We have discussed “obesogens,” or chemicals that compromise our metabolism in depth in past issues. They do so mainly by interfering with cell membrane function, which leads to insulin resistance, and by compromising how we detoxify said chemicals in the liver. The more compromised we are in liver function (think drugs, alcohol, genetics,) the less efficiently we eliminate chemicals like Bisphenol A in plastics. A marker for suboptimal liver detoxification is a “fatty Liver,” seen all too often in Ultrasounds for Gall Bladder issues, or other problems.
It turns out that “Children with NAFLD (Fatty Liver) Are More Sensitive to the Adverse Metabolic Effects of Fructose Beverages than Children without NAFLD.” This means that many kids are caught up in a metabolic vicious cycle: the more High Fructose Corn Syrup they eat, the worse their liver gets. The worse the liver gets, the more problems they have with HFCS.
Don’t believe the commercials telling you that HFCS is OK: follow the money.
Hugo Rodier, MD
If we become insulin resistant, energy/sugar cannot enter our cells; where is it going to go? To fat cells, which do not need insulin to incorporate glucose. This is how we end up with not only a Fatty Liver, but also a Fatty Ass, and Fatty muscles. How fatigued do you think you will be, packing all that extra weight, detoxifying poorly and moving around under the power of muscles infiltrated with fat? Take a look:
“Intramyocellular Lipid Is Associated with Visceral Adiposity, Markers of Insulin Resistance, and Cardiovascular Risk in Prepubertal Children: The EPOCH Study,”
“First-Degree Relatives of Type 2 Diabetic Patients Have Reduced Expression of Genes Involved in Fatty Acid Metabolism in Skeletal Muscle.”
“Skeletal Muscle Lipid Peroxidation and Insulin Resistance in Humans,”
Don’t be like the Tin Man
Obesogens affect our metabolism by oxidizing and inflaming our cell membranes, which then become insulin resistant. Again, the plot “sickens:” the same process of oxidation and inflammation also occurs on the originating end, that is, where insulin is produced, the Beta cells in the pancreas, further compounding metabolic problems. How can you minimize these issues? Eat a lot of antioxidants, and consider taking glutathione precursors as discussed in previous issues. The following is an abstract from the Journal Endocrinology that only egg heads will find interesting..
“Growing evidence indicates that the regulation of intracellular reactive oxygen species (ROS) and reactive nitrogen species (RNS) levels is essential for maintaining normal β-cell glucose responsiveness. While long-term exposure to high glucose induces oxidative stress in β cells, conflicting results have been published regarding the impact of ROS on acute glucose exposure and their role in glucose stimulated insulin secretion (GSIS). Although β cells are considered to be particularly vulnerable to oxidative damage, as they express relatively low levels of some peroxide-metabolizing enzymes such as catalase and glutathione (GSH) peroxidase, other less known GSH-based antioxidant systems are expressed in β cells at higher levels. Herein, we discuss the key mechanisms of ROS/RNS production and their physiological function in pancreatic β cells. We also hypothesize that specific interactions between RNS and ROS may be the cause of the vulnerability of pancreatic β cells to oxidative damage. In addition, using a hypothetical metabolic model based on the data available in the literature, we emphasize the importance of amino acid availability for GSH synthesis and for the maintenance of β-cell function and viability during periods of metabolic disturbance before the clinical onset of diabetes.”
Yeah, boring, but your doctor may need to read this, if he/her has not caught on to the dramatic importance of a good diet and the antioxidant/anti-inflammatory activity therein, particularly in those with metabolic problems.
Metabolism and your brain
“No effective treatments are currently available for the prevention or cure of Alzheimer’s disease (AD), the most frequent form of dementia in the elderly. The most recognized risk factors, advancing age and having the apolipoprotein E Ɛ4 gene,cannot be modified or treated. Increasingly, scientists are looking toward other risk factors to identify preventive and therapeutic strategies. Much attention recently has focused on the metabolic syndrome (MetS), with a strong and growing body of research suggesting that metabolic disorders and obesity may play a role in the development of dementia.”
The brain is the organ that needs the most energy; any derangement in the processes that fuel neurons, like insulin resistance, will cause significant dysfunction. Refined diets promote more inflammation and oxidation in the brain, as do pollutants and chemicals like Bisphenol A. Mixed with less education, these toxins are likely to promote more cognitive dysfunction as we age. Throw in childhood adversity and we are likely to see a higher rate of brain inflammation that may manifest itself in most neurologic problems, from seizures to migraines. Of course, inflammation is not really the problem, but a normal reaction to a challenge, that is bad diets, stress and pollutants. If the brain mounts an anti-inflammatory response that leads to lifestyle changes and avoidance of pollutants, a lower rate of Alzheimer’s disease may be seen. For example, meditation, by ameliorating loneliness, has also been shown to decrease inflammation by modulating genetic expression and thereby “inducing positive structural brain changes.”
While genetics are involved in the chances of getting Alzheimer’s Disease that may hasten death, we may be able to lower the risk of brain disorders like AD according to the field of epigenetics. By optimizing how genes are copied or transcribed, functions that are optimized by plant based foods, clean environments and managing stress better, we stand a better chance of avoiding neurodegenerative diseases. The bottom line is to optimize energy to the brain, which is why Metformin, a drug to treat Diabetes and Pre Diabetes, has been shown to renew neurons.
Previous issues have discussed other things you could do. Here is an update from the latest research:
Medical drink high in anti-oxidants,
N-Acetyl-Cysteine, an amino acid,
Lastly, there is now “More Evidence Links Common Parasite to Suicidal Behavior.” I leave it to you to figure out why…
 J. Clinical Endocrinology & Metabolism 2012;97: E1088
 J. Clinical Endocrinology & Metabolism 2012;97: E1088
 J. Clinical Endocrinology & Metabolism 2012;97: E1332
 J. Clinical Endocrinology & Metabolism 2012;97: E1182
 “Reactive oxygen and nitrogen species generation, antioxidant defenses, and β-cell function: a critical role for
amino acids,” J Endocrinology 2012;214: 11
 Link between Metabolic Disorders and Alzheimer’s Disease Examined. Need for New Lines of Research Stressed
in a Supplement to Journal of Alzheimer’s Disease, June 15, 2012
 “Biomarkers of Insulin Resistance and Inflammation and the Risk for All-Cause Dementia and AD: results from
the Framingham Heart Study,” J. Archives of Neurology 2012;69:594
 “Prenatal Bisphenol A Exposure and Child Behavior in an Inner-City Cohort,”
J. Environmental Health Perspectives 2012;120:1190
 Exposure to solvents with less than HS education = higher risk MCI later in life, J. Neurology May 29th 2012
 J. Headache April 25th 2012 Epub
 J. Neurology. Published online August 15, 2012
 J. Archives of Neurology, Epub July 23rd 2012
 J. Cell Stem Cell 2012 July 5th Epub
 Med Scape Medical News August 24th 2012
 J. Stroke, Epub August 24th 2012
 “Impact of Smoking on Cognitive Decline in Early Old Age,” : The Whitehall II Cohort Study
J. J. Archives Gen Psychiatry. 2012;69:627
 J. Hypertension, Epub August 14th 2012
 “Medical drink improved cognition in Alzheimer’s Disease,” J. Alzheimer’s Disease, July 2012:
Eicospentaenoic acid, 300 mg, Docosahexaenoic acid, 1200 mg, Phospholipids 106 mg, Choline, 400 mg, Uridine monophosphate, 625 mg, Vitamin E 40 mg, Selenium, 60 µg, Vitamin B12, 3 µg, Vitamin B6, 1 µg, Folic acid, 400 µg
 NAC 900mg x1 month, then BID for 1 month, then TID 1 month may ease autism symptoms,
J. Biological Psychiatry June 1st 2012. It has been shown to help BPD in the past.
 “Maternal periconceptional folic acid intake and risk of autism spectrum disorders and developmental delay in the CHARGE (Childhood Autism Risks from Genetics and Environment) case-control study,”
American J. Clinical Nutrition 2012;96:80
 “Relationship Between Vitamin B12 and Sensory and Motor Peripheral Nerve Function in Older Adults,”
J. American Geriatric Society 2012;60:1057
 J. Clinical Psychiatry, Epub August 2012