Showing posts with label AntiAging. Show all posts
Showing posts with label AntiAging. Show all posts

Sunday, October 11, 2026

Common Drugs May Pave Way To Extending Human Lifespan

A commonly used drug may be the secret to a longer, healthier life, new research suggests. Aging is a complex process, which many of us consider to be an inevitable consequence of life on Earth. But thanks to modern technology, many scientists now consider aging to be a disease that we can treat, or at least delay. “You can think about life span like a candle it depends on how fast it burns,” Michael Lisanti, a professor in cancer research and metabolism…..Story continues….

Source: Newsweek

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Critics:

The heritability of lifespan is estimated to be less than 10%, meaning the majority of variation in lifespan is attributable due to differences in environment rather than genetic variation. However, researchers have identified regions of the genome which can influence the length of life and the number of years lived in good health.

For example, a genome-wide association study of 1 million lifespans found 12 genetic loci which influenced lifespan by modifying susceptibility to cardiovascular and smoking-related disease. The locus with the largest effect is APOE. Carriers of the APOE ε4 allele live approximately one year less than average (per copy of the ε4 allele), mainly due to increased risk of Alzheimer’s disease.

In July 2020, scientists identified 10 genomic loci with consistent effects across multiple lifespan-related traits, including healthspan, lifespan, and longevity. The genes affected by variation in these loci highlighted haem metabolism as a promising candidate for further research within the field. This study suggests that high levels of iron in the blood likely reduce, and genes involved in metabolising iron likely increase healthy years of life in humans.

A follow-up study which investigated the genetics of frailty and self-rated health in addition to healthspan, lifespan, and longevity also highlighted haem metabolism as an important pathway, and found genetic variants which lower blood protein levels of LPA and VCAM1 were associated with increased healthy lifespan.

In developed countries, the number of centenarians is increasing at approximately 5.5% per year, which means doubling the centenarian population every 13 years, pushing it from some 455,000 in 2009 to 4.1 million in 2050. Japan is the country with the highest ratio of centenarians (347 for every 1 million inhabitants in September 2010). Shimane Prefecture had an estimated 743 centenarians per million inhabitants.

In the United States, the number of centenarians grew from 32,194 in 1980 to 71,944 in November 2010 (232 centenarians per million inhabitants). Mental illness is reported to occur in approximately 18% of the average American population. The mentally ill have been shown to have a 10- to 25-year reduction in life expectancy.

Generally, the reduction of lifespan in the mentally ill population compared to the mentally stable population has been studied and documented. The greater mortality of people with mental disorders may be due to death from injury, from co-morbid conditions, or medication side effects. For instance, psychiatric medications can increase the risk of developing diabetes.

It has been shown that the psychiatric medication olanzapine can increase risk of developing agranulocytosis, among other comorbidities. Psychiatric medicines also affect the gastrointestinal tract; the mentally ill have a four times risk of gastrointestinal disease. As of 2020 and the COVID-19 pandemic, researchers have found an increased risk of death in the mentally ill.

The life expectancy of people with diabetes, which is 9.3% of the U.S. population, is reduced by roughly 10–20 years. People over 60 years old with Alzheimer’s disease have about a 50% life expectancy of 3–10 years. Other demographics that tend to have a lower life expectancy than average include transplant recipients and the obese.

Education on all levels has been shown to be strongly associated with increased life expectancy. This association may be due partly to higher income, which can lead to increased life expectancy. Despite the association, among identical twin pairs with different education levels, there is only weak evidence of a relationship between educational attainment and adult mortality.

According to a paper from 2015, the mortality rate for the Caucasian population in the United States from 1993 to 2001 is four times higher for those who did not complete high school compared to those who have at least 16 years of education. In fact, within the U.S. adult population, people with less than a high school education have the shortest life expectancies.

Preschool education also plays a large role in life expectancy. It was found that high-quality early-stage childhood education had positive effects on health. Researchers discovered this by analyzing the results of the Carolina Abecedarian Project, finding that the disadvantaged children who were randomly assigned to treatment had lower instances of risk factors for cardiovascular and metabolic diseases in their mid-30s.

Various species of plants and animals, including humans, have different lifespans. Evolutionary theory states that organisms which—by virtue of their defenses or lifestyle—live for long periods and avoid accidents, disease, predation, etc. are likely to have genes that code for slow aging, which often translates to good cellular repair. One theory is that if predation or accidental deaths prevent most individuals from living to an old age, there will be less natural selection to increase the intrinsic life span.

That finding was supported in a classic study of opossums by Austad;however, the opposite relationship was found in an equally prominent study of guppies by Reznick. One prominent and very popular theory states that lifespan can be lengthened by a tight budget for food energy called caloric restriction. Caloric restriction observed in many animals (most notably mice and rats) shows a near doubling of life span from a very limited calorific intake. Support for the theory has been bolstered by several new studies linking lower 

basal metabolic rate to increased life expectancy. That is the key to why animals like giant tortoises can live so long. Studies of humans with life spans of at least 100 have shown a link to decreased thyroid activity, resulting in their lowered metabolic rate. The ability of skin fibroblasts to perform DNA repair after UV irradiation was measured in shrew, mouse, rat, hamster, cow, elephant and human. It was found that DNA repair capability increased systematically with species life span

Since this original study in 1974, at least 14 additional studies were performed on mammals to test this correlation. In all, but two of these studies, lifespan correlated with DNA repair levels, suggesting that DNA repair capability contributes to life expectancy. See DNA damage theory of aging. In a broad survey of zoo animals, no relationship was found between investment of the animal in reproduction and its life span.

Life expectancy forecasting is usually based on one of two different approaches:

1. Forecasting the life expectancy directly, generally using ARIMA or other time-series extrapolation procedures. This has the advantage of simplicity, but it cannot account for changes in mortality at specific ages, and the forecast number cannot be used to derive other life table results. Analyses and forecasts using this approach can be done with any common statistical/mathematical software package, like EViews, R, SAS, Stata, Matlab, or SPSS.

2. Forecasting age-specific death rates and computing the life expectancy from the results with life table methods. This is usually more complex than simply forecasting life expectancy because the analyst must deal with correlated age-specific mortality rates, but it seems to be more robust than simple one-dimensional time series approaches. It also yields a set of age-specific rates that may be used to derive other measures, such as survival curves or life expectancies at different ages.

The most important approach in this group is the Lee-Carter model, which uses the singular value decomposition on a set of transformed age-specific mortality rates to reduce their dimensionality to a single time series, forecasts that time series, and then recovers a full set of age-specific mortality rates from that forecasted value. The software includes Professor Rob J. Hyndman’s R package called ‘demography’ and UC Berkeley’s LCFIT system

Louisiana law classifies abortion drugs as controlled, dangerous substances Voice of America 03:24 

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LongevityDrugs ,AntiAging ,HealthSpan ,LifeExtension ,Wellness ,HealthyLiving ,PharmaceuticalInnovation ,FutureOfMedicine ,AgeReversal ,Biohacking ,ScientificBreakthrough ,LongevityScience ,YouthfulLiving ,GetOldSlow ,SmartSupplements ,AgingWell ,MedicalResearch ,LongevityLifestyle ,HealthRevolution

Wednesday, July 29, 2026

Tweakments, Fillers and Botox How Much Does It Really Cost To Knock a Decade Off Your Face?

 Getty

Whether it’s friends, neighbours or celebrities posturing on social media – what people have had ‘done’ to their face is an irresistible topic of conversation. From Botox to fillers, to Morpheus 8 and profilo, its quite likely that what’s commonly known as ‘tweakments’ has piqued your curiosity. But how do you make sure you look youthful rather than slightly odd?…….Continue reading….

By:

Source: Telegraph

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Critics:

Botulinum toxin is used to treat a number of disorders characterized by overactive muscle movement, including cerebral palsy, post-stroke spasticity, post-spinal cord injury spasticity, spasms of the head and neck, eyelid, vagina, limbs, jaw, and vocal cords. Similarly, botulinum toxin is used to relax the clenching of muscles, including those of the esophagus, jaw, lower urinary tract and bladder, or clenching of the anus which can exacerbate anal fissure. Botulinum toxin appears to be effective for refractory overactive bladder

Strabismus, otherwise known as improper eye alignment, is caused by imbalances in the actions of muscles that rotate the eyes. This condition can sometimes be relieved by weakening a muscle that pulls too strongly, or pulls against one that has been weakened by disease or trauma. Muscles weakened by toxin injection recover from paralysis after several months, so injection might seem to need to be repeated, but muscles adapt to the lengths at which they are chronically held, so that if a paralyzed muscle is stretched by its antagonist, it grows longer, while the antagonist shortens, yielding a permanent effect.

In January 2014, botulinum toxin was approved by UK’s Medicines and Healthcare products Regulatory Agency for treatment of restricted ankle motion due to lower-limb spasticity associated with stroke in adults. In July 2016, the US Food and Drug Administration (FDA) approved abobotulinumtoxinA (Dysport) for injection for the treatment of lower-limb spasticity in pediatric patients two years of age and older.

Abobotulinumtoxin A is the first and only FDA-approved botulinum toxin for the treatment of pediatric lower limb spasticity. In the US, the FDA approves the text of the labels of prescription medicines and for which medical conditions the drug manufacturer may sell the drug. However, prescribers may freely prescribe them for any condition they wish, also known as off-label use.Botulinum toxins have been used off-label for several pediatric conditions, including infantile esotropia.

Botulinum toxin is also used to treat disorders of hyperactive nerves including excessive sweating, neuropathic pain, and some allergy symptoms. In addition to these uses, botulinum toxin is being evaluated for use in treating chronic pain. Studies show that botulinum toxin may be injected into arthritic shoulder joints to reduce chronic pain and improve range of motion. The use of botulinum toxin A in children with cerebral palsy is safe in the upper and lower limb muscles. 

While botulinum toxin is generally considered safe in a clinical setting, serious side effects from its use can occur. Most commonly, botulinum toxin can be injected into the wrong muscle group or with time spread from the injection site, causing temporary paralysis of unintended muscles. In at least three cases temporary diplopia was reported due to subcutenious injections for cosmetic purposes. Side effects from cosmetic use generally result from unintended paralysis of facial muscles.

These include partial facial paralysis, muscle weakness, and trouble swallowing. Side effects are not limited to direct paralysis, however, and can also include headaches, flu-like symptoms, and allergic reactions.[74] Just as cosmetic treatments only last a number of months, paralysis side effects can have the same durations. At least in some cases, these effects are reported to dissipate in the weeks after treatment.

Bruising at the site of injection is not a side effect of the toxin, but rather of the mode of administration, and is reported as preventable if the clinician applies pressure to the injection site; when it occurs, it is reported in specific cases to last 7–11 days.  When injecting the masseter muscle of the jaw, loss of muscle function can result in a loss or reduction of power to chew solid foods. With continued high doses, the muscles can atrophy or lose strength; research has shown that those muscles rebuild after a break from Botox.

Side effects from therapeutic use can be much more varied depending on the location of injection and the dose of toxin injected. In general, side effects from therapeutic use can be more serious than those that arise during cosmetic use. These can arise from paralysis of critical muscle groups and can include arrhythmia, heart attack, and in some cases, seizures, respiratory arrest, and death. Additionally, side effects common in cosmetic use are also common in therapeutic use, including trouble swallowing, muscle weakness, allergic reactions, and flu-like syndromes.

In response to the occurrence of these side effects, in 2008, the FDA notified the public of the potential dangers of the botulinum toxin as a therapeutic. Namely, the toxin can spread to areas distant from the site of injection and paralyze unintended muscle groups, especially when used for treating muscle spasticity in children treated for cerebral palsy. In 2009, the FDA announced that boxed warnings would be added to available botulinum toxin products, warning of their ability to spread from the injection site.

However, the clinical use of botulinum toxin A in cerebral palsy children has been proven to be safe with minimal side effects. Additionally, the FDA announced name changes to several botulinum toxin products, to emphasize that the products are not interchangeable and require different doses for proper use. Botox and Botox Cosmetic were given the generic name of onabotulinumtoxinA, Myobloc as rimabotulinumtoxinB, and Dysport retained its generic name of abobotulinumtoxinA.

In conjunction with this, the FDA issued a communication to health care professionals reiterating the new drug names and the approved uses for each. A similar warning was issued by Health Canada in 2009, warning that botulinum toxin products can spread to other parts of the body. Botulinum toxin exerts its effect by cleaving key proteins required for nerve activation. First, the toxin binds specifically to presynaptic surface of neurons that use the neurotransmitter acetylcholine.

Once bound to the nerve terminal, the neuron takes up the toxin into a vesicle by receptor-mediated endocytosis. As the vesicle moves farther into the cell, it acidifies, activating a portion of the toxin that triggers it to push across the vesicle membrane and into the cell cytoplasm. Botulinum neurotoxins recognize distinct classes of receptors simultaneously (gangliosides, synaptotagmin and SV2).

Once inside the cytoplasm, the toxin cleaves SNARE proteins (proteins that mediate vesicle fusion, with their target membrane bound compartments) meaning that the acetylcholine vesicles cannot bind to the intracellular cell membrane, preventing the cell from releasing vesicles of neurotransmitter. This stops nerve signaling, leading to flaccid paralysis. 

The toxin itself is released from the bacterium as a single chain, then becomes activated when cleaved by its own proteases. The active form consists of a two-chain protein composed of a 100-kDa heavy chain polypeptide joined via disulfide bond to a 50-kDa light chain polypeptide.

Letybo- letibotulinumtoxina-wlbg injection, powder, lyophilized, for solution”.

Therapeutic Goods Administration (TGA)

Relfydess (relabotulinumtoxinA, purified Botulinum toxin type A)”.

FDA-sourced list of all drugs with black box warnings (Use Download Full Results and View Query links.)”.

 

Nuceiva (PPD Australia Pty Ltd)”. 

Nuceiva prabotulinumtoxinA 100 Units Powder for Solution for Injection vial (381094)”. 

Prescription medicines: registration of new chemical entities in Australia, 2014″. 

 Therapeutic Goods Administration (TGA)”.

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Tweakments ,Fillers ,Botox ,BeautyTips ,AntiAging ,SkinCare ,CosmeticEnhancement ,FacialRejuvenation ,YouthfulGlow ,AestheticTreatments ,DermalFillers ,BotoxCosmetic ,LookGoodFeelGood ,BeautyTrends ,SelfCare ,GlowingSkin ,ConfidenceBoost ,SmoothSkin ,EnhanceYourBeauty ,RadiantComplexion, BeautyProduts, PlasticSurgery, Surgery, SkinCareProducts

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How To Battle Boredom At Work

Vladimir Vladimirov/E+ via Getty Images Though neuroscience suggests that boredom can be good for us , we all try to avoid it. Even the most...