Arterial Stiffening Correlates with Raised Calcium Levels
Researchers here note a correlation between age-related arterial stiffening, likely the primary cause of hypertension, and rising levels of calcium in the blood. It is an open question as the degree to which calcification contributes to stiffening of blood vessel tissues in comparison to the contribution of cross-links to that stiffening. The processes leading to calcification are arguably not as comprehensively understood as those of cross-linking, but at least some of it is a secondary consequence of specific mechanisms - such as inflammation - in blood vessel walls that lead to atherosclerosis.
The progression of arterial stiffness is accelerated by aging, although the underlying mechanisms have not yet been clarified. This prospective observational study was conducted to clarify whether longitudinal changes in the serum calcium/phosphate levels are associated with the accelerated progression of arterial stiffness with age. In a cohort of employees at a construction company (1507 middle-aged Japanese men), the serum calcium/phosphate levels and brachial-ankle pulse wave velocity (baPWV) were measured at the start and at the end of a 3-year study period.A general linear model multivariate analysis revealed a significant interaction of the 2 factors - age and longitudinal changes of the serum calcium levels (delCa) during the follow-up period - on the longitudinal changes of the baPWV during the study period (delPWV). The delCa was significantly correlated with the delPWV even after adjustments for covariates in subjects aged ≥48 years. The delPWV in subjects aged ≥48 years with the delCa in the upper tertile was significantly larger than that in the other groups even after adjustments for covariates. Thus the association between the arterial stiffness and serum calcium levels differed with age. Pathophysiological abnormalities related to increased serum calcium levels appeared to be associated with accelerated progression of arterial stiffness with age.
Link: http://dx.doi.org/10.1016/j.atherosclerosis.2015.10.002
Yes, as the hormonal signal (estrogen in females) is lost to hold calcium in bone, it is deposited from bone to arterial wall which results in stiffening. The effort to consume supplemental calcium is futile --like pouring calcium in a barrel with a hole in the bottom. Osteoporosis is not a calcium deficiency it is a hormone deficiency. Numerous studies now show supplemental calcium among post-menopausal women increases the risk of a heart attack. Around $2 billion of calcium supplements are sold annually, sold primarily to older misdirected women. This also speaks for the misdirection of statin drugs and cholesterol control. Nature provides four anti-calcifying agents: magnesium, vitamins K2 and D3 and IP6 phytate from bran.
AGE crosslinks are known to cause increased levels of TGF-beta which spurs stem cell dysfunction and inhibition of said factor reverses this situation as the conboys have demonstrated. So would removing the crosslinks directly mediate this issue?
It seems the more I research the SENS proposal to remove crosslinks would clear a slew of problems up in particular stem cell decline and loss of signalling due to TGF-beta increasing and increasing inflamation and B2M etc...
So the question is if we remove crosslinks thus reducing TGF-beta levels would we potentially mitigate this calcium issue too? After all the stem cells would be helping maintain and repair more efficiently.
I might be wrong but removing Glucosepane should improve stem cell signalling and allow better clearing of waste which could perhaps include this calcium?
Unless I have the wrong end of the stick here I am starting to see the staggering potential SENS proposes here by removing Glucosepane.
I am hoping to get ALK5 inhibition tested soon in aged mice which will show what SENS gets for free if they remove Glucosepane crosslinks. It is the hope to test Alk-5 ala conboys alone and in combination with Senlyotic agents Dasatinib & Quercetin.