Delayed hepatic caffeine metabolism in NAFLD and increased caffeine transport to the brain with aging-induced mitophagy in neurons is associated with the induction of Type 3 diabetes and neurodegenerative disease. Caffeine content in feed should be carefully assessed to prevent accelerated mitophagy with unexpected death rates over the next 20 years.
A single gene cannot be of relevance to the SURVIVAL of a living being (neither to the survival of an Industry).
On the other hand, I do not understand the issue with caffeine but caffeine is not bad for humans and I would not think it may be "bad" for cattle
Dear Rafael Franco,
Thank you for your mail.
The effects of caffeine becomes toxic as we develop non alcoholic fatty liver disease (NAFLD). [Reference 1,2,3]. In the current global NAFLD epidemic caffeine consumption should be reduced so that excess transport to the brain does not interfere with neuron calcium homeostasis with relevance to circadian rhythm abnormalities[Reference 1,2,3,5]. In individuals with NAFLD the liver caffeine metabolism is defective. The food intake determines caffeine metabolism and the excess amount of fat consumed delays caffeine metabolism [Reference 6]. The calculated amount of fat for rapid hepatic caffeine metabolism does not allow caffeine to reach brain toxic levels with the aging process. The survival of the species can be determined by a single gene such as Sirtuin 1 since its inactivation leads to no mitochondrial biogenesis with neuron apoptosis and the induction of NAFLD [7]. Sirtuin 1 inactivation [8] leads to diabetes (Type 1,2,3) [9,10] with insulin resistance linked to NAFLD, brain dysfunction and pancreatic dysfunction. In populations that have limited Sirt 1 activators diabetes will occur (developing world) and in the presence of Sirt 1 inhibitors no neuron proliferation with the induction of NAFLD [Reference 5].
REFERENCES:
1. Martins IJ. Caffeine with Links to NAFLD and Accelerated Brain Aging. Chapter: Non-Alcoholic Fatty Liver Disease - Molecular Bases, Prevention and Treatment. InTech - Open Science Open Minds | InTechOpen
2. Martins IJ. Caffeine Consumption and Induction of Obesity in the Developed World. Ann Obes Disord. 2017; 2(1): 1018.
3. Martins IJ. Caffeine consumption with Relevance to Type 3 diabetes and accelerated brain aging. Research and Reveiws: Neuroscience. 1,1, December, 2016.
4. Martins IJ. Nutrigenomic Diets and Caffeine Determines the Intelligence Quotient and Thinking in Developing Countries. Research and Reveiws: Neuroscience. 2017.1:2.
5. Martins IJ. Nutrition Therapy Regulates Caffeine Metabolism with Relevance to NAFLD and Induction of Type 3 Diabetes. J Diabetes Metab Disord. 2017; 4: 019.
6. Martins IJ. FOOD INTAKE AND CAFFEINE DETERMINE AMYLOID BETA METABOLISM WITH RELEVANCE TO MITOPHAGY IN BRAIN AGING AND CHRONIC DISEASE. European Journal of Food Science and Technology. 2016;4:11-17.
7. Martins IJ. Unhealthy Nutrigenomic Diets Accelerate NAFLD and Adiposity in Global communities. Journal of Molecular and Genetic Medicine: 03/2015; 9(1).
8. Martins IJ (2017) Single Gene Inactivation with Implications to Diabetes and Multiple Organ Dysfunction Syndrome. J Clin Epigenet. Vol. 3 No. 3:24.
9. Martins IJ. Diabetes and Organ Dysfunction in the Developing and Developed. Global Journal of Medical Research: F Diseases Volume 15 Issue 1 Version 1.0 Year 2015.
10. Martins IJ. Diabetes and Organ Dysfunction in the Developing and Developed. World Global Journal of Medical Research: F Diseases Volume 15 Issue 1 Version 1.0 Year 2015.
Yours sincerely,
Ian Martins (Ph D)
Fellow of International Agency for Standards and Ratings (IASR)
Centre of Excellence for Alzheimer's Disease Research and Care School of Medical Sciences Edith Cowan University 270 Joondalup Drive Joondalup Western Australia 6027
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