Why is overcoming chronic fear so critical to Good Energy? Because in many ways, our mind controls our metabolism. When it comes to Good Energy and the brain, itβs a vicious cycle: a lack of healthy habits weakens the brainβs defenses to chronic stress, and chronic stress and fear can directly cause more metabolic dysfunction that worsens mood and resilience.
Consider that 75 to 90 percent of human diseases are related to activation of Β stress-βΒ related biology, and much evidence points to a common pathway between psychological stressors and metabolic dysfunction. Your cells βlistenβ to all your thoughts through biochemical signals, and the message they are getting from chronic stress is to halt the production of Good Energy. In fact, intense acute stress and chronic stress trigger all the hallmarks of Bad Energy:
1. Chronic Inflammation: In mice, just six hours of acute stress leads to a βrapid mobilizationβ of the immune system, with the increase in concentration of inflammatory cytokines. Cytokines are specific immune chemicals involved in early attacks of infections and wounds, as well as gene expression of pathways related to immune cell migration (the way immune cells get to the place they need to go to fight).
Stressful thoughts trigger neuroinflammation (inflammation in the brain). Neuroinflammation leads to metabolic dysfunction in the brain and predisposes us to metabolic diseases, like depression and neurodegeneration. It also impacts the whole body by kicking off the βstress armβ of the nervous Β systemββΒ the sympathetic nervous system (SNS) or fightβΒ orβΒ flight system. Overactivation of the SNS drives insulin resistance, hyperglycemia, and mobilization of inflammatory cells and cytokines throughout the body, further compounding Bad Energy everywhere.
Longer periods of psychological stress, like childhood abuse, are associated with elevated levels of the inflammatory cytokines CRP, TNFβΒ Ξ±, and ILβΒ 6. One researcher notes that chronicΒ stressββΒ induced inflammation represents the βcommon soilβ of a wide variety of metabolic diseases like cancer, fatty liver disease, heart disease, and type 2 diabetes. Remember, inflammation directly leads to Bad Energy by blocking the expression of glucose channels, blocking the insulin signal from transmitting inside the cell, and promoting the release of free fatty acids from fat cells, which can then be taken up by the liver and muscle and generate insulin resistance.
2. Oxidative Stress: In 2004, a study examined the blood of fifteen medical students both before and after their significant exams to measure oxidative stress biomarkers. The findings showed that the students had lower levels of antioxidants leading up to the exams and experienced higher levels of DNA and lipid damage from oxidation. These results suggest that their cells were subjected to oxidative stress during the stressful period. There is evidence to suggest that Β work-βΒ related stress also contributes to oxidative stress.
For example, a study in Japan demonstrated a correlation between 8βΒ hydroxydeoxyguanosine (8βΒ OHβΒ dG), an oxidative stress marker, and female workersβ perceived workload, psychological stress, and sense of impossibility in reducing stress. Similarly, a study in Spain found a relationship between high levels of Β work-βΒ related stress and malondialdehyde, another oxidative stress biomarker.
In rats, chronic stress induces oxidation of fats and decreases antioxidant activity. This correlated with higher LDL cholesterol and triglycerides, lower HDL, and, ultimately, plaque development in the rodentsβ arteries. Interestingly, animal studies have shown that ingested antioxidants may protect against Β stress-βΒ induced mitochondrial dysfunction, βindicating the existence of Β stress-Β sensitizing and Β stress-βΒ buffering factors for the effects of induced stress on mitochondria.β Similarly, when mice are engineered to overexpress mitochondrial antioxidant enzymes, they seem to have increased capacity to handle stressors.
3. Mitochondrial Dysfunction: While almost all research on psychosocial stress and mitochondrial function has been done in animals, the results indicate a clear theme that βchronic stress induced through a form of psychosocial stressor decreases mitochondrial energy production capacity and alters mitochondrial morphology.β This showed up as reduction in the function of mitochondrial proteins, lower rate of oxygen consumption (which is needed to make ATP in the mitochondria), and lower mitochondrial content.
4. High Glucose Levels: Elevations of stress hormones resulting from acute psychological stressors can lead to diabetogenic effects, meaning that they immediately raise blood sugar rapidly while also causing fat cells to break down fat and release it into the bloodstream, which promotes insulin resistance. During stress, the body mobilizes a βquickβ and robust source of energy, so stress hormones prompt the rapid breakdown of stored glucose from the liver (glycogenolysis) and increase production of glucose from the liver (gluconeogenesis).
As stress hormones trigger the rapid breakdown of triglycerides (stored fat) in fat cells, one of the breakdown products is glycerol, which can be transported to the liver to manufacture glucose via gluconeogenesis. Researchers believe that repeated acute stress responses could βinduce repeated exposure to transient hyperglycemia and hyperlipidemia, and insulin resistance, which could evolve toward type 2 diabetes onset in the long term.β Levels members often report being surprised by the impact a stressful day at work can have on their blood sugar, and how increases in blood sugar can indicate stress.
5. Worse Metabolic Biomarkers: Chronic stress is associated with obesity, lower HDL, increased visceral fat, larger waist circumference, and higher blood pressure, LDL, heart rate, insulin levels, and triglycerides. Whatβs more, cortisol levels have been shown to be a predictor of elevated levels of HOMAβΒ IR, a key marker of insulin resistance.
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