Extending Lifespan by Preventing the Diseases of Aging

I have developed a biotechnology which will enable people to live longer and enjoy better quality lives.

Over the past 30 years I have been researching and refining a measurement assay for, as well as technologies to increase, a naturally occurring protein in blood that ameliorates the negative effects of very low density lipoprotein (VLDL). VLDL injures/kills the white cells in the blood (leukocytes) and the cells lining the interior surface of the blood vessel (endothelial cells). The former injury compromises the immune system resulting in more frequent infections and impaired ability to eliminate precancerous cells. The latter injury clearly contributes to stroke, cardiovascular disease and kidney disease. Besides researching VLDL toxicity, I discovered a protein in blood eliminates VLDL toxicity and allows leukocytes and endothelial cells to remain viable and function normally. The ratio of these two factors, protective albumin and VLDL, determines whether cells live or die. Studies have shown that people with high VLDL levels and/or low levels of the protective protein develop cardiovascular disease at a faster rate than the rest of the population. This represents a major advancement in cardiovascular disease research since we can now identify individuals at risk prior to the onset of irreversible disease. Numerous epidemiological studies show that VLDL increases during aging and we have shown that the protective fraction decreases. Total albumin, of which the protective factor is a part, is inversely correlated with people dying not just from cardiovascular disease but from any disease. The lower a person’s total albumin (and therefore their protective factor) after the age of 45, the more likely s/he is to die of any disease. I have developed a therapy that increases the level of the protective albumin and should result in a longer, healthier lifespan.

Humans begin to develop age-related diseases (cardiovascular-problems, kidney disease and cancer) after the age of 45; in evolutionary terms humans did not have this long a life-span until recently. What changes occur that allow these diseases to progress? My research indicates that an age-associated decrease in a specific hormone changes the body’s metabolism from primarily glucose to primarily lipid metabolism. Increased lipid metabolism, important during times of stress, causes a decrease in protective albumin. If reliance on lipid metabolism continues over a long time, there is increased susceptibility to the diseases of aging. The protective albumin-VLDL hypothesis is a completely new concept supported by research from my laboratory and a number of clinical trials from other researchers. If my hypothesis is correct, increasing protective albumin might extend the human lifespan by 10 or 20 years.

A straightforward clinical trial will establish this technology. Hospitalized patients offer the least expensive and quickest way to test whether increasing protective albumin decreases the risk of death. Intensive-care-unit patients (ICU) would be divided into two groups, one treated with our hormonal therapy and one not. Blood samples would be collected before and after treatment and hormone levels adjusted to achieve a protective albumin level in the treated group. Outcomes such as length of stay, hospital morbidity and hospital mortality in the two groups would be recorded. Two hundred patients in each group would be sufficient. Success with the ICU patients would be expanded to all hospitalized patients within a short period of time and eventually to everyone over 45.

The people who would benefit the most would be those over the age of 45 who are developing the diseases of aging. As people age their protective albumin would decrease and their VLDL would increase. At some point they would become susceptible to the diseases of aging (cardiovascular disease, kidney disease and cancer). By increasing protective albumin (or decreasing VLDL) the diseases of aging would not progress. This would prolong the productive period of their lifespan. The ones who would not benefit from this technology would be people that died from accidental death. Just as the treatment of infectious diseases with penicillin led to an increase in average lifespan, this technology could be as equally dramatic.

Optimally preventive measures could be initiated in persons identified as having increased risk by routinely screening blood at the age of 45. Individuals having a level below 2 would be treated to raise their protective albumin level to more closely resemble the metabolic profile of a younger person. This would significantly delay or prevent the progression of diseases of aging and result in a longer life span. This technology would also help people already affected with the diseases of aging. By increasing protective albumin by means of a very low cost and readily available therapy, disease could be halted or even reversed. By delaying the diseases of aging, productive lifespan and quality of life would be significantly increased. Not only will this technology have an immediate impact on people’s lives, but it will establish a basis for new breakthroughs in the treatment of chronic disease.