HEALTH TRAIN EXPRESS
Mission: To promulgate health education across the internet:
Follow or subscribe to Health Train Express as well as Digital Health Space for all the updates for health policy, reform, public health issues. Health Train Express is published several times a week.Subscribe and receive an email alert each time it is published. Health Train Express has been published since 2006.
These factors contribute to the ongoing challenges faced by physicians in maintaining their practices and providing necessary care.
6 Sources
How are we still in business> The answer is, we are not. Individual practice is about gone. Medicine has gone coporate. Individual doctors or small groups have been. forced to sell to hospitals, venture capitalists,or whoever is foolish enough to purchase their practices. Gross income looks abundant, but the details are in payables, overhead, and bureaucracy from Medicare, and Private payers.
Key Medicare Incentive Programs
Merit-based Incentive Payment System (MIPS): The main component of the QPP, MIPS scores clinicians across four areas:
Quality: Reporting on patient outcomes and measures.
Cost: Tracking patient-specific costs.
Advancing Care Information (ACI): Meaningful use of Electronic Health Records (EHRs).
Clinical Practice Improvement Activities (CPIA): Participation in activities improving care.
Outcome: Positive scores can lead to bonus payments, while poor scores can result in penalties (up to 9% adjustments).
Promoting Interoperability Program (formerly EHR Incentive Program): Incentivizes hospitals and eligible professionals to adopt and meaningfully use certified EHR technology.
Electronic Prescribing (eRx) Incentive Program: Rewards successful electronic prescribing for Medicare Part B beneficiaries and penalizes non-prescribers.
The Medicare budget is balanced by reducing payments to providers and incentivizing Medicare Advantage plans. The insurance lobby rules Congress.
By Ben Shenhar, Glen Pridham, ThaÃs Lopes De Oliveira, et al.Science29 Jan 2026
The shapes of aging
Life span varies strikingly across the tree of life. Baker’s yeast survive for days, fruit flies for weeks to months, bowhead whales for more than two centuries, and bristlecone pines for millennia (1). Comparative studies have uncovered conserved biological mechanisms that regulate aging (2), leaving little doubt that genetics places strong constraints on how long organisms live. Nevertheless, classical aging experiments in animals show that there is considerable variability in life span, even among isogenic littermates, indicating that there’s more to aging than genetics (3). Indeed, population-level studies on twins estimate that the heritability of human life span may be as little as 10 to 25% (4, 5), as do studies on pedigrees (6, 7). The prevailing view is that individual longevity is influenced largely by environmental factors and lifestyle. On page 504 of this issue, Shenhar et al. (8) challenge this notion, reporting that human heritability is 55%, considerably higher than previous estimates.
Shenhar et al. reexamined how mortality is conceptualized and quantified. In their framework, life span reflects the combined influence of intrinsic mortality, which is driven by biological aging processes, and extrinsic mortality, which arises from external hazards such as infections or accidents. Because extrinsic deaths may occur independently of inherited differences in the rate of biological aging, the causes of extrinsic death introduce variance unrelated to genetic contributions to intrinsic aging. As a result, the authors conclude that analyses that do not distinguish intrinsic from extrinsic mortality tend to systematically underestimate the heritability of aging, even when substantial genetic differences in intrinsic aging processes are present. Across human twin-cohort datasets, Shenhar et al. found that heritability estimates increased as extrinsic mortality declined and rose further when extrinsic deaths were mathematically removed from their model. Accordingly, they found that birth cohorts with progressively lower extrinsic mortality showed a parallel increase in estimated life-span heritability. Taking these observations into consideration, Shenhar et al. arrived at an intrinsic heritability of 55%.
Why might previous estimates be wrong? Although susceptibility to external hazards can be genetically influenced, mortality in historical human populations was largely dominated by variation in exposure, medical care, and chance. Many classical life-span studies therefore rely on cohorts born during periods when premature death from external causes was common. Such early deaths truncate survival independently of biological aging, reducing similarity among genetically related individuals and suppressing heritability estimates. Further, some studies have also relied on data spanning several hundred years with potentially poor data quality. The effect is that additional variance is introduced that masks correlations.
These considerations carry important implications. If life span is largely fixed by genetics, then the scope for influencing the rate of aging is limited, particularly for lifestyle interventions. Conversely, if genetic contributions are minimal, efforts to understand aging through genetic approaches are difficult to justify. Clarifying the role of inherited variation in aging-related mortality is therefore central to both biological understanding and societal expectations.
Several observations suggest that inherited factors make a meaningful contribution to the rate of aging. Rare genetic disorders marked by accelerated aging lead to early onset of multiple age-associated pathologies and markedly shortened life span, demonstrating that perturbations in single genes can substantially alter the rate of aging (9). Individuals with exceptionally long-lived relatives tend to experience lower mortality across adulthood, indicating that inherited factors contribute to such longevity (10). Consistent with this, twin studies have shown greater similarity in life span between identical twins than between fraternal twins, pointing to a genetic contribution to longevity (11). Genome-wide association studies have identified numerous variants associated with human life span and age-related traits, yet their combined explanatory power remains limited (12).
Another interesting finding of Shenhar et al. is that different diseases show different levels of heritability. They note that cardiovascular disease and dementia display higher heritability than cancer, an observation previously described in other patient cohorts (13, 14). A key ramification of this finding is that cancer is either more extrinsically influenced or more stochastic than other chronic diseases. Indeed, it makes sense that stochastic processes could drive rare cellular events leading to malignant transformation.
By reframing life-span heritability through the lens of intrinsic mortality, the study of Shenhar et al. has important consequences for aging research. A substantial genetic contribution strengthens the rationale for large-scale efforts to identify longevity-associated variants, refine polygenic risk scores, and link genetic differences to specific biological pathways that regulate aging. It also suggests that the limited success of previous genome-wide association studies may reflect phenotypic noise introduced by extrinsic mortality rather than inherently weak genetic effects. Further, the findings of Shenhar et al. agree with the observed 50% heritability of other complex traits (15). Perhaps this means that intrinsic rates of aging are tightly optimized through evolution, in line with other traits such as cognitive function and metabolism.
In Summary. Only about 50% of aging is heritable. Our next post will cover extrinsic causes for biological aging
It happens to all of us: A random backache, a wrinkle, a new slang phrase you have no idea the meaning of — something that leads us to question, “when did I start to get so old?” As a mother of teenagers, I of course have had my own experiences, but as a family medicine doctor, I often help patients navigate the part that comes after: The “how do I make it stop?” phase.
Mona Brownfield, MD, Family Medicine Provider
Sun Exposure
Now, don’t get me wrong. Daily sunlight can have quite a few advantages for our mental and physical health, but we don’t need that much sun to experience the benefits — ten minutes is plenty enough to get our recommended vitamin D. Anything beyond, without proper sun protection, starts to put our skin at risk for cancer and premature aging.
Aging Effects: Paper-Thin Skin, Sagging Skin, Dark Spots
One of the biggest misconceptions I hear is sun exposure just makes your skin thick and leathery, when in fact, the opposite can be just as true. Too much sun exposure can break down our skin’s elasticity causing it to be thick like leather or thin like tissue paper. Not only that, UV rays can damage collagen proteins in the skin, leading to sagging or loose skin, and speed up the production of melanin (cells that give the skin its color) causing dark age spots.
How to Prevent It
Sunscreen. I know, that’s not the most exciting answer, especially with a multibillion-dollar skin care industry, but sunscreen and other forms of sun protection are the best way to prevent sun damage and premature aging. I’ve found the easiest way to make sure I’m protecting my skin is to build it into my morning routine. There are a lot of creams and makeup products available with a sun protection factor (SPF) or 35 or more that can make it an easy integration. There’s even clothing with SPF ratings as well. Just remember to protect your hands — they’re easy to forget but can be one of the first spots to age.
Smoking
The health reasons alone should be enough to avoid smoking — after all, it’s considered the number one cause of preventable disease, disability and death according to the World Health Organization — but in terms of premature aging, smoking is definitely not one to preserve our youth.
Not only does smoking break down our skin’s elasticity and strength, it can shrink the size of our blood vessels and limit the oxygen our skin receives, leading to wrinkled, sagging skin. We don’t often consider DNA in our hair follicles to be a living thing, but toxic chemicals found in cigarettes can actually damage that DNA and cause hair to thin, turn gray or fall out altogether. And nicotine, the most popular chemical associated with tobacco, is the reason for stained teeth and skin, leading to that aged yellow look.
How to Prevent It
Don’t smoke. I know for some, that’s easier said than done, but there are plenty of resources out there designed to help people break the habit, including MU Health Care’s free tobacco cessation program. Try to find one, or multiple, that can fit your needs and offer support.
Exposure to Loud Noise
Long-lasting exposure to loud noises isn’t usually one that’s on my patients’ radar until they start to experience its adverse effects on their hearing. When I say loud noises, I’m not just talking about rock concerts and industrial machinery, which are usually the first things people think of; I’m talking about boats, lawn mowers, movie theaters and even vacuuming.
Aging Effects: Hearing Loss
Exposure to loud noise can damage the little hair cells in our ears that carry sound to our brain. Once those hairs are broken, they can’t regrow, and the less hairs we have, the worse our hearing.
How to Prevent It
Be sure to wear earplugs or other protective gear when dealing with any long-lasting volumes that are louder than a normal conversation. When listening to music with headphones, do a quick test beforehand to see if the volume is too loud. While the music is playing, hold your headphones as far away from your ears as possible. If you can still hear the music, it’s too loud.
Stress
Stress has a fascinating way of impacting our bodies, whether it’s the more obvious physical stress or the subtler emotional stress. In terms of short-term effects, stress can boost our energy and focus. Think about the last time you had a quick deadline to meet — did the adrenaline kick in to get it done? While stressful, a moment of stress here and there isn’t problematic. It’s the chronic, long-term stress that can wear our bodies down and lead to premature aging.
Aging Effects: Memory Loss, High Blood Pressure, Aged Immune System
Research has found the hormones produced with chronic stress can age our brain and immune systems. Those who are constantly stressed have higher instances of dementia and memory loss, as well as more damaged cells within their immune systems. Stress also lends itself to high blood pressure, making you more susceptible to heart disease and other conditions typically found in older populations.
How to Prevent It
Managing stress is all about mindfulness. Try to regularly quiet your mind with activities like yoga or meditation. If you’re feeling overwhelmed with the to-do list, reach out for help and delegate the tasks you can give up. Another way to reduce stress is by looking for positivity in every situation — make a list of three things you’re thankful for or give a silver lining for every negative thought you have. Getting outside, exercising and being social with friends are also great ways to reduce stress.
The Medicare budget is balanced by reducing payments to providers and incentivizing Medicare Advantage plans. The insurance lobby rules Congress.
