You don't have to attack me first thing in the morning

Older adults with depression are actually aging faster than their peers, UConn Center on Aging researchers report.

“These patients show evidence of accelerated biological aging, and poor physical and brain health,” which are the main drivers of this association, says Breno Diniz, a UConn School of Medicine geriatric psychiatrist and author of the study, which appears in Nature Mental Health on March 22.

Diniz and colleagues from several other institutions looked at 426 people with late-in-life depression. They measured the levels of proteins associated with aging in each person’s blood. When a cell gets old, it begins to function differently, less efficiently, than a “young” cell. It often produces proteins that promote inflammation or other unhealthy conditions, and those proteins can be measured in the blood. Diniz and the other researchers compared the levels of these proteins with measures of the participants’ physical health, medical problems, brain function, and the severity of their depression.

To their surprise, the severity of a person’s depression seemed unrelated to their level of accelerated aging. However, they did find that accelerated aging was associated with worse cardiovascular health overall. People with higher levels of aging-associated proteins were more likely to have high blood pressure, high cholesterol, and multiple medical problems. The accelerated aging was also associated with worse performance on tests of brain health such as working memory and other cognitive skills.

https://www.nature.com/articles/s44220-023-00033-z

In a several decade study made by Stamford I think they concluded that people who were positive about becoming old lived on average 7.8 years longer than those negative about it.

Mind over matter, its literally about perspective.

Yes I recognize that I will die early.

Limitations per abstract:

“As highlighted, our study’s main limitation is that we did not include a healthy control group and did not collect longitudinal data. Therefore, we cannot test for causal relationships. Furthermore, future studies should build on our findings and use causal statistical models to examine the relationship among LLD, physical health and the SASP index.

In addition, our analyses were limited by the nature of our data. For instance, the number of participants from under-represented groups was too small, and we could not assess the influence of race or ethnicity on the SASP index. However, previous studies have suggested associations between race/ethnicity and physical health or LLD65.

Also, we did not have information on socioeconomic status except for the indirect measure of years of education.

Similarly, we did not have information on childhood adversity or past traumas, which might mediate the relationship between neuropsychiatric symptoms and ageing. While we included a large selection of carefully pre-selected clinical measures, other variables might be relevant to capture the clinical heterogeneity of LLD. In particular, more detailed information on smoking and alcohol consumption, other physical comorbidities (for example, cerebrovascular disease) and general markers of quality of life, activities of daily living and physical activities should be included in future studies66.”

They used 22 protein levels to assess an aging index called SASP:

Here are the 22 proteins:

> As in our previous studies28,30, the 22 proteins included in the SASP index used in the present study are IGFBP-6, IGFBP-2, MIP-1β, IL-1β, GMC-SF, PLGF, Angiogenin, MIF-1, MIP-1α, Gro-α, IL-6, MCP-4, Gp130, ICAM-1, MCP-1, IL-8, MIP-3 α, Osteoprotegerin, TIMP-1, uPAR, TNFRI and TNFRII. The raw values were log transformed and standardized to z scores, and the SASP index for each participant was calculated

> Cellular senescence11 has emerged as a pivotal hallmark of the biology of ageing. It is a complex stress response in which cells irreversibly lose their proliferative capacity, become resistant to apoptosis12 and develop a multicomponent secretory phenotype13, referred to as the senescence-associated secretory phenotype (SASP)12. The SASP includes proteins involved in cycle control, intercellular communication, the immune-inflammatory response and tissue remodelling14. Under non-pathological conditions, SASP proteins are essential for embryonic development and tissue patterning throughout life15. However, the accumulation of senescent cells and the increased secretion of SASP proteins with age is linked to tissue deterioration and the emergence of physical disorders prevalent in older adults16. Human and animal studies found that the increased expression of SASP proteins drives multiple age-related phenotypes, such as atherosclerosis17, osteoarthritis18, cancer19, kidney dysfunction20 and a shortened health span21. In humans, an increase in SASP proteins is related to obesity, cardiometabolic dysregulation22 and frailty14. Several studies characterized the role of cellular senescence and SASP proteins in the brain. Aged microglia, astrocytes and neurons exhibit various features of senescence, including the expression of SASP proteins23,24,25.

> While the cellular source of SASP proteins is unknown, some evidence suggests that the SASP index is relevant to brain health and that brain cells express SASP proteins23,24,25. In ageing and psychiatric disorders, the blood–brain barrier permeability is increased71, leading to an enhanced passage of proteins. Some studies suggest that plasma from old mice accelerates brain ageing in young mice72, and senolytic interventions targeting the periphery alleviate the effect of SASP proteins on the brain71.

Unknown !

Blood brain barrier permeability increased.

I feel personally attacked.

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I recommend researching autophagy

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