Metformin is an inexpensive oral hypoglycemic drug from the class of biguanides, discovered 1957 and used to treat Type II Diabetes Mellitus; apparently no other newer drug has been able to consolidate its position for such length of time in treatment of diabetes.
Recently, it has been seen to have cancer inhibitory properties, more prominently a prostate cancer. A number of trails are going on to explore its' potential benefit in cancer prevention and treatment; among which breast, prostate and lungs cancer are prominent.
Prostate cancer is among the top five leading causes of cancer death worldwide, according to an estimate of the World Health Organisation.
It is projected that approximately 1 in 7 men in the U.S. will be diagnosed with prostate cancer at some point in their lives, with roughly two-thirds of these cases found between the ages of 55-74.
According to the National Cancer Institute, more than 29,000 American men will die from prostate cancer in 2013.
Likewise, the World Health Organization estimates that 347 million people worldwide have diabetes, and that it will be the seventh leading cause of death by 2030.
According to the U.S. Centers for Disease Control and Prevention, more than 25 million Americans are affected by diabetes and over one-quarter of people older than age 65 have the disease.
Now, it has been seen that diabetic prostate cancer patients on metformin survive longer than those who are not on metformin. Whereas, the metformin group die of some other disease, those not on metformin succumb to cancer of prostate.
How exactly metformin has prostate cancer preventing property is not known. Some research suggests that high insulin levels along with Insulin Growth Factor 1 can influence cancer growth. Metformin decreases insulin level in blood what is called hyperinsulinemia; reduction in level of insulin and insulin like growth factor (IGF) may inhibit the cell proliferation.
Metformin decreases the neoglucogenesis and prevents glycolysis in liver, thereby decreases the blood level of glucose and insulin. Typical side effects of the drug are mild diarrhea and stomach problems that usually subside after one or two weeks.
Metformin may also have direct action at cellular level. The drug has been observed to act directly on prostate cancer cells to cause death and/or inhibit proliferation.
By decreasing obesity metformin may also have negative impact on the growth of prostate cancer, as obesity is a predisposing factor for cancer prostate.
This involves an action of the drug that interferes with cellular energy metabolism: metformin interferes with the process by which nutrients are converted to energy : under some circumstances, cells react to the energy deficiency by adjusting their functions to use less energy – but a cancer cell that is minimizing energy consumption cannot exhibit aggressive metastatic or proliferative behaviour. The energy stress caused by metformin is sufficient to cause cell death.
It may have also some other mode of action, a direct anti-proliferative effect occurs characterized by the activation of phospho-AMPK [Adenosine Mono-Phosphate-activated protein kinase (AMPK)] with subsequent inhibition of downstream mTOR signalling and altered cycle distribution with cell cycle arrest in G1/S phase.
The beneficial effect on prostate cancer is seen in time dependent manner. Its use in non-diabetic prostate cancer is being explored.
At present, pending further research on the subject, metformin can be used in diabetic prostate cancer patients, if otherwise not contraindicated.
For further information on the subject and to know about ongoing trials go here.
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| Galega officinalis, for metformin. |
Recently, it has been seen to have cancer inhibitory properties, more prominently a prostate cancer. A number of trails are going on to explore its' potential benefit in cancer prevention and treatment; among which breast, prostate and lungs cancer are prominent.
Prostate cancer is among the top five leading causes of cancer death worldwide, according to an estimate of the World Health Organisation.
It is projected that approximately 1 in 7 men in the U.S. will be diagnosed with prostate cancer at some point in their lives, with roughly two-thirds of these cases found between the ages of 55-74.
According to the National Cancer Institute, more than 29,000 American men will die from prostate cancer in 2013.
Likewise, the World Health Organization estimates that 347 million people worldwide have diabetes, and that it will be the seventh leading cause of death by 2030.
According to the U.S. Centers for Disease Control and Prevention, more than 25 million Americans are affected by diabetes and over one-quarter of people older than age 65 have the disease.
Now, it has been seen that diabetic prostate cancer patients on metformin survive longer than those who are not on metformin. Whereas, the metformin group die of some other disease, those not on metformin succumb to cancer of prostate.
How exactly metformin has prostate cancer preventing property is not known. Some research suggests that high insulin levels along with Insulin Growth Factor 1 can influence cancer growth. Metformin decreases insulin level in blood what is called hyperinsulinemia; reduction in level of insulin and insulin like growth factor (IGF) may inhibit the cell proliferation.
Metformin decreases the neoglucogenesis and prevents glycolysis in liver, thereby decreases the blood level of glucose and insulin. Typical side effects of the drug are mild diarrhea and stomach problems that usually subside after one or two weeks.
Metformin may also have direct action at cellular level. The drug has been observed to act directly on prostate cancer cells to cause death and/or inhibit proliferation.
By decreasing obesity metformin may also have negative impact on the growth of prostate cancer, as obesity is a predisposing factor for cancer prostate.
This involves an action of the drug that interferes with cellular energy metabolism: metformin interferes with the process by which nutrients are converted to energy : under some circumstances, cells react to the energy deficiency by adjusting their functions to use less energy – but a cancer cell that is minimizing energy consumption cannot exhibit aggressive metastatic or proliferative behaviour. The energy stress caused by metformin is sufficient to cause cell death.
It may have also some other mode of action, a direct anti-proliferative effect occurs characterized by the activation of phospho-AMPK [Adenosine Mono-Phosphate-activated protein kinase (AMPK)] with subsequent inhibition of downstream mTOR signalling and altered cycle distribution with cell cycle arrest in G1/S phase.
The beneficial effect on prostate cancer is seen in time dependent manner. Its use in non-diabetic prostate cancer is being explored.
At present, pending further research on the subject, metformin can be used in diabetic prostate cancer patients, if otherwise not contraindicated.
For further information on the subject and to know about ongoing trials go here.
