How LED Lighting is Draining Focus, Energy, and Mental Calm | by Czarif | ILLUMINATION’S MIRROR | Feb, 2026 | Medium

Much of your brain is devoted to signals from the retina. Visual input is one of the greatest senses providing stimuli for the fight or light reflexes.  Animals also have these pathways because survval means escaping from predators.

 LEDs don’t just hurt your eyes. They quietly drain your nervous system.

Your eyes are not just cameras. They are sensors wired straight into the brain’s control centers.

Inside the retina are specialized cells called intrinsically photosensitive retinal ganglion cells. These cells do not help you see objects. They help regulate alertness, hormone release, body temperature, and the sleep wake cycle. They send signals directly…

Where do they go?

Besides the primary pathway to the visual cortex (via the Lateral Geniculate Nucleus), visual stimuli are sent to several subcortical structures for specialized processing, including reflex control, circadian rhythms, and rapid emotional responses. 

Key brain regions receiving visual input include:

Superior Colliculus (Midbrain): This structure controls rapid, reflexive eye and head movements (saccades) to direct gaze toward a visual stimulus. It is heavily involved in visual attention and orientation, particularly for stimuli in the peripheral field.

Suprachiasmatic Nucleus (Hypothalamus): This is the body's internal clock, which regulates circadian rhythms and sleep/wake cycles based on light intensity.

Pretectum (Midbrain): This area is responsible for the pupillary light reflex, managing the constriction of the pupil in response to bright light.

Amygdala (Limbic System): A direct, "fast-track" pathway from the retina (via the pulvinar nucleus of the thalamus) allows the amygdala to receive raw visual information quickly—often before the cortex conscious processes it—enabling rapid detection of potential threats, such as angry or fearful faces.

Pulvinar Nucleus (Thalamus): This nucleus connects with the superior colliculus and the amygdala, contributing to the "subcortical pathway" that enables rapid, non-conscious "blindsight" and emotional processing. 

Cortical Pathways Beyond V1

Once visual information reaches the primary visual cortex (V1), it is distributed to higher-order areas via two main streams: 

Dorsal Stream ("Where" or "How" pathway): Travels to the parietal cortex for spatial awareness, motion processing, and guiding motor actions.

Ventral Stream ("What" pathway): Travels to the inferior temporal lobe for object recognition, face recognition, and color processing. 

 

 

Medicare Expense Constantly Rising, Why?

Even as Medicare Expenses rise and inflation causes increased cost, incresasing premiums, physician reimbursement are reduced annually. 

Physician reimbursements have been reduced annually due to several factors:

• The 2025 Medicare Physician Fee Schedule introduced a 2.83% cut, marking the fifth consecutive year without meaningful congressional action to address declining reimbursement rates. 

  2
• This reduction is attributed to the expiration of a temporary increase in payment rates and the expiration of the Medicare Access and CHIP Reauthorization Act, which froze fee schedule inflation updates until 2026. 

  2
• Over the past two decades, physician payments have declined significantly, with a 33% drop since 2001 when adjusted for inflation, while practice costs have risen sharply. 

  1
• The ongoing debate focuses on balancing cost control with fair compensation and ensuring access to care for Medicare beneficiaries. 

  2

  
  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.

Medical Economics

Medicare reimbursement rates explained: Why they keep declining, and ...

Recent Trends in GLP-1 Use and Spending in Medicare | KFF

Rethinking the heritability of aging

The genetic contribution to human longevity is greater than previously thought

Daniela Bakula and Morten Scheibye-KnudsenAuthors Info & Affiliations

Science

29 Jan 2026

Vol 391, Issue 6784

p. 448

DOI: 10.1126/science.aee3844

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Related Research Article

Heritability of intrinsic human life span is about 50% when confounding factors are addressed

By Ben Shenhar, Glen Pridham, Thaís 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