Melatonin to Induce Apoptosis

[Guest guest]

I found this quite interesting on its own. But in light of the

research done by the National CFIDS Foundation which involved P53 deficiency in

those with ME/CFS, this should motivate further research - in my opinion. " The

data indicate that native p53 protein is fragmented at a later point in the

disease cycle than RNase L protein. The loss of functional p53 protein in PBMCs

render these cells unable to respond to normal growth inhibitory stimuli and

provide the means whereby unregulated cell growth occurs, ultimately giving rise

to hematopoitic tumours. " from Unmasked Research: STAT1-alpha and p53

Deficiencies Are Found In Patients With Chronic Fatigue Syndrome

http://www.ncf-net.org/forum/P1-STAT1.htm

I would appreciate any ideas or theories or perceptions regarding

this please?

blessings

Shan

 

Melatonin to Induce Apoptosis

 

http://www.drlam.com/A3R_brief_in_doc_format/2001-No6-CancerStrategies.cfm#3Mela\

tonintoInduceApoptosis

 

Every cell in the human body has a gene called the P53 gene. This gene tracks

the degeneration of the cell and when it finds that the cell is damaged

beyond repair, it triggers its self-destruction. The P53 gene triggers old cells

that died through this natural self-destruction process. New cells are then

created through cell division.

 

The function of the P53 gene gets suppressed in tumor cells. The tumor cells

lose the ability to die naturally. This insight about the P53 gene has led to

the development of a new way to re-enliven the function of the suppressed P53

gene and bring back its ability to naturally self-destruct the cell upon

recognizing that the cell is degenerated. What this means is that malignant

tumors

can be reduced and/or eliminated from the body by re-activating the cells

suppressed P53 function. It is postulated that melatonin fights cancer by the

re-expression of the P53 gene. With this function re-energized, the tumor cells

recognize their own degenerated state and naturally die on their own thus

allowing the body to manage the process of elimination of the dead tumor cell.

 

Melatonin is therefore much more than a natural sleeping pill. It is the

agent used to induce programmed cell death (apoptosis). Melatonin's link to

cancer

was first reported when researchers discovered that flight attendants have

twice the normal rate while blind people have half the normal rate of breast

cancer. Blind people are known to have high levels of melatonin in their bodies.

It is believed that is why blind people have half the normal rate of breast

and other cancers. Flight attendants, on the other hand, have frequent jet lag

and sleep disturbance. They have less melatonin, which according to

researchers, accounts for the doubling rate of breast cancer.

 

According to an article in the American Journal of Epidemiology (April,

1987), the nighttime production of melatonin inhibits the body's production of

estrogen. But exposure to either light at night or to electromagnetic fields can

suppress the secretion of melatonin. Chronic exposures of this sort could lead

to an increase in an individual's cumulative lifetime dose of estrogen and

therefore to an increased breast cancer risk. Two researchers later showed that

melatonin directly inhibited the proliferation of human breast cancer cells in

culture. In fact, melatonin has been shown to increase the level of naturally

occurring antioxidants in breast cancer cells.

 

One established center of melatonin and cancer studies today is the Division

of Radiation Oncology of the San Gerardo Hospital, Milan, Italy. Doctors there

have developed a " neuroimmunotherapeutic " protocol that includes a low-dose

of IL-2 (Interlukin 2) (three million IU/day for six days per week, for four

weeks) with the addition of melatonin taken by mouth (40 mg/day, starting seven

days before IL-2).

 

In a randomized clinical trial reported in 1994, patients with advanced

diseases (other than melanoma or kidney cancer) received either low-dose IL-2

alone

or IL-2 plus the orally administered melatonin.

 

There was just one (partial) response out of 39 patients in the IL-2 group.

However, when melatonin was added, there were 11 complete or partial responses.

After one year on the treatment, there were just six survivors out of 39

patients on IL-2, but 19 survivors in the melatonin +IL-2 group. This was

statistically significant and was reported in the British Journal of Cancer

(1994;

69:196-199).

 

In another randomized study, patients with end stage inoperable brain

metastases were given either just supportive care or supportive care and

melatonin

(20 mg/day taken orally). Survival at one year as well as freedom from brain

tumor progression and mean survival time were all significantly higher in

patients who were treated with melatonin than in those who received supportive

care

alone (Cancer 1994; 73:699-701).

 

Although studies like these and others are encouraging, they must be

interpreted with caution. The studies were not placebo-controlled, so it is

uncertain

whether the results were caused by melatonin or a placebo effect. Further

studies are needed for confirmation. It should also be noted that the doses of

melatonin used in these cancer studies (20-40 mg per night) were considerably

higher than the over-the-counter doses (3-6 mg) recommended for sleep. Those

unfamiliar with melatonin dosing should note that the dosage to induce sleep is

highly variable. Many have reported better sleep with lower dose melatonin (0.5

mg to 1 mg) than at high dose (5 mg and up).