Biophysica Incorporated

Phone: 416-784-0463 or Toll Free 1-800-488-2032 from Canada, US and Territories -or- E-mail:



 and Possible Telomere Regeneration using our

Pinealstim Tesla Technology Generator or

TransCranial Magnetic Stimulator (TMS) or

Hunza Water antioxidant

A major thrust of Biophysica’s research since 1992, originally supported by a grant from the National Research Council of Canada, is in possible regeneration of Pineal, Pituitary and Telomeres using electromagnetic energy, signals and frequencies emitted by the Pinealstim generator.  We now have  Trans-Cerebral and whole body stimulation devices which emit longitudinal Scalar EM waves.  This new technology  might possibly be promising in protecting and regenerating telomeres and we invite interested research investors.

The Pinealstim Cellular Regenerator emits a magnetic field, pulsed light pulses and repetitive high voltage pulses, containing within each pulse, high frequency information and Scalar Waves using a Caduceus Coil.  Repetition rate is scanned and controlled by feedback circuitry.  The energy is powerful and palpable and can penetrate deeply into cellular structures.  We are developing a portable model for applying to limbs, abdomen etc.

Telomeres are specialized DNA-protein complex at ends of linear chromosomes. They are essential for proper maintenace of chromosomes, and play a major role in aging and cancer. Telomerases are specialized reverse transcriptases that are involved in synthesis of telomeres in most organisms. They are very interesting DNA polymerases in that they carry RNA template within them.

T he excitement over telomerase continues to mount as evidence accumulates that makes the connection between telomere length and cell lifespan likely to be more than a coincidence. The most recent findings show that the age span of cultured cells, normally limited to around 50 to 90 cell doublings–the so-called Hayflick limit, named for the scientist who first observed that the lifespan of cultured cells was finite–can be more than doubled by transfecting them with telomerase genes (A.G. Bodnar et al., Science, 279:349-52, 1998). These findings come on the heels of a series of observations correlating the loss of telomerase activity and/or the shortening of the ends of chromosomes (telomeres) with the loss of proliferative capacity, an observation that holds true in a number of situations: somatic (limited proliferative capacity) as compared to germ cells (larger proliferative capacity); normal tissue (limited) versus malignant tumors (unlimited); and normal T cells versus HIV-infected T cells, whose telomeres resemble those of aged individuals.


Accelerated telomere shortening is a response to life stress

Chronicity of stress—is significantly associated with higher oxidative stress, lower telomerase activity, and shorter telomere length, which are known determinants of cell senescence and longevity, in peripheral blood mononuclear cells. Women with the highest levels of perceived stress have demonstrated telomeres shorter on average by the equivalent of at least one decade of additional aging compared.  Elissa S. Epel, Elizabeth H. Blackburn, Jue Lin, Firdaus S. Dhabhar, Nancy E. Adler, Jason D. Morrow, and Richard M. Cawthon,PNAS 2004 101: 17312-17315;

Broken chromosomes can be healed by adding new telomeres

Chromosome healing through terminal deletions generated by de novo telomere additions.  534 independent de novo telomere additions were achieved within a 12-kb region of chromosome by de novo genome rearrangement and addition of a telomere.

In most organisms studied, telomere DNA sequences are tandem array of simple G- rich repeat on the strand running from centromere to telomere.

This site is a part of GenLink database at Washington University, and collects telomere related references.

Special Issue: TELOMERE, TELOMERASE, CANCER, AND AGING  This issue contains recent reviews concerning telomere biology. The entire text is available on-line. Nice starting point for understanding recent telomere studies.


Tetrahymena Telomeres and Mitosis by Brian Harmon

Brian Harmon is a graduate student in the Sedat lab.   He discusses here new evidences suggesting telomeres are important in sister chromatid segregation during mitosis.

Lists of NIH Funded Research Groups [Gopher Search]
[Telomere] [Telomerase]

Lists of NSF Funded Research Groups [Gopher Search]
[Telomere] [Telomerase]

Geron Corporation
Geron Corporation is a biopharmaceutical company focused on the development of therapeutic products of aging, including cancer by controlling telomerase activity in cells.

Boehringer-Mannheim now sells Telomerase RCR ELISA kit.

Oncor also sells TRAP-eze, an telomerase detection kit. (Order Information)

Recommendations and Summary 

from workshop on telomerase activity and early detection of cancer (June 6-7, 1996)

Aging by Biology 52 Project:

The Aging Research Centre (ARC) Home Page

Telomere & Telomerase Research Information

By Toru Nakamura at the University of Colorado, Boulder, contains information on telomere and related gene sequences.

Old Cells Can Be Young Again

(telomeres can be repaired)

When you get sick, your immune system makes copies of its disease-fighting white blood cells called T-cells. These cells divide over and over again to fight off the bacteria or virus that’s invading your body.

The more often these cells reproduce, the shorter their telomeres become until they stop copying. The older you get, the fewer active T-cells you have because they’ve fought off as much sickness as they can. The bottom line is that when your telomeres are short, your immune system looks and acts old.

This makes your risk for infection and disease much higher. One study looked at about 150 people from 60-75 years old. The ones who had shorter telomeres were three times more likely to die from heart disease. And they were eight times more likely to die from an infectious disease.

Shortened telomeres also appear to be the mechanism for many chronic diseases like:

Diabetes. When you eat too many carbohydrates, your pancreas is asked to create more insulin than it’s supposed to. And to get the job done, the pancreas has to create more of a factory to create the insulin it needs by making more cells. If the pancreas is continually challenged to produce more and more insulin, the cells have to continue to divide. When their telomeres are too short, they can’t reproduce anymore. And your body can’t make the insulin you need. This is what causes diabetes. (4)

Atherosclerosis. One study I read looked at men with high blood pressure. Those with shorter telomeres in their white blood cells were more likely to get heart disease. (5)

Alzheimer’s disease. Alzheimer’s patients’ glial cells, the maintenance cells to the brain, have short telomeres. Some kind of toxic environmental hazard caused those cells to replicate to defend themselves.(6)
But you don’t have to let your immune system grow old. When telomerase is activated, you strengthen your cells by keeping the telomeres long, strong and young. And the younger your cells are, the more powerful they are at fighting sickness and disease.

In fact, for most of the people in a brand new study, telomerase activation therapy reduced the percentage of immune cells with short telomeres by 10-50 percent. And the amount of older immune cells decreased by 10-20 percent.7 This represents an “apparent age reversal of 5-20 years!”(8)

Grow Younger Naturally

Tons of research is going on every day and you’ll be reading more and more about telomerase in the coming months. But in the meantime, you can help slow the aging of your cells with nutrients.

One of the best nutrients for activating your telomerase is trusty omega-3. A new study in the Journal of the American Medical Association followed about 600 people over a full five years. They found that daily supplements of omega-3 significantly increased telomerase activity.(9)


1 Cong, Yusheng, Shay, Jerry W., “Actions of human telomerase beyond telomeres,” Cell Research June 2008; 18:725-732
2 Simon, R., Chan, W. L., Blackburn, Elizabeth H., “Telomeres and telomerase,” Phil. Trans. R. Soc. Lond. B 2004; 359, 109-121
3 Cawthon, R.M., Smith, K.R., O’Brien, E., et al, “Association between telomere length in food and mortality in people aged 60 years or older,” Lancet 2003; 361(9355): 393-395
4 Sampson, M., Winterbone, M., et al, “Monocyte Telomere Shortening and Oxidative DNA Damage in Type 2 Diabetes,” Diabetes Care 2006
5 Benetos, A., Gardner, J., et al, “Short Telomeres are Associated with Increased Carotid Atherosclerosis in Hypertensive Subjects,” Hypertension 2004
6 Farfara, D., Lifshitz, V., et al, “Neuroprotective and neurotoxic properties of glial cells in the pathogenesis of Alzheimer’s disease,” Journal of Cellular and Molecular Medicine 2008
7 Harley, C., Weimin, L., et al, “A Natural Product Telomerase Activator as Part of a Health Maintenance Program,” Rejuvenation Research 2010
8 Ibid.
9 Ramin Farzaneh-Far, M.D., “Association of Marine Omega-3 Fatty Acid Levels with Telomeric Aging in Patients with Coronary Heart Disease,” JAMA 2010; 303(3):250-257