Michael Fossel Michael is President of Telocyte

February 1, 2018

Aging and Disease: 1.0 – Aging, Our Purpose, Our Perspective:

Aging is poorly understood, While the process seems obvious, the reality is far more complex than we realize. In this series of blogs I will explain how aging works and how aging results in disease. In passing, I will touch upon why aging occurs and will culminate in an explanation of the most effect single point of intervention, both clinically and financially. We will likewise explore the techniques, costs, and hurdles in taking such intervention into common clinical use in the next few years.

The approach will be magesterial, rather than academic. I do not mean to preclude differences of opinion, but my intent is not to argue. I will explain how aging works, rather than engage in theoretical disputes. Many of the current academic disputes regarding aging are predicated on unexamined assumptions and flawed premises, resulting in flawed conclusions. Rather than argue about the conclusions; I will start from basics, highlight common pitfalls in our assumptions and premises, then proceed to show how aging and age-related diseases occur.

Since this is not and is not intended to be an “Academic” series (capitalization is intentional), I will aim at the educated non-specialist and will usually omit references, in order to make engagement easier for all of us as the series proceeds. If any of you would like references, more than 4,200 academic references are available in my medical textbook on this topic, Cells, Aging, and Human Disease (Oxford University Press, 2004). For those of you with a deep intellectual exploration of this topic, I recommend you read my textbook. Ironically, my academic textboo is still largely up-to-date with regard to the patholgy and to the aging process in general, if not so with regard to current interventional techniques for human clinical use.

The first book and medical articles that explained aging were published two decades ago, including Reversing Human Aging (1996) and the first two articles in the medical literature (both in JAMA, in 1997 and 1998). There are no earlier or more complete explanations of how aging works, nor of the potential for effective clinical intervention in aging and age-related disease. Since then, I have published additional articles and books that explain the aging process and potentially effective clinical interventions. The most recent, and most readable of these (The Telomerase Revolution, 2015) is meant for the lay reader and is available in 7 languages and 10 global editions. For those of you who want to know more, I encourage you to explore this book, which was praisde in both The London Times and the Wall Street Journal.

Finally, the focus will be the theory of aging; a theory that is valid, accurate, consistant with known data, predictively valid, and testable. This will not be a narrow discussion of the “telomere theory of aging”, which is a misnomer, but a detailed discussion of how aging works and what can be done about it using current techniques. A factual and accurate explanation of aging relies on telomeres, but also must addrss mechanisms of genes and genetics, gene expression changes and epigenetics, cell senescence and changes in cell function, mitochondrial changes and ROS, molecular turnover and recycling, DNA damage and cancer, “bystander” cells and “direct aging”, tissue pathology and human disease, and – above all – how we may intervene to alleviate and prevent such disease. The proof is not “in the pudding”, but in the ability to save lifes, prevent tragedy, and improve health.

The proof is in human lives.

This theory of aging has several key features. It is the only theory that accounts for all of the current biological and medical data. It is internally consistent. It is predictively valid: for the past 20 years, it has predicted both academic research results and the clinical outcomes of pharmaceutical trials accurately and reliably in every case. These predictions include the results of monoclonal antibody trials in Alzheimer’s disease, as well as other Alzheimer’s clinical trials, other clinical trials for age-related disease, and animal research (in vivo and in vitro). Perhaps the most fundamental feature of this theroy of aging is that it is an actual theory, i.e., testable and falsiable. A “theory” that cannot be disproven isn’t science, but philosophy. Many of what we think of as “theories of aging” cannot meet this criteria. If they cannot be disproven, they are not science, but mere will-o’-the-wisps.

If the theory of aging has a single name – other than the “telomere theory of aging” — it might be the epigenetic theory of aging. Despite misconceptions and misunderstandings about what it says (both of which I will try to remedy here), the epigenetic theory of aging has stood the test of time for the past two decades. It remains the only rational explanation of the aging process, while remaining consistent, comprehensive, and predictively valid. When it predicted failure of an intervention, the intervention has failed. When it predicted an effective intervention, the intervention has proven effective. Whether it’s the telomere theory of aging or the epigenetic theory of aging, in this series, we will proceed to get our conceptual hands dirty and look carefully at what happens when aging occurs, why it happens, where it happens, and what can be done about it. We’re going to go at this step-by-step, going into detail, and showing why we can intervene in both the basic aging process and human age-related diseases.

I doubt you’ll be disappointed.

 

Next blog:       1.1 – Aging, What is Isn’t

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