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Gout, a painful form of arthritis, occurs when high levels of uric acid in the blood cause crystals to form and accumulate around a joint.
Uric acid is produced when the body breaks down a chemical called purine. Purine occurs naturally in your body, but it’s also found in certain foods. Uric acid is eliminated from the body in urine.
Grounding may reduce your risk of cardiovascular disease and may thin your blood, both good things when you want to reduce your risk for gout. If you want to try grounding, start by walking in a dewy, grassy area barefoot.
If you live near a large body of water, that’s a great location for walking barefoot, as seawater is a good conductor.
1. Apple Cider Vinegar: ACV is considered king when it comes to a gout natural home remedy and it’s my most popular post voted by social media. ACV helps your body become more alkaline and the acidity helps relieve acute gout pain. Many gout sufferers report drinking 1-2 tablespoons of raw unfiltered and organic apple cider vinegar in a glass of at least 8 ounces of water. Some will drink this 2-3 times a day for better results. ACV can also be used as topical treatment. You you can soak your foot for about 30 minutes in a bucket full of 4 cups of hot water and 1 cup of apple cider vinegar. You can also soak a clean, dry cloth in apple cider vinegar and wrap it around the affected area for about 15 minutes.
2. Baking Soda: Another extremely popular natural home remedy for gout sufferers is baking soda. Like apple cider vinegar, it makes your body more alkaline. Many consume ½ a teaspoon in a glass of 8 oz. water.Many will repeat this throughout the day until they have consumed at least 3 teaspoons of baking soda. It helps lower uric acid providing with relief from the pain at the same time. Avoid this home remedy if suffering from high blood pressure and try to limit salt intake in your meals during the day when taking baking soda. Baking soda is very high in sodium. The maximum recommended dose is 4 teaspoons throughout the day.
3. Cherries: Whether sweet or sour, cherries have been known to be extremely effective in treating gout and lowering uric acid due to their high antioxidant properties. In one study conducted with 600 people suffering from gout, it was concluded that eating half a cup serving of cherries daily (10-12 cherries) resulted in a 35% reduced risk of a successive gout attack. For those eating 2 or even 3 servings in a day, their risk dropped to 50%! But that is too much sugar as well which can cause other health ailments. Best recommendation is to use a tart cherry extract supplement and avoid the sugar intake if you can!
4. Ginger and/or Turmeric: The powerful anti-inflammatories present in ginger root and turmeric can be very helpful in easing gout pain and inflammation. I basically chop off a little piece the size of an inch and boil it for about 20 minutes and drink it as tea. You can also add ginger root and/or turmeric in cooking recipes. Some may also eat a small piece raw daily. Others use it topically to reduce swelling by making a paste of ginger root with water and then apply it to the affected area, leaving it on for about 30 minutes.
A thrombus occurs when the hemostatic process, which normally occurs in response to injury, becomes activated in an uninjured or slightly injured vessel. A thrombus in a large blood vessel will decrease blood flow through that vessel (termed a mural thrombus). In a small blood vessel, blood flow may be completely cut off (termed an occlusive thrombus), resulting in death of tissue supplied by that vessel. If a thrombus dislodges and becomes free-floating, it is considered an embolus.
Some of the conditions which elevate risk of blood clots developing include atrial fibrillation (a form of cardiac arrhythmia), heart valve replacement, a recent heart attack (also known as a myocardial infarction), extended periods of inactivity (see deep venous thrombosis), and genetic or disease-related deficiencies in the blood’s clotting abilities.
Platelet activation can occur through different mechanisms such as a vessel wall breach that exposes collagen, or tissue factor encryption.[clarification needed] The platelet activation causes a cascade of further platelet activation, eventually causing the formation of the thrombus.This process is regulated through thromboregulation.
Blood clot prevention and treatment reduces the risk of stroke, heart attack and pulmonary embolism. Heparin and warfarin are often used to inhibit the formation and growth of existing thrombi; the former binds to and activates the enzyme inhibitor antithrombin III, while the latter inhibits vitamin K epoxide reductase, an enzyme needed to synthesize mature clotting factors.
Some treatments have been derived from bacteria. One drug is streptokinase, which is an enzyme secreted by several streptococcal bacteria. This drug is administered intravenously and can be used to dissolve blood clots in coronary vessels. However, streptokinase is nonspecific and can digest almost any protein, which can lead to many secondary problems. Another clot-dissolving enzyme that works faster and is more specific is called tissue plasminogen activator (tPA). This drug is made by transgenic bacteria and it converts plasminogen into the clot-dissolving enzyme plasmin. There are also some anticoagulants that come from animals that work by dissolving fibrin. For example, Haementeria ghilianii, an Amazon leech, produces an enzyme called hementin from its salivary glands. As of 2012, this enzyme has now been successfully produced by genetically engineered bacteria and administered to cardiac patients.
Thrombus formation can have one of four outcomes: propagation, embolization, dissolution, and organization and recanalization.
A number of factors are likely behind the surprising rise in strokes in women, including:
Earlier this year, research presented at the American Stroke Association’s International Stroke Conference showed that people who drink just one diet soda a day may increase their risk of stroke by 48 percent!
According to the authors:
“This study suggests that diet soda is not an optimal substitute for sugar-sweetened beverages, and may be associated with a greater risk of stroke, myocardial infarction, or vascular death than regular soda.”
While more research will likely be needed to confirm this potential link, there’s plenty of evidence showing that artificial sweeteners such as aspartame and sucralose (Splenda) can be dangerous to your health. I believe aspartame is, by far, the most dangerous artificial sweetener on the market. Reports of adverse reactions to the US FDA also support this, as aspartame accounts for over 75 percent of the adverse reactions to food additives reported to the FDA.
An embolism is the lodging of an embolus, a blockage-causing piece of material, inside a blood vessel. The embolus may be a blood clot (thrombus), a fat globule, a bubble of air or other gas (gas embolism), or foreign material. An embolism can cause partial or total blockage of blood flow in the affected vessel. Such a blockage (a vascular occlusion) may affect a part of the body distant from where the embolus originated. An embolism in which the embolus is a piece of thrombus is called a thromboembolism. Thrombosis, the process of thrombus formation, often leads to thromboembolism.
An embolism is usually a pathologic event (that is, part of illness or injury). Sometimes it is created intentionally for a therapeutic reason, such as to stop bleeding or to kill a cancerous tumor by stopping its blood supply. Such therapy is called embolization.
In health care, gender disparities are especially pernicious. If you are a woman, studies have shown, you are not only less likely to receive blood clot prophylaxis, but you may also receive less intensive treatment for a heart attack. If you are a woman older than 50 who is critically ill, you are at particular risk of failing to receive lifesaving interventions. If you have knee pain, you are less likely to be referred for a knee replacement than a man, and if you have heart failure, it may take longer to get EKGs.
When Dr. Elliott Haut and his team at Johns Hopkins Hospital in Baltimore designed their blood clot prevention protocol back in 2006, they didn’t expect to discover systemic gender bias. But the data were clear and the implications were alarming: Women who were trauma patients at Johns Hopkins Hospital were in considerably greater danger of dying of preventable blood clots than men.
Why? Because doctors were less likely to provide them with the appropriate blood clot prevention treatment. At Hopkins, as at many hospitals, both men and women were receiving treatment at less than perfect rates, but while 31 percent of male trauma patients were failing to get proper clot prevention, for women, the rate was 45 percent. That means women were nearly 50 percent more likely to miss out on blood clot prevention.
Blood clots, gelatinous tangles that can travel through the body and block blood flow, kill more people every year than breast cancer, AIDS and car crashes combined. But many of these clots can be avoided — if doctors prescribe the right preventive measures.
Such implicit bias, as researchers now understand, happens when we unintentionally use stereotypes or associations to make judgments. “Perhaps we take women’s symptoms less seriously, or we interpret them as having an emotional cause as opposed to a physical cause,” said Dr. Christine Kolehmainen, the associate director for women’s health at the Middleton Memorial Veterans Hospital in Madison, Wis. Studies bear this out: in one study of patients with irritable bowel syndrome, doctors were more likely to suggest that male patients receive X-rays and more likely to offer female patients tranquilizers and lifestyle advice.
In the case of blood clot prevention, doctors’ assumptions about women’s risk factors could lead to disparities in treatment. “There might be stereotypes about women’s biology or environment or occupation that could all play into medical decision-making,” Kolehmainen said.
Whether unintentional, unconscious or simply based on erroneous assumptions, treatment differentials clearly exist. Interventions like the Hopkins checklist can help correct them.
A University of Virginia study was conducted to determine if stress enhance or impair memory Consolidation.
Overall results provide consistent evidence that stress does not uniformly enhance memory consolidation. Although prior research has shown that stress during recall can interfere with memory, the current experiments obtained evidence of interference when stress was introduced after learning and participants had returned to baseline levels of arousal before recall. This is the first evidence of which the authors are aware that stress can actually impair consolidation of declarative memories. We tested several hypotheses for these effects, including those concerned with stimulus type, rehearsal, gender, hormonal influences (from menstrual cycle and oral contraceptive use), and opportunity for post-encoding processing. Nevertheless, we continued to obtain the same robust finding that stress-induced arousal impairs long term memory.
In each experiment, exposure to a stressor interfered with, rather than enhanced, long term memory for associated material.
Another was conducted to determine if chronic stress induces a hyporeactivity of the autonomic nervous system in response to acute mental stressor and impairs cognitive performance in business executives.
The study is the first to demonstrate a blunted reactivity of the ANS when male subjects with chronic psychological stress were subjected to an acute mental stressor, and this change could contribute to impairments in cognitive performance.
Another study also demonstrated that it is better not to deal with two tasks at the same time when stressed since acute psychosocial stress reduces task shielding in dual-task performance.
Following successful stress induction, as indicated by increases in salivary α-amylase (sAA) and cortisol that reflect increases in sympathetic nervous system and hypothalamus-pituitary-adrenal (HPA) axis activity, respectively, stressed individuals displayed reduced task shielding relative to controls. This result was further substantiated by a correlation between treatment-related increase in cortisol, but not sAA, and between-task interference, suggesting a potential role of the HPA stress response for the development of the observed effects. As an additional finding, when the volunteers were categorized with regard to their action-state orientation, their orientation did not interact with stress but did reveal generally increased between-task interference, and thus inferior task shielding, for state-oriented as compared to action-oriented individuals.
Connie’s comments: Chronic stress, experiencing stressors over a prolonged period of time, can result in a long-term drain on the body.
Summary: Researchers report they have established a link between emotional stress and diabetes.
Source: Rice University.
Connection established between anxiety control, inflammation and Type 2 diabetes.
A Rice University study has found a link between emotional stress and diabetes, with roots in the brain’s ability to control anxiety.
That control lies with the brain’s executive functions, processes that handle attention, inhibition, working memory and cognitive flexibility and are also involved in reasoning, problem-solving and planning.
The study published in Psychoneuroendocrinology establishes a metabolic chain reaction that starts with low inhibition, aka attention control, which leaves a person vulnerable to tempting or distracting information, objects, thoughts or activities. Previous studies have shown that such vulnerability can lead to more frequent anxiety, and anxiety is known to activate a metabolic pathway responsible for the production of pro-inflammatory cytokines, signaling proteins that include interleukin-6 (IL-6).
Along with cognitive tests that measured attention control, the Rice study measured levels of both blood glucose and IL-6 in more than 800 adults. IL-6 is a protein the body produces to stimulate immune response and healing. It is a biomarker of acute and chronic stress that also has been associated with a greater likelihood of diabetes and high blood glucose.
The research showed individuals with low inhibition were more likely to have diabetes than those with high inhibition due to the pathway from high anxiety to IL-6. The results were the same no matter how subjects performed on other cognitive tests, like those for memory and problem-solving.
Researchers have suspected a link between anxiety and poor health, including diabetes, for many years but none have detailed the biological pathway responsible, said lead author Kyle Murdock, a postdoctoral research fellow in psychology. He said the Rice study takes a deeper look at how inflammation bridges the two.
“The literature shows individuals with poor inhibition are more likely to experience stressful thoughts and have a harder time breaking their attention away from them,” Murdock said. “That made me wonder if there’s a stress-induced pathway that could link inhibition with inflammation and the diseases we’re interested in, such as diabetes.
“Plenty of research shows that when individuals are stressed or anxious or depressed, inflammation goes up,” he said. “The novel part of our study was establishing the pathway from inhibition to anxiety to inflammation to diabetes.”
Murdock works in the Rice lab of Christopher Fagundes, assistant professor of psychology. The Fagundes lab investigates processes that happen along the border of psychology and physiology, and how those processes affect overall health and potential treatments.
The data came from a Midlife Development in the United States study of 1,255 middle-aged adults whose cognitive abilities were tested two years apart. More than 800 of those also underwent blood tests to check IL-6 and glucose levels. The Rice researchers found not only the positive link between inhibition and diabetes, but the absence of a link between other cognitive functions and the disease. They also determined that the pathway only went in one direction: Inflammation never appeared to affect inhibition. Murdock said a year as a clinical psychology intern at the Oregon Health and Science University, where he studied with co-author and psychologist Danny Duke, led the researchers to think there could also be a feedback loop at play in those with diabetes. “Individuals who are anxious are more likely to avoid treatment and use maladaptive strategies (like smoking or unhealthy diets) that enhance their blood glucose, which is problematic. It’s a snowball effect: The further they go, the worse it gets,” he said.
“We also know that extremely high blood glucose can impact cognition as well. We talked about how, if we’re going to treat these individuals appropriately, it won’t be by sitting them down in a room and saying, ‘Hey, you need to eat better,’ or ‘You need to use your insulin on time.’”
The researchers listed several possible interventions, including mindfulness therapy, stimulant or anti-inflammatory medications and cognitive behavioral therapy. “Research shows that people who practice mindfulness do better on the inhibition tests over time,” Murdock said, suggesting that shifting one’s attention away from stressful thoughts may affect physiological responses.
“I’m a firm believer that mindfulness-based approaches to treatment are a great idea, for a lot of reasons,” Fagundes said. “That doesn’t mean medicines that promote inhibition, such as stimulants, shouldn’t be considered, but a combination of the two could be really helpful.”
Co-authors of the paper are Angie LeRoy, a Rice staff member and a graduate student at the University of Houston; and Tamara Lacourt, a postdoctoral researcher, and Cobi Heijnen, a professor of symptom research at the University of Texas MD Anderson Cancer Center.
Funding: The National Institute on Aging and the National Heart, Lung and Blood Institute supported the research.
Source: Jeff Falk – Rice University
Image Source: This NeuroscienceNews.com image is credited to Andrea Lugo/Rice University.
Original Research Abstract “Executive functioning and diabetes: The role of anxious arousal and inflammation” by Kyle W. Murdock, Angie S. LeRoy, Tamara E. Lacourt, Danny C. Duke, Cobi J. Heijnen, and Christopher P. Fagundes in Psychoneuroendocrinology. Published online May 18 2016 doi:10.1016/j.psyneuen.2016.05.006
Executive functioning and diabetes: The role of anxious arousal and inflammation
Individuals who perform poorly on measures of the executive function of inhibition have higher anxious arousal in comparison to those with better performance. High anxious arousal is associated with a pro-inflammatory response. Chronically high anxious arousal and inflammation increase one’s risk of developing type 2 diabetes. We sought to evaluate anxious arousal and inflammation as underlying mechanisms linking inhibition with diabetes incidence. Participants (N = 835) completed measures of cognitive abilities, a self-report measure of anxious arousal, and donated blood to assess interleukin-6 (IL-6) and glycated hemoglobin (HbA1c). Individuals with low inhibition were more likely to have diabetes than those with high inhibition due to the serial pathway from high anxious arousal to IL-6. Findings remained when entering other indicators of cognitive abilities as covariates, suggesting that inhibition is a unique cognitive ability associated with diabetes incidence. On the basis of our results, we propose several avenues to explore for improved prevention and treatment efforts for type 2 diabetes.
“Executive functioning and diabetes: The role of anxious arousal and inflammation” by Kyle W. Murdock, Angie S. LeRoy, Tamara E. Lacourt, Danny C. Duke, Cobi J. Heijnen, and Christopher P. Fagundes in Psychoneuroendocrinology. Published online May 18 2016 doi:10.1016/j.psyneuen.2016.05.006
About 10–15% of human couples are infertile, unable to conceive. In approximately in half of these cases, the underlying cause is related to the male. The underlying causative factors in the male infertility can be attributed to environmental toxins, systemic disorders such as, hypothalamic–pituitary disease, testicular cancers and germ-cell aplasia. Genetic factors including aneuploidies and single-gene mutations are also contributed to the male infertility.
Patients suffering from nonobstructive azoospermia or oligozoospermia show microdeletions in the long arm of the Y chromosome and/or chromosomal abnormalities, each with the respective frequency of 9.7% and 13%. A large percentage of human male infertility is estimated to be caused by mutations in genes involved in primary or secondary spermatogenesis and sperm quality and function. Single-gene defects are the focus of most research carried out in this field.
NR5A1 mutations are associated with male infertility, suggesting the possibility that these mutations cause the infertility. However, it is possible that these mutations individually have no major effect and only contribute to the male infertility by collaboration with other contributors such as environmental factors and other genomics variants. Vice versa, existence of the other alleles could reduce the phenotypic effects of impaired NR5A1 proteins and attenuate the expression of abnormal phenotypes and manifest male infertility solely.
Nuclear receptor subfamily 5 group A member 1 (NR5A1), also known as SF1 or Ad4BP (MIM 184757), is located on the long arm of chromosome 9 (9q33.3). The NR5A1 is an orphan nuclear receptor that was first identified following the search for a common regulator of the cytochrome P450 steroid hydroxylase enzyme family. This receptor is a pivotal transcriptional regulator of an array of genes involved in reproduction, steroidogenesis and male sexual differentiation and also plays a crucial role in adrenal gland formation in both sexes. NR5A1 regulates the mullerian inhibitory substance by binding to a conserved upstream regulatory element and directly participates in the process of mammalian sex determination through mullerian duct regression.
Targeted disruption of NR5A1 (Ftzf1) in mice results in gonadal and adrenal agenesis, persistence of Mullerian structures and abnormalities of the hypothalamus and pituitary gonadotropes. Heterozygous animals demonstrate a milder phenotype including an impaired adrenal stress response and reduced testicular size. In humans, NR5A1 mutations were first described in patients with 46, XY karyotype and disorders of sex development (DSD), Mullerian structures and primary adrenal failure (MIM 612965). After that, heterozygous NR5A1 mutations were described in seven patients showing 46, XY karyotype and ambiguous genitalia, gonadal dysgenesis, but no adrenal insufficiency. Since then, studies have confirmed that mutations in NR5A1 in patients with 46, XY karyotype cause severe underandrogenisation, but no adrenal insufficiency, establishing dynamic and dosage-dependent actions for NR5A1. Subsequent studies revealed that NR5A1 heterozygous mutations cause primary ovarian insufficiency (MIM 612964).
Recently, NR5A1 mutations have been related to human male infertility (MIM 613957). These findings substantially increase the number of NR5A1 mutations reported in humans and show that mutations in NR5A1 can be found in patients with a wide range of phenotypic features, ranging from 46, XY sex reversal with primary adrenal failure to male infertility. For the first time, Bashamboo et al. (2010) conducted a study on the nonobstructive infertile men (a non-Caucasian mixed ancestry n = 315), which resulted in the report of all missense mutations in the NR5A1 gene with 4% frequency. Functional studies of the missense mutations revealed impaired transcriptional activation of NR5A1-responsive target genes. Subsequently, three missense mutations were identified as associated with and most likely the cause of the male infertility, according to computational analyses. The study indicated that the mutation frequency is below 1% (Caucasian German origin, n = 488). In another study the coding sequence of NR5A1 has been analysed in a cohort of 90 well-characterised idiopathic Iranian azoospermic infertile men versus 112 fertile men. Heterozygous NR5A1 mutations were found in 2 of 90 (2.2%) of cases. These two patients harboured missense mutations within the hinge region (p.P97T) and ligand-binding domain (p.E237K) of the NR5A1 protein.
Semen is only one percent sperm; the rest is composed of over 200 separate proteins, as well as vitamins and minerals including vitamin C, calcium, chlorine, citric acid, fructose, lactic acid, magnesium, nitrogen, phosphorus, potassium, sodium, vitamin B12, and zinc .
Endocrine disruptors are chemicals that, at certain doses, can interfere with endocrine (or hormone) systems. These disruptions can cause cancerous tumors, birth defects, and other developmental disorders. Any system in the body controlled by hormones can be derailed by hormone disruptors.
Pituitary Gland in the brain is responsible for sleep, sex hormones, food cravings and stress hormones.
|ACTH||Adrenals||Stimulates the adrenal gland to produce a hormone called cortisol. ACTH is also known as corticotrophin.|
|TSH||Thyroid||Stimulates the thyroid gland to secrete its own hormone, which is called thyroxine. TSH is also known as thyrotrophin.|
|LH & FSH||Ovaries (women)
|Controls reproductive functioning and sexual characteristics. Stimulates the ovaries to produce oestrogen and progesterone and the testes to produce testosterone and sperm. LH and FSH are known collectively as gonadotrophins. LH is also referred to as interstitial cell stimulating hormone (ICSH) in males.|
|PRL||Breasts||Stimulates the breasts to produce milk. This hormone is secreted in large amounts during pregnancy and breast feeding, but is present at all times in both men and women.|
|GH||All cells in the body||Stimulates growth and repair. Research is currently being carried out to identify the functions of GH in adult life.|
|MSH||Exact role in humans is unknown.|
|ADH||Kidneys||Controls the blood fluid and mineral levels in the body by affecting water retention by the kidneys. This hormone is also known vasopressin or argenine vasopressin (AVP).|
|Affects uterine contractions in pregnancy and birth and subsequent release of breast milk.|
“One chemical of note involved in the HPA axis’ work is corticotropin-releasing hormone (CRH). The hypothalamus releases CRH in response to stress, illness, exercise, cortisol in the blood and sleep/wake cycles. It peaks soon after waking and slowly declines throughout the rest of the day. In a stressed individual, however, cortisol levels are elevated for prolonged periods of time.
During stress, the body believes it is in imminent danger, so cortisol triggers a number of metabolic changes to ensure that enough energy is available in case a fight or flight is necessary. One of these energy-saving tactics is to suppress the metabolically expensive immune system, saving vital glucose for the approaching life-threatening event …
In this way, ongoing stress can reduce the capabilities of the immune system as the body saves its energy for a physical exertion that never comes.”
On the other hand, oxytocin — a hormone that has long been associated with physical and emotional closeness — helps suppress the HPA axis, thereby promoting healthy immune function and improved wound healing.
The brain was once considered to lack normal immune surveillance. This was assumed to be the case because normal immune responses like swelling do not regularly occur inside the brain. If they did, people would be dying from it on a regular basis. However, considering the brain “immune privileged” turned out to be overly simplistic.
As noted above, research shows that your brain does in fact interact with your peripheral immune system, albeit in unique ways. In 2015, researchers discovered lymphatic vessels in the brain,13 again showing the connection between the brain and the immune system.
Neuropeptides may also be part of the puzzle, as they’ve been implicated in a number of functions involving emotions. For example, they play a role in social-, reproductive-, and reward-seeking behaviors. More than 100 neuropeptides are also used by your central nervous system; they influence both gene expression and the building of new brain synapses.
|Sudden death||Research shows that during the first week after the death of a spouse, mortality skyrockets to double the normal rate|
|Heart and cardiovascular disease, stroke, and heart attacks||Letting your anger out explosively may be harmful because it triggers surges in stress hormones and injures blood vessel linings.
One study11 found that people over the age of 50 who express their anger by lashing out are more likely to have calcium deposits in their coronary arteries — an indication that you’re at a high risk for a heart attack — than their mellower peers.
A systematic review12 involving data on 5,000 heart attacks, 800 strokes and 300 cases of arrhythmia also revealed that anger increases your risk of heart attack, arrhythmia and stroke — and the risk increases with frequent anger episodes.
|Gastrointestinal (GI) problems||Sustained or chronic stress has been linked to a number of GI problems, including inflammatory bowel disease and irritable bowel syndrome.
It’s becoming increasingly clear that your brain, your immune system and your gut microbes are intricately linked.
Autism, for instance, is associated with gastrointestinal problems and potentially an over-reaction in the immune system
|Cancer||Your outlook has an effect on your ability to recover from cancer. The quality and quantity of psychological support also makes a difference in survival rates|
|HIV||Heightened stress and dwindling support from family and friends has been shown to accelerate the progression of HIV infection|
|Allergies||Skin complaints like psoriasis and eczema have psychological underpinnings. Ditto for asthma. All tend to worsen when stress is elevated|
|Wound healing||The psychological state of the patient has been shown to affect their rate of healing. As noted in the featured article:
“For instance, increased levels of fear or distress before surgery have been associated with worse outcomes, including longer stays in the hospital, more postoperative complications and higher rates of re-hospitalization.
In one study on patients with chronic lower leg wounds, those who reported the highest levels of depression and anxiety showed significantly delayed healing.”
|Inflammation||Stress-relieving strategies such as meditation has been shown to promote antiviral gene activity and reduce inflammatory gene expression|
Interestingly, while both are positive emotional states associated with happiness, the gene expressions they produced were not identical.
Those whose sense of happiness was rooted in the eudaimonic camp had favorable gene-expression profiles, while hedonic well-being produced gene profiles similar to those seen in people experiencing stress due to adversity.
Professor Cole’s theory8 as to these differences is that when you’re driven by materialistic values, your happiness depends on circumstances that may or may not be within your control. If you run into adversity, it can cause a great deal of stress because it impedes your perceived ability to be happy.
On the other hand, those driven by a sense of “purpose” are largely buffered against the uncertainty that comes with adversity, and their happiness is not dependent on having or experiencing anything in particular that can at any moment be taken away.