As we begin a new year we reflect upon our health and mortality. Some are thus led to plastic surgery and hormonal therapies that only delay the inevitable. This is understandable, but not healthy. Aging properly and maintaining health as long as possible while we travel through this valley of tears is best accomplished by being mindful of “energy” issues: the energy of our relationships, the energy of good food, and the energy sources that pollute our environment.
1. Aging well depends upon maintaining the right “metabolism,” or fueling our body cells properly with the whole foods, not processed garbage:
- “The metabolic regulation of aging.”[1]
2. Aging depends on our metabolism being supported, or mitigated by the right amounts and types of antioxidants. Oxidation is the basic and unavoidable result of energy-consumption in the mitochondria of each cell:
- “Mitochondria-targeted antioxidants.”[2]
- “Association of habitual dietary resveratrol (grapes) exposure with the development of frailty in older age: the Invecchiare in Chianti study.”[3]
3. Aging depends on how clean we are able to maintain our environment:
- “Aging: toward avoiding the inevitable:”[4]
“Aging is receiving more attention as a risk factor for human disease. With the correct modeling of human heterogeneity and consideration of environmental factors in the aging process, we may delay the onset of human disease.”
4. Aging depends on proper relationships wherein we learn to be unselfish in the service of others:
- “Personality Traits and Inflammation in Men and Women in Their Early 70s: The Lothian Birth Cohort 1936 Study of Healthy Aging.”[5]
Hugo Rodier, MD
Ignoring the root of diseases
Aging poorly is a sure result of not properly addressing the root of diseases listed above. Trying to address the consequences of toxic living with drugs is not only foolish, but unsustainable. While pharmaceutical products are occasionally needed, particularly in emergent situations, they may have dire side effects:
“Antidepressant Use During Pregnancy and the Risk of Autism Spectrum Disorder in Children:”[6]
“Children of women who took antidepressants during the second and third trimesters of pregnancy were 87 percent more likely to develop autism than kids born to women who didn’t take the drugs.”
Yet, we continue to ignore the cause of the explosion of Autism in our children, despite clear evidence that it is due to poor diets and toxic environments affecting genetic expression. Please, do read about EPIGENETICS. The same applies to practically all other organs:
“Road Repairs: Does Exposure to Traffic Affect Mechanisms of Vascular Injury and Repair.”[7]
- “Pivotal Role for the Visceral Fat Compartment in the Release of Persistent Organic Pollutants During Weight Loss.”[8]
- “Circulating Markers of Liver Function and Cardiovascular Disease Risk.”[9]
- “The Association Between Body Mass Index and Disability, Depression, History of Abuse, Medications, and Comorbidities.”
Yet, it has been amply demonstrated that “Healthy eating lowers mortality risk in a large cohort of cardiac patients who received state-of-the-art drug treatment.”[10] I am sure many of these patients could have avoided pharmaceutical treatment altogether if they had minded the concepts discussed above. Sounds nuts? Read on…
“Effects of tree nuts on blood lipids, apolipoproteins, and blood pressure: systematic review, meta-analysis, and dose-response of 61 controlled intervention trials.”[11]
“Eating a handful of walnuts each day may be particularly good for people at risk of developing diabetes, a U.S. study suggests. When people in the study added 56 grams of walnuts (2 ounces, or about 14 walnuts) to their daily diet for six months, they had improvements in blood vessel function and reductions in LDL cholesterol.”[12]
Of course, one thing is to eat the right foods; another is to maintain the right gut flora. These are two sides of the same coin. See articles below and the January blog.
Gut Update
“Psyllium fiber improves glycemic control proportional to loss of glycemic control: a meta-analysis of data in euglycemic subjects, patients at risk of type 2 diabetes mellitus, and patients being treated for type 2 diabetes mellitus.”
Am J Clin Nutr 2015 102: 1604
“Prebiotic (fiber) consumption and the incidence of overweight in a Mediterranean cohort: the Seguimiento Universidad de Navarra Project.”
Am J Clin Nutr 2015 102: 1554
“Comparative metabolomics in vegans and omnivores reveal constraints on diet-dependent gut microbiota metabolite production.”
J. Gut 2016;65:63
“Dietary Fiber-Induced Improvement in Glucose Metabolism Is Associated with Increased Abundance of Prevotella.”[13]
“The gut microbiota plays an important role in human health by interacting with host diet, but there is substantial inter-individual variation in the response to diet. Here we compared the gut microbiota composition of healthy subjects who exhibited improved glucose metabolism following 3-day consumption of barley kernel-based bread (BKB) with those who responded least to this dietary intervention. The Prevotella/Bacteroides ratio was higher in responders than non-responders after BKB. Metagenomic analysis showed that the gut microbiota of responders was enriched in Prevotella copri and had increased potential to ferment complex polysaccharides after BKB. Finally, germ-free mice transplanted with microbiota from responder human donors exhibited improved glucose metabolism and increased abundance of Prevotella and liver glycogen content compared with germ-free mice that received non-responder microbiota. Our findings indicate that Prevotella plays a role in the BKB-induced improvement in glucose metabolism observed in certain individuals, potentially by promoting increased glycogen storage.”
“Gut Microbiota Orchestrates Energy Homeostasis during Cold:”[14]
“Microbial functions in the host physiology are a result of the microbiota-host co-evolution. We show that cold exposure leads to marked shift of the microbiota composition, referred to as cold microbiota. Transplantation of the cold microbiota to germ-free mice is sufficient to increase insulin sensitivity of the host and enable tolerance to cold partly by promoting the white fat browning, leading to increased energy expenditure and fat loss. During prolonged cold, however, the body weight loss is attenuated, caused by adaptive mechanisms maximizing caloric uptake and increasing intestinal, villi, and microvilli lengths. This increased absorptive surface is transferable with the cold microbiota, leading to altered intestinal gene expression promoting tissue remodeling and suppression of apoptosis—the effect diminished by co-transplanting the most cold-downregulated strain Akkermansia muciniphila during the cold microbiota transfer. Our results demonstrate the microbiota as a key factor orchestrating the overall energy homeostasis during increased demand.”
“Microbiota-Dependent Hepatic Lipogenesis Mediated by Stearoyl CoA Desaturase 1 (SCD1) Promotes Metabolic Syndrome in TLR5-Deficient Mice.”[15]
“The gut microbiota plays a key role in host metabolism. Toll-like receptor 5 (TLR5), a flagellin receptor, is required for gut microbiota homeostasis. Accordingly, TLR5-deficient (T5KO) mice are prone to develop microbiota-dependent metabolic syndrome. Here we observed that T5KO mice display elevated neutral lipids with a compositional increase of oleate [C18:1 (n9)] relative to wild-type littermates. Increased oleate contribution to hepatic lipids and liver SCD1 expression were both microbiota dependent. Analysis of short-chain fatty acids (SCFAs) and 13C-acetate label incorporation revealed elevated SCFA in ceca and hepatic portal blood and increased liver de novo lipogenesis in T5KO mice. Dietary SCFAs further aggravated metabolic syndrome in T5KO mice. Deletion of hepatic SCD1 not only prevented hepatic neutral lipid oleate enrichment but also ameliorated metabolic syndrome in T5KO mice. Collectively, these results underscore the key role of the gut microbiota-liver axis in the pathogenesis of metabolic diseases.”
- Journal Nature Medicine December 2015 Volume 21,pp1416 – 1423 ↑
- FASEB J. December 2015 29:4766 ↑
- Am J. Clin Nutr 2015 102: 1534 ↑
- Journal Nature Medicine December 2015 Volume 21,p1373 ↑
- J. Psychosom Med January 2013;75:11↑
- JAMA Pediatr. Published online December 14, 2015 ↑
- J.Arterioscler Thromb Vasc Biol. 2015;35:2266 ↑
- Journal Clinical Endocrinology Metabolism 2015 100(12), pp. 4463 ↑
- J. Arterioscler Thromb Vasc Biol. 2015;35:229 ↑
- J. Am J Clin Nutr 2015 102: 1527↑
- Am J. Clin Nutr 2015 102: 1347 ↑
- BMJ Open Diab Res Care Nov 2015 ↑
- J. Cell Metab Volume 22, Issue 6 , p971–982, 1 December 2015 ↑
- J Cell Volume 163, Issue 6 , p1360–1374, 3 December 2015 ↑
- J Cell Metab Volume 22, Issue 6 , p983–996, 1 December 2015 ↑
