Superlongevity and Extreme Life Extension

Living Longer and Healthier

Funding Aging Research


posted on August 11, 2009

Okay. Let™s say we solve the aging puzzle on time. You won™t get sick. You won™t get old. You™ll be youthful and happy for as long as you want.

Or will you?

Don™t forget, more time will magnify the good and the not so good. If you enjoy high self-esteem, life will be good. If it™s not as high as you™d like, it might be a drag. That™s true no matter how long we live. So shouldn™t self-esteem be something we might want to pay attention to? Shouldn™t it be the foundation upon which we build our lives?

First, exactly what is self-esteem? I have the most sensible answer for you. It comes straight from Dr. Nathaniel Branden, often referred to as œthe father of self-esteem, and a cherished friend.

According to Dr. Branden, œSelf-esteem is an experience. It is a particular way of experiencing the self. It is a good deal more than a mere feeling. It involves emotional, evaluative, and cognitive components. It also entails certain action dispositions: to move toward life rather than away from it; to move toward consciousness rather than away from it; to treat facts with respect rather than denial; to operate self-responsibly rather than the opposite.

œSelf-esteem is the disposition to experience oneself as being competent to cope with the basic challenges of life and of being worthy of happiness. It is confidence in the efficacy of our mind, in our ability to think. By extension, it is confidence in our ability to learn, make appropriate choices and decisions, and respond effectively to change. It is also the experience that success, achievement, fulfillment”happiness”are right and natural for us.

œSelf-esteem is not the euphoria or buoyancy that may be temporarily induced by a drug, a compliment, or a love affair. It is not an illusion or hallucination. Lots of things (some of them quite dubious) can make us œfeel good”for a while. If self-esteem is not grounded in reality, if it is not built over time through the appropriate operation of mind”for example, through operating consciously, self-responsibly, and with integrity--it is not self-esteem.

œRationally, one does not focus on self-esteem per se; one focuses on the practices that support and nurture self-esteem”such as the practice of living consciously, of self-acceptance, of self-responsibility, of self-assertiveness, of purposefulness, and of integrity, as I discuss in The Six Pillars of Self-Esteem.

œSelf-esteem demands a high reality-orientation; it is grounded in a reverent respect for facts and truth. Excessive and inappropriate self-absorption is symptomatic of poor self-esteem, not high self-esteem. If there is something we are confident about, we do not obsess about it”we get on with living.

Well said Nathaniel.

Extreme life extension is as much about the quality of your life as the quantity. Both take work. If you™re willing to invest in your mind as well as your body, then I suggest you devour a copy of The Six Pillars of Self-Esteem.

This is such an important issue that I am going to cover more next week. Meanwhile, why not visit some of Dr. Branden™s historical blogs for more information? Start with:


In the near future it will be possible to increase the rate at which new neurons and neural connections are created in the brain. This looks promising as a way to tackle some aspects of age-related decline: "Newborn neurons are continuously produced in the hippocampus, which may be involved in several cognitive functions, including learning and memory, throughout life. However, both hippocampus-dependent cognitive functions and the level of adult neurogenesis are gradually attenuated as aging progresses. Few studies have explored the relationship between adult neurogenesis and cognitive functions, especially in primates. In this study, we evaluated learning performance and hippocampal neurogenesis utilizing young and aged cynomolgus monkeys. Significant attenuations in learning performance and adult neurogenesis were detected in aged monkeys. Interestingly, there was a positive correlation between learning performance and the level of neurogenesis. Our findings suggest that cognitive functions and adult neurogenesis may have some interdependent relationships during aging."

The immune system declines and malfunctions with age, but researchers are making strides towards methods of reprogramming that might restore an age-damaged immune system to better operation: researchers have "identified a protein that could serve as a target for reprogramming immune system cells exhausted by exposure to chronic viral infection into more effective "soldiers" against certain viruses like HIV, hepatitis C, and hepatitis B, as well as some cancers, such as melanoma. The protein Blimp-1 (B-lymphocyte-induced maturation protein 1) represses the normal differentiation of CD8 T cells into memory T cells, which recognize disease-causing agents from previous infections and enable the body to mount faster, stronger immune responses. The team also reports that Blimp-1 causes exhausted CD8 T cells to express inhibitory receptors, which prevent recognition of specific antigens, further weakening immune response. The researchers describe how complete deletion of Blimp-1, which is overexpressed in CD8 T cells during chronic viral infection, reversed these aspects of T cell exhaustion." Note that one important cause of immune system aging is chronic infection by cytomegalovirus - this work probably has relevance to aging.

A snapshot of ongoing work to develop cost-effective tools for building targeted cancer therapies: "Scientists have spent more than a decade trying to direct liposomes to specific cancer cells, with limited success. A common approach involves attaching an antibody to the liposome membrane. Ideally the antibody will bind to a cancer cell receptor so that it can deliver the liposome - and the cancer drug - into the cell. Developing such antibodies is costly and time-consuming, however, and the process of attaching them to liposomes is difficult to control. Aptamers are short strands of DNA or RNA; they are highly efficient binders, and are very easy to make, label and manipulate. Researchers] used an aptamer that binds to nucleolin receptors, which are found in abundance on certain breast cancer cells. The researchers then developed an effective method for attaching the aptamer to a liposome loaded with cisplatin, a drug that effectively kills cancer cells but has troublesome side effects when administered intravenously. Tests in cells grown in the lab yielded promising results. Four days after they exposed the cells to the new drug-delivery system, 59.5 percent of the breast cancer cells had died, while less than 12 percent of breast cancer cells treated with cisplatin alone had died. Another advantage of using aptamers as targeting agents is that they are easily disabled. They readily bind to complementary DNA, which prevents them from interacting with cell receptors."

Here, Chemical & Engineering News looks at the practice of calorie restriction: "lthough Paul McGlothin and Meredith Averill are in their early 60s, the married couple from New York State says that they feel at least 20 years younger. This is no idle claim: Their blood pressures, resting heart rates, and body fat percentages rival those of Olympic athletes. So what's their antiaging secret? For the past 16 years, McGlothin and Averill have been eating a carefully controlled, calorie-restricted diet. Scientists have known for decades that caloric restriction - reducing calorie intake without malnutrition - slows aging and extends life span in model organisms ranging from yeast to mice. Exactly why and how it confers these benefits in animals, and whether similar effects could be attained in humans, have been a mystery. Caloric restriction is about more than just being thin and fit. Something about eating a diet that is low in calories but nutritionally complete causes a dramatic reprogramming of cellular metabolism that can't be replicated by exercise or by eating smaller amounts of high-calorie foods. In laboratory animals such as fruit flies, roundworms, and mice, caloric restriction switches biochemical pathways on or off, resulting in higher insulin sensitivity, decreased inflammation, enhanced cardiovascular functioning, reduced muscle wasting with age, and improved resistance to cellular stress. Not only is normal aging slowed, but calorie-restricted animals are also less likely to develop age-associated diseases such as diabetes and cancer."

I don't think I've pointed out the Healthy Life Extension Society, or Heales before; it's a group based in Belgium, and so you'll find more French and Dutch content than English material at the Society's website.
For the rest of us English-speaking monolinguists, there's always Google Translate: "Each day 100,000 people die due to the effects of old age. Aging is responsible for 90% of deaths in the richest countries and two-thirds of deaths in the world. It doesn't just cause innumerable deaths, it is also the source of horrible suffering - Alzheimer's Disease, muscular atrophy, damage to vision and hearing, osteoporosis, rheumatoid arthritis The only way to prevent these illnesses linked to aging is to attack the root cause “ that is aging itself. It is time to start working towards solutions to this universal human tragedy. Heales raises awareness of new developments in the area of biogerontolgy (the science of aging). We promote and support anti-aging research." As I noted in the latest Longevity Meme newsletter, Heales is holding a fundraising music festival for LysoSENS research next month.

Here is an example of how looking at observable data on aging - such as mortality rates - can inform us of the nature of underlying mechanisms of aging: "What do you think are the odds that you will die during the next year?  Try to put a number to it - 1 in 100?  1 in 10,000?  Whatever it is, it will be twice as large 8 years from now. This startling fact was first noticed by the British actuary Benjamin Gompertz in 1825 and is now called the 'Gompertz Law of human mortality.' Your probability of dying during a given year doubles every 8 years.  For me, a 25-year-old American, the probability of dying during the next year is a fairly miniscule 0.03% - about 1 in 3,000.  When I'm 33 it will be about 1 in 1,500, when I'm 42 it will be about 1 in 750, and so on.  By the time I reach age 100 (and I do plan on it) the probability of living to 101 will only be about 50%.  This is seriously fast growth - my mortality rate is increasing exponentially with age. There is one important lesson, however, to be learned from Benjamin Gompertz's mysterious observation.  By looking at theories of human mortality that are clearly wrong, we can deduce that our fast-rising mortality is not the result of a dangerous environment, but of a body that has a built-in expiration date." You might also look at the reliability theory of aging for a similar process of insight.

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