male genitalia in humans.

Cavernous nerve injury (CNI) is the main cause of erectile dysfunction (ED) following pelvic surgery. Our previous studies have demonstrated that transplantation of different sources of mesenchymal stem cells (MSCs) was able to alleviate ED induced by CNI in rat models. However, little is known about the therapeutic effects of human gingiva-derived MSCs (hGMSCs) in CNI ED rats. Herein, we injected the hGMSCs around the bilateral major pelvic ganglia (MPG) in a rat model of CNI and evaluated their efficacy. The results showed that treatment of hGMSCs could significantly promote the recovery of erectile function, enhance smooth muscle and endothelial content, restore neuronal nitric oxide synthase (nNOS) expression, and attenuate cell apoptosis in penile tissue. Moreover, penile fibrosis was significantly alleviated after hGMSC administration. In addition, potential mechanism exploration indicated that hGMSCs might exert its functions via skewed macrophage polarity from M1 toward M2 anti-inflammatory phenotype. In conclusion, this study found that transplantation of hGMSCs significantly improved CNI-related ED, which might provide new clues to evaluate their pre-clinical application.

There are many causes of erectile dysfunction (ED), which include psychological factors, neurological disorders (such as multiple sclerosis, temporal lobe epilepsy, and cavernous nerve injury), and vasculogenic disorders (such as atherosclerosis, hypertension, and diabetes mellitus). Neurogenic sexual dysfunction makes up about 10–19% in all causes of erectile dysfunction. Neurotic erectile dysfunction is one of most important complications after radical prostatectomy and rectectomy, owing to intraoperative damage of the pelvic cavernous nerve (CN). It affects not only the physical but also mental health in postoperative patients. Despite the improvement of nerve-sparing techniques, the incidence of neurotic ED still has no substantial improvement. The incidences of ED range from 75 to 80% after pelvic surgery (Schauer et al., 2015).