Aging

Cawthorn et al examined the telomeres of 143 people over the age of 60.¹ Telomeres are DNA sequences on the ends of chromosomes that are gradually lost as cells replicate. The team found that those with shorter telomeres in blood DNA had significantly poorer survival, attributable in part to a 3.18-fold higher mortality rate from heart disease and, tellingly, a 8.54-fold higher mortality rate from infectious disease.

A number of the sickest patients on the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis., who are killing intracellular bacteria at the fastest rate possible, take over three years to completely recover their health. This hints at the large amount of pathogen-altered DNA that many people, even those who are not yet displaying the hallmarks of Th1 disease, are carrying.

Vitamin D3 homeostasis regulates physiological aging as demonstrated in this study, “Premature aging in vitamin D receptor mutant mice.”²

VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response. knockout mice – that is, mice that have their Vitamin D Receptors removed – show signs of premature aging:

Overall, VDR KO mice showed several aging related phenotypes, including poorer survival, early alopecia, thickened skin, enlarged sebaceous glands and development of epidermal cysts…. Unlike the wildtype controls, VDR KO mice lose their ability to swim after 6 months of age. Expression of all the genes was lower in old VDR KO mice, but only NF-kappaBA protein that stimulates the release of inflammatory cytokines in response to infection, Fgf-23, p53 and IGF1R were significantly lower. Since the phenotype of aged VDR knockout mice is similar to mouse models with hypervitaminosis D(3), our study suggests that VDR genetic ablation promotes premature aging in mice, and that vitamin D(3) homeostasis regulates physiological aging.

T. Keisala et al.³

As far as I can see, Th1 pathogens start to dictate the 'health' of just about everyone as they age. If you draw a graph of 25-DThe vitamin D metabolite widely (and erroneously) considered best indicator of vitamin D "deficiency." Inactivates the Vitamin D Nuclear Receptor. Produced by hydroxylation of vitamin D3 in the liver. levels vs age, they drop steadily after age 40. Something is happening, even during 'healthy aging', that we really ought to understand a little more :)

There is a branch of medicine which is starting to look at Immunity and Aging. Here is a short letter I recently wrote to the editor of one of the journals: http://www.immunityageing.com/content/3/1/12/comments

Trevor Marshall, PhD

Study shows that most older adults have signs of brain damage http://bacteriality.com/2008/01/04/brain/

Aging is a super-category. We’ve gradually lumped together more and more symptoms under the category of natural aging. Many of these symptoms are the same as those caused by diseases that surely have an infectious cause. In that sense, you could view much of what we now call aging as an incapacitating illness that leads to a decrease in function. We know that inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. and the interaction of the immune system with pathogens can destroy tissue. So it’s not surprising that the tissues of a person who harbors a lot of pathogens would age earlier and alter their biological structure earlier in life. I do believe it is inevitable that people will eventually die of old age, but I suspect that this should generally happen when they are 80-100 years old. But we are increasingly seeing signs of aging-related diseases in people who are much younger.

Paul Ewald, Bacteriality interview

There is speculation that some persistent bacteria may be associated with the aging process, especially since diseases and symptoms of aging from cancer and cardiovascular disease to aches and pains– basically everything that makes getting older such a drag– are at their essence, inflammatory conditions. Because bacteria cause the immune system to mount a constant inflammatory response, the presence of L-formDifficult-to-culture bacteria that lack a cell wall and are not detectable by traditional culturing processes. Sometimes referred to as cell wall deficient bacteria. or other Th1 pathogens may very well be responsible for aging skin, wrinkles, and the wear and tear on organs.

People who haven’t completed the MP consider it inevitable that as they age, they will need to stock up on any number of medications including thyroid medications, cardiac meds, statins, NSAIDS, B/P meds, etc. But people who have reached the later stages of the MP see no reason why they cannot take their level of healing to a maximum – to a point where they will never need these medications and may experience great health during their elder years.

Amy Proal, Top 14 misconceptions about the MP: addressed and explained

Mice without a VDR have been shown to age prematurely.⁴

Vitamin D and aging.

Tuohimaa P. Medical School, 33014 University of Tampere, Finland. pentti.tuohimaa@uta.fi Recent studies using genetically modified mice, such as FGF23-/- and Klotho-/- mice that exhibit altered mineral homeostasis due to a high vitamin D activity showed features of premature aging that include retarded growth, osteoporosis, atherosclerosis, ectopic calcification, immunological deficiency, skin and general organ atrophy, hypogonadism and short lifespan. The phenotype reversed by normalizing vitamin D and/or mineral homeostasis. Thus, hypervitaminosis D due to an increased 1alpha-hydroxylase activity seems to be a cause of the premature aging. In several studies, we have described that a complete or partial lack of vitamin D action (VDR-/- mice and CYP27B1-/-) show almost similar phenotype as FGF23-/- or Klotho-/- mice. VDR mutant mice have growth retardation, osteoporosis, kyphosis, skin thickening and wrinkling, alopecia, ectopic calcification, progressive loss of hearing and balance as well as short lifespan. CYP27B1-/- mice do not show alopecia nor balance deficit, which might be apoVDR-dependent or calcidiol-dependent. The features are typical to premature aging. The phenotype is resistant to a normalization of the mineral homeostasis by a rescue diet containing high calcium and phosphate. Taken together, aging shows a U-shaped dependency on hormonal forms of vitamin D suggesting that there is an optimal concentration of vitamin D in delaying aging phenomena. Our recent study shows that calcidiol is an active hormone. Since serum calcidiol but not calcitriol is fluctuating in physiological situations, calcidiol might determine the biological output of vitamin D action. Due to its high serum concentration and better uptake of calcidiol-DBP by the target cells through the cubilin-megalin system, calcidiol seems to be an important circulating hormone. Therefore, serum calcidiol might be associated with an increased risk of aging-related chronic diseases more directly than calcitriol. Aging and cancer seem to be tightly associated phenomena. Accumulation of damage on DNA and telomeres cause both aging and cancer, moreover the signalling pathways seem to converge on tumour suppressor protein, p53, which seems to be regulated by vitamin D. Also, the insulin-like growth factor signalling pathway (IGF-1, IGFBPs, IGFR) and fibroblast growth factor-23 (FGF-23) regulate growth, aging and cancer. Vitamin D can regulate these signalling pathways, too. Also NF-kappaB and telomerase reverse transcriptase (TERT) might be molecular mechanisms mediating vitamin D action in aging and cancer. Calcidiol serum concentrations show a U-shaped risk of prostate cancer suggesting an optimal serum concentration of 40-60 nmol/L for the lowest cancer risk. Therefore, it is necessary to study several common aging-associated diseases such as osteoporosis, hypertension and diabetes known to be vitamin D-dependent before any recommendations of an optimal serum concentration of calcidiol are given.

PMID: 19444937