Tuesday, November 17, 2015

Withania somnifera & GABA

The botanical known as Ashwagandha (Withania somnifera) is often used for its adaptogenic properties, which modulate general conditions like insomnia, stress, anxiety, and cognitive function. GABA is the inhibitory neurotransmitter in the central nervous system mediating pathological processes such as anxiety, depression, epilepsy, and other cognitive disorders.  The study completed by Candelario et al.(2015) aimed to examine the root extract of Ashwagandha and its constituents, and how they inhibit GABA receptors in the CNS. Results of the study suggest that the key constituents in Ashwagandha may beneficially influence the signaling dysfunction found in general anxiety disorders, sleep disorders, and cognitive disorders by targeting GABA in the CNS. 

Candelario M. et al.(2015) Direct evidence for GABAergic activity of Withania somnifera on mammalian ionotropic GABAa and GABAp receptors.  Journal of Ethnopharmacology, 171 (May 2015), 264-272. http://dx.doi.org/10.1016/j.jep.2015.05.058
   

Monday, November 16, 2015

Novel Mechanistic non-linear model & Circadian Oscillations of hormones in HPA-axis related to Depression

The etiology of depression is discussed in a study by Gudmand-Hoeyer et al. (2014).  While depression is associated with dysregulation of the HPA-axis many of the resulting hormones synthesized in this system are affected and downstream concentrations directly influence the energy in the brain and muscles. These hormones are synthesized at different rates and times during the day.  Utilizing a multi-scale modeling approach, this study was able to show both the circadian and ultradian oscillations of hormones as it is related to depression.  The three parameters varying between groups that were examined in this study reveal hypocortisolemic depressed, hypercortisolemic depressed, and non-depressed. The model utilized in this study allows for the complex interpretation of ACTH levels and the resulting synthesis of cortisol and associated depression. 

J. Gudmand-Hoeyer et al.(2014). Patient-specific modeling of the neuroendocrine HPA-axis and its relation to depression: Ultradian and circadian oscillations, Mathematical Biosciences, 257(September 2014), 23-32. http://dx.doi.org/10.1016/j.mbs.2014.07.013

Depression & HPA-Axis

Regulation of our internal environment involves three systems: the nervous system, immune system, and endocrine system. The hypothalamic-pituitary-adrenal (HPA) axis is integral to all three of these systems and is often disrupted and hyperactive in major depression (MD).  Neuroendocrine stimulation research suggests that negative coping strategies predicts the plasma cortisol response, which is controlled by the HPA-axis. Results of the study by N.Hohne et al.(2014) indicate that subjects with a lifetime history of major depression have HPA-axis dysregulation and negative coping strategies, compared to individuals that have never been depressed. 

N. Hohne et al.(2014). Increased HPA axis response to pyschosocial stress in remitted depression: the influence of coping style, Biological Psychology, 103 (September 2014), 265-267. http://dx.doi.org/10.1016/j.biopsycho.2014.09.008


Tuesday, June 23, 2015

Laughter Interventions & Quality of Life

The Laughter Club movement (laughter yoga) has inspired researchers to investigate the health effects of simulated laughter. Some health practitioners require researched evidence to suggest laughter as an intervention to patients. Why? I'm not sure. For those of you that need the evidence, here it is…Available evidence on laughter research suggests that laughter has a positive, quantifiable physiological and psychological effect on health leading to an improved quality of life. Specifically, laughter affects the muscular, cardiovascular, respiratory, endocrine, immune, and central nervous systems. 

Ramon Mora-Ripoll (2011). Potential health benefits of simulated laughter: A narrative review of the literature     
and recommendations for future research. Complementary Therapies in Medicine. (May 25 2011) 19: 170-1 

Memorial Sloan Kettering Cancer Center & Rx

Memorial Sloan Kettering Cancer Center now offers a tool for patients to review cancer drugs and the modifiable price components. Check out DrugAbacus here.


Wednesday, February 25, 2015

Vitamins & Cancer

The relationship between vitamins and cancer, specifically vitamin A, B complex, vitamin C, vitamin D, vitamin E, and vitamin K are discussed in a review completed by Mamede et al. (2012).  The pathway in which vitamin A achieves anticarcinogenic effects is poorly understood, but research has demonstrated promising roles in the prevention and treatment of many cancers. B complex functions as many coenzymes and are important methylators in cellular processes, thus influencing cancer via proto-oncogenes. Research has repeatedly demonstrated the benefits of vitamin C where pharmacologic concentrations act as proxidants harming cancer cells without damaging normal cells in the body.


Mamede, A. C., Tavares, S. D., Abrantes, A. M., Trindade, J., Maia, J. M., & Botelho, M. F. (2011). The role of vitamins in cancer: a review. Nutrition and Cancer, 63(December 2012), 479–494. doi:10.1080/01635581.2011.539315



Vitamin D & Cancer

Garland et al. (2009) review the evidence supporting high serum levels of vitamin D and it's role in lowering the risk of colon, breast, ovarian, renal, pancreatic, aggressive prostate and other cancers. Data extrapolated from NHANES reports that women with higher exposure to UVB light had half the risk of breast cancer compared to those with lower UVB exposure.  15-year survival and metastatic rates in breast cancer are improved with 25(OH) D serum levels higher than 29 ng/mL. Statistics cited in this review indicate that an intake of 2,000 IU/day of vitamin D3 would lead to 25% reduction in risk of breast cancer and 27% reduction of risk in colorectal cancer in North America.


Garland, Cedric F., Gorham, Edward D., Mohr, Sharif B., Garland, F. C. (2009). Garland_2009_Vitamin_D_for_Cancer_Prevention_Global_Perspective.Pdf. Aep.