Biological Link Between Stress and Obesity

Summary: Researchers revealed the molecular elements that bridge anxiety and metabolism.

Source: Hebrew University of Jerusalem.

For the first time — researchers revealed a connection between anxiety and metabolic disorders at the molecular level; the discovery opens new possibilities for detecting and treating both symptoms.

Metabolic and anxiety-related disorders both pose a significant healthcare burden, and are in the spotlight of contemporary research and therapeutic efforts. Although intuitively we assume that these two phenomena overlap, the link has not been proven scientifically.

Now, a team of researchers from the Hebrew University of Jerusalem, headed by Prof. Hermona Soreq from the Edmond and Lily Safra Center for Brain Sciences and the Department of Biological Chemistry at the Faculty of Mathematics and Sciences, revealed the molecular elements that bridge anxiety and metabolism – a type of microRNA that influences shared biological mechanisms.

“We already know that there is a connection between body and mind, between the physical and the emotional, and studies show that psychological trauma affects the activity of many genes. Our previous research found a link between microRNA and stressful situations – stress and anxiety generate an inflammatory response and dramatically increase the expression levels of microRNA regulators of inflammation in both the brain and the gut, for example the situation of patients with Crohn’s disease may get worse under psychological stress, “says Prof. Soreq.

“In the present study, we added obesity to the equation. We revealed that some anxiety-induced microRNA are not only capable of suppressing inflammation but can also potentiate metabolic syndrome-related processes. We also found that their expression level is different in diverse tissues and cells, depending on heredity and exposure to stressful situations,” explains Prof. Soreq.

The family of microRNA genes is part of the human genome, which was considered until not too long ago as “junk-DNA”. However, microRNAs are now known to fulfill an important role in regulating the production process of proteins by other genes. These tiny RNA molecules, which are one percent of the average size of a protein-coding gene, act as suppressors of inflammation and are able to halt the production of proteins.

The research paper, published in the journal Trends in Molecular Medicine, details the evidence linking microRNA pathways, which share regulatory networks in metabolic and anxiety-related conditions. In particular, microRNAs involved in these disorders include regulators of acetylcholine signaling in the nervous system and their accompanying molecular machinery.

Image shows Laurel and Hardy and a DNA strand.

Metabolic disorders, such as abdominal obesity and diabetes, have become a global epidemic. In the USA, the prevalence of metabolic syndrome is as high as 35 percent. In other countries, such as Austria, Denmark and Ireland it affects 20-25 percent of the population.

Anxiety disorders are harder to quantify than metabolic ones. They include obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD) and phobia. The full burden of the anxiety spectrum is difficult to assess, due to under-diagnosis and poorly defined pathophysiological processes.

This newly revealed link offers novel opportunities for innovative diagnoses and treatment of both metabolic and anxiety-related phenomena.

“The discovery has a diagnostic value and practical implications, because the activity of microRNAs can be manipulated by DNA-based drugs,” explains Prof. Soreq. “It also offers an opportunity to reclassify ‘healthy’ and ‘unhealthy’ anxiety and metabolic-prone states, and inform putative strategies to treat these disorders.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The study was supported by The European Research Council, Legacy Heritage Biomedical Partnership Program of the Israel Science Foundation, The Israeli Ministry of Science.

Source: Avivit Delgoshen – Hebrew University of Jerusalem
Image Source: This NeuroscienceNews.com image is credited to Petra Pollins.
Original Research: Abstract for “MicroRNA Regulators of Anxiety and Metabolic Disorders” by Chanan Meydan, Shani Shenhar-Tsarfaty, and Hermona Soreq in Trends in Molecular Medicine. Published online August 22 2016 doi:10.1016/j.molmed.2016.07.001


Abstract

MicroRNA Regulators of Anxiety and Metabolic Disorders

Anxiety-related and metabolic disorders are under intense research focus. Anxiety-induced microRNAs (miRNAs) are emerging as regulators that are not only capable of suppressing inflammation but can also induce metabolic syndrome-related processes. We summarize here evidence linking miRNA pathways which share regulatory networks in metabolic and anxiety-related conditions. In particular, miRNAs involved in these disorders include regulators of acetylcholine signaling in the nervous system and their accompanying molecular machinery. These have been associated with anxiety-prone states in individuals, while also acting as inflammatory suppressors. In peripheral tissues, altered miRNA pathways can lead to dysregulated metabolism. Common pathways in metabolic and anxiety-related phenomena might offer an opportunity to reclassify ‘healthy’ and ‘unhealthy’, as well as metabolic and anxiety-prone biological states, and inform putative strategies to treat these disorders.

Trends
Anxiety-related and metabolic disorders pose a significant healthcare burden, and are in the spotlight of contemporary research and therapeutic efforts.

miRNAs continue to emerge as molecular elements with diverse regulatory functions. Recent data support a role for miRNAs in clinical scenarios linking anxiety and metabolic disorder-related diseases.

Dually linked miRNAs may bridge anxiety and metabolism by influencing shared biological mechanisms.

miRNAs can influence both metabolic and anxiety-related signaling pathways, and control inflammation, as well as modulating enzymes associated with autonomic nervous system functioning.

This emerging link may offer novel opportunities for innovative diagnoses, follow-up, risk stratification, and management, while cautiously assessing potential off-target effects and risks.

“MicroRNA Regulators of Anxiety and Metabolic Disorders” by Chanan Meydan, Shani Shenhar-Tsarfaty, and Hermona Soreq in Trends in Molecular Medicine. Published online August 22 2016 doi:10.1016/j.molmed.2016.07.001

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Contributing factors to aging

aging-genes-3aging-genes-2aging-genes-1
It has been a long standing goal to develop molecular biomarkers of biological age. Recent studies demonstrate that powerful epigenetic biomarkers of aging can be defined based on DNA methylation levels. For example, the epigenetic clock (PMID: 24138928) is a multivariate age estimation method that applies to sorted cell types (CD4T cells or neurons), complex tissues, and organs and even prenatal brain samples. The epigenetic clock is an attractive biomarker of aging because a) it applies to most human and chimpanzee tissues, b) its accurate measurement of chronological age is unprecedented, c) it is predictive of all-cause mortality even after adjusting for a variety of known risk factors, d) it correlates with measures of cognitive and physical fitness in the elderly, and e) it has been found useful for detecting accelerated aging effects due to obesity, Down syndrome, and HIV infection. Recent genomewide association studies shed light on the underlying biological mechanisms.

For more information go to https://oir.nih.gov/wals

Author: Steve Horvath, Sc.D., Ph.D., University of California, Los Angeles

Permanent link: http://videocast.nih.gov/launch.asp?1…

High BMI linked to cognitive decline through systemic inflammation

There are plenty of reasons it’s important to maintain a healthy weight, and now you can add one more to the list: It may be good for your brain.

Researchers from the University of Arizona have found that having a higher body mass index, or BMI, can negatively impact cognitive functioning in older adults.

How? They say inflammation is to blame.

“The higher your BMI, the more your inflammation goes up,” said Kyle Bourassa, lead author of the study, which is published in the journal Brain, Behavior and Immunity. “Prior research has found that inflammation — particularly in the brain — can negatively impact brain function and cognition.”

Previous studies also have linked higher BMI — an index of body fat based on height and weight — to lower cognitive functioning. But how and why the two are connected was far less clear.

“We saw this effect, but it’s a black box. What goes in between?” said Bourassa, a UA psychology doctoral student. “Establishing what biologically plausible mechanisms explain this association is important to be able to intervene later.”

Bourassa and his co-author, UA psychology professor David Sbarra, analyzed data from the English Longitudinal Study of Aging, which includes over 12 years’ worth of information on the health, well-being and social and economic circumstances of the English population age 50 and older.

Using two separate samples from the study — one of about 9,000 people and one of about 12,500 — researchers looked at aging adults over a six-year period. They had information on study participants’ BMI, inflammation and cognition, and they found the same outcome in both samples.

“The higher participants’ body mass at the first time point in the study,” Bourassa said, “the greater the change in their CRP levels over the next four years. CRP stands for C-reactive protein, which is a marker in the blood of systemic inflammation in your body. Change in CRP over four years then predicted change in cognition six years after the start of the study. The body mass of these people predicted their cognitive decline through their levels of systemic inflammation.”

The findings support existing literature linking inflammation to cognitive decline and take it a step further by illuminating the important role of body mass in the equation.

Sbarra added a word of caution in trying to understand the findings.

“The findings provide a clear and integrative account of how BMI is associated with cognitive decline through systemic inflammation, but we need to remember that these are only correlational findings,” he said. “Of course, correlation does not equal causation. The findings suggest a mechanistic pathway, but we cannot confirm causality until we reduce body mass experimentally, then examine the downstream effects on inflammation and cognition.”

“Experimental studies finding whether reducing inflammation also improves cognition would be the gold standard to establish that this is a causal effect,” Bourassa added.

Cognitive decline is a normal part of aging, even in healthy adults, and can have a significant impact on quality of life. The current research may provide valuable insights for possible interventions and new research directions in that area.

“If you have high inflammation, in the future we may suggest using anti-inflammatories not just to bring down your inflammation but to hopefully also help with your cognition,” Bourassa said.

Of course, maintaining a healthy weight is also good for overall health, he added.

“Having a lower body mass is just good for you, period. It’s good for your health and good for your brain,” Bourassa said.

Source:

University of Arizona


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Colorectal, ovarian-uterine, prostate, kidney, liver and bladder cancer risk Factor

COPKL: Colorectal, ovarian/uterine, prostate, kidney, liver and bladder cancer risk Factor, formula by Connie Dello Buono , ©12Sept2016

Assumption: Female/Male, over 50yrs of age, on western diet, lives in Northern hemisphere, have families with cancer, diabetes and polyps, prone to allergies (lack zinc), digestive disorders, high dairy and sugar consumption (low magnesium and calcium,iron) and had used some medications in the past

COPKL Risk Factor = Blood sugar (0.2) + history (0.1) + sugar/processed foods consumption (0.1) + Exercise and sun exposure (0.1) + number of medications (0.1) + obesity/night time worker (0.1) + exposure to copper,fungus,molds,aflatoxins (0.1) + genes (0.2)

  • COPKL Risk Factor =1.0 (High)
  • COPKL Risk Factor = 6- 4 (Medium)
  • COPKL Risk Factor = < 3 (Low)

Please email your entries to motherhealth@gmail.com to create a database and get health data insights on Prostate,Colorectal,kidney,liver and ovarian/uterine disease.

Modified Colon and other cancer risk factor

Blood sugar
Normal/low =0High = 0.2
Med =0.1
Previous history of cancer/bowel disease, family cancer/polyps
Normal/low=0
High = 0.1
Race = 0.1 racial/ethnic background (African American, Eastern European Jews)
Exercise and sun exposure, 3x per week = 0
No exercise = 0.1
Exposure to copper,fungus,molds,toxins, smoking,alcohol,narcotics, aluminum, air pollution, char broiled meat, aflatoxin, virus,bacteria, medications > 5
(H,M,L)
Yes = H,M = 0.1
Metabolic and diet:
Diabetes 0.1Night time work, obesity (H,M,L)
H = 0.1
Age > 45 yrs old Genes:
0.2 = MSH2, MLH1, MSH6, PMS2, PMS1, TGFBR2, MLH3 , RCC, APC, HPC1, tmprss2-erg ,  TMPRSS2-ETV1/4, HBOC,BRCA,BRCA2,BRCA1
(0.2 more than 2 genes, 0.1 one gene),
Weak immune and metabolic system:
Infection and allergy 0.1
 

colo-rectal-kidney-cancer-risk-factors

risk-factor

Having an inherited syndrome

About 5% to 10% of people who develop colorectal cancer have inherited gene defects (mutations) that can cause family cancer syndromes and lead to them getting the disease. The most common inherited syndromes linked with colorectal cancers are familial adenomatous polyposis (FAP) and Lynch syndrome (hereditary non-polyposis colorectal cancer, or HNPCC), but other rarer syndromes can also increase colorectal cancer risk.

Familial adenomatous polyposis (FAP): FAP is caused by changes (mutations) in the APC gene that a person inherits from his or her parents. About 1% of all colorectal cancers are due to FAP.

In the most common type of FAP, hundreds or thousands of polyps develop in a person’s colon and rectum, usually in their teens or early adulthood. Cancer usually develops in 1 or more of these polyps as early as age 20. By age 40, almost all people with this disorder will have developed colon cancer if the colon isn’t removed first to prevent it. People with FAP are also at increased risk for cancers of the stomach, small intestines, and some other organs.

In attenuated FAP, which is a subtype of this disorder, patients have fewer polyps (less than 100), and colorectal cancer tends to occur at a later age.

Gardner syndrome is a type of FAP that also has non-cancerous tumors of the skin, soft tissue, and bones.

Lynch syndrome (hereditary non-polyposis colon cancer, or HNPCC): Lynch syndrome accounts for about 2% to 4% of all colorectal cancers. In most cases, this disorder is caused by an inherited defect in either the MLH1 or MSH2 gene, but changes in other genes can also cause Lynch syndrome. These genes normally help repair DNA damage. (See Do we know what causes colorectal cancer? for more details.)

People with this syndrome develop cancers when they are relatively young, although not as young as in FAP. People with Lynch syndrome may have polyps, but they tend to only have a few, not hundreds as in FAP. The lifetime risk of colorectal cancer in people with this condition may be as high as 80%, although this depends on which gene is affected.

Women with this condition also have a very high risk of developing cancer of the endometrium (lining of the uterus). Other cancers linked with Lynch syndrome include cancer of the ovary, stomach, small intestine, pancreas, kidney, brain, ureters (tubes that carry urine from the kidneys to the bladder), and bile duct.

For more information on Lynch syndrome, see Do we know what causes colorectal cancer? and Can colorectal cancer be prevented?

Turcot syndrome: This is a rare inherited condition in which people have a higher risk of adenomatous polyps and colorectal cancer, as well as brain tumors. There are actually 2 types of Turcot syndrome:

One is caused by gene changes similar to those seen in FAP, in which cases the brain tumors are medulloblastomas.

The other is caused by gene changes similar to those seen in Lynch syndrome, in which cases the brain tumors are glioblastomas.

Peutz-Jeghers syndrome: People with this rare inherited condition tend to have freckles around the mouth (and sometimes on the hands and feet) and a special type of polyp in their digestive tracts (called hamartoma). These people are at greatly increased risk for colorectal cancer, as well as several other cancers, which usually appear at a younger than normal age. This syndrome is caused by mutations in the STK1 gene.

MUTYH-associated polyposis: People with this syndrome develop colon polyps which will become cancerous if the colon is not removed. These people also have an increased risk of cancers of the small intestine, skin, ovary, and bladder. This syndrome is caused by mutations in the MUTYH gene.

These syndromes often lead to cancer at a younger age than is usual. They are also linked to some other types of cancer. Identifying families with these inherited syndromes is important because it lets doctors recommend specific steps such as screening and other preventive measures when the person is younger.

Information on risk assessment, and genetic counseling and testing for these syndromes can be found in Colorectal Cancer Prevention and Early Detection.

Your racial and ethnic background

African Americans have the highest colorectal cancer incidence and mortality rates of all racial groups in the United States. The reasons for this are not yet understood.

Jews of Eastern European descent (Ashkenazi Jews) have one of the highest colorectal cancer risks of any ethnic group in the world. Several gene mutations leading to an increased risk of colorectal cancer have been found in this group. The most common of these gene changes, called the I1307K APC mutation, is present in about 6% of American Jews.

Having type 2 diabetes

People with type 2 (usually non-insulin dependent) diabetes have an increased risk of colorectal cancer. Both type 2 diabetes and colorectal cancer share some of the same risk factors (such as being overweight or obese). But even after taking these factors into account, people with type 2 diabetes still have an increased risk. They also tend to have a less favorable prognosis (outlook) after diagnosis.

Factors with unclear effects on colorectal cancer risk

Night shift work

Results of one study suggested working a night shift at least 3 nights a month for at least 15 years may increase the risk of colorectal cancer in women. The study authors suggested this might be due to changes in levels of melatonin (a hormone that responds to changes in light) in the body. More research is needed to confirm or refute this finding.

Previous treatment for certain cancers

Some studies have found that men who survive testicular cancer seem to have a higher rate of colorectal cancer and some other cancers. This might be because of the treatments they have received.

Several studies have suggested that men who had radiation therapy to treat prostate cancer might have a higher risk of rectal cancer because the rectum receives some radiation during treatment. Most of these studies are based on men treated in the 1980s and 1990s, when radiation treatments were less precise than they are today. The effect of more modern radiation methods on rectal cancer risk is not clear.


Calculate your Alzheimer’s risk factor

https://clubalthea.com/2016/09/12/alzheimers-disease-data-insigths/

Calculate your Blood cancer risk factor

https://clubalthea.com/2016/09/16/prenatal-health-of-mother-may-contribute-to-childhood-leukemia/


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Behavior, brain SPECT scan, hormones, gratitude, neuroplasticity

Neuroplasticity, also known as brain plasticity, is an umbrella term that describes lasting change to the brain throughout an individual’s life course. The term gained prominence in the latter half of the 20th century, when new research[1] showed many aspects of the brain remain changeable (or “plastic”) even into adulthood.[2] This notion contrasts with the previous scientific consensus that the brain develops during a critical period in early childhood, then remains relatively unchangeable (or “static”) afterward.[3]

Neuroplastic change can occur at small scales, such as physical changes to individual neurons, or at whole-brain scales, such as cortical remapping in response to injury; however cortical remapping only occurs during a certain time period meaning that if a child were injured and it resulted in brain damage then cortical remapping would most likely occur, however if an adult was injured and it resulted in brain damage, then cortical remapping would not occur since the brain has made the majority of its connections.[4] Behavior, environmental stimuli, thought, and emotions may also cause neuroplastic change through activity-dependent plasticity, which has significant implications for healthy development, learning, memory, and recovery from brain damage.[4][5][6]

Neuroscientists distinguish synaptic plasticity, which refers to changes in how neurons connect to each other, from non-synaptic plasticity, which refers to changes in the neurons themselves.

Chronic pain

Main article: Chronic pain

Individuals who suffer from chronic pain experience prolonged pain at sites that may have been previously injured, yet are otherwise currently healthy. This phenomenon is related to neuroplasticity due to a maladaptive reorganization of the nervous system, both peripherally and centrally. During the period of tissue damage, noxious stimuli and inflammation cause an elevation of nociceptive input from the periphery to the central nervous system. Prolonged nociception from periphery then elicit a neuroplastic response at the cortical level to change its somatotopic organization for the painful site, inducing central sensitization.[32] For instance, individuals experiencing complex regional pain syndrome demonstrate a diminished cortical somatotopic representation of the hand contralaterally as well as a decreased spacing between the hand and the mouth.[33] Additionally, chronic pain has been reported to significantly reduce the volume of grey matter in the brain globally, and more specifically at the prefrontal cortex and right thalamus.[34] However, following treatment, these abnormalities in cortical reorganization and grey matter volume are resolved, as well as their symptoms. Similar results have been reported for phantom limb pain,[35] chronic low back pain[36] and carpal tunnel syndrome.[37]

Meditation

A number of studies have linked meditation practice to differences in cortical thickness or density of gray matter.[38][39][40] One of the most well-known studies to demonstrate this was led by Sara Lazar, from Harvard University, in 2000.[41] Richard Davidson, a neuroscientist at the University of Wisconsin, has led experiments in cooperation with the Dalai Lama on effects of meditation on the brain. His results suggest that long-term, or short-term practice of meditation results in different levels of activity in brain regions associated with such qualities as attention, anxiety, depression, fear, anger, the ability of the body to heal itself, and so on. These functional changes may be caused by changes in the physical structure of the brain.[42][43][44][45]

Fitness and exercise

Aerobic exercise promotes adult neurogenesis by increasing the production of neurotrophic factors (compounds that promote growth or survival of neurons), such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor 1 (IGF-1), and vascular endothelial growth factor (VEGF).[46][47][48] Exercise-induced neurogenesis in the hippocampus is associated with measurable improvements in spatial memory.[49][50][51][52] Consistent aerobic exercise over a period of several months induces marked clinically significant improvements in executive function (i.e., the “cognitive control” of behavior) and increased gray matter volume in multiple brain regions, particularly those that give rise to cognitive control.[48][49][53][54] The brain structures that show the greatest improvements in gray matter volume in response to aerobic exercise are the prefrontal cortex and hippocampus;[48][49][50] moderate improvements seen in the anterior cingulate cortex, parietal cortex, cerebellum, caudate nucleus, and nucleus accumbens.[48][49][50] Higher physical fitness scores (measured by VO2 max) are associated with better executive function, faster processing speed, and greater volume of the hippocampus, caudate nucleus, and nucleus accumbens.[49]

Human echolocation

Human echolocation is a learned ability for humans to sense their environment from echoes. This ability is used by some blind people to navigate their environment and sense their surroundings in detail. Studies in 2010[55] and 2011[56] using functional magnetic resonance imaging techniques have shown that parts of the brain associated with visual processing are adapted for the new skill of echolocation. Studies with blind patients, for example, suggest that the click-echoes heard by these patients were processed by brain regions devoted to vision rather than audition.[57]

ADHD stimulants

Reviews of magnetic resonance imaging (MRI) studies on individuals with ADHD suggest that the long-term treatment of attention deficit hyperactivity disorder (ADHD) with stimulants, such as amphetamine or methylphenidate, decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in several parts of the brain, such as the right caudate nucleus of the basal ganglia.[58][59][60] Based upon rodent models, the authors of one review proposed that “juvenile exposure to methylphenidate may cause abnormal prefrontal function and impaired plasticity in the healthy brain”.[61] The same authors noted in another review that in juvenile rats, methylphenidate reduced levels of NR2B subunit of the NMDA receptor without altering NR2A levels in the prefrontal cortex, thereby affecting long-term plasticity in the prefrontal cortex.[

brain  101