Save for half the amount of a use car, less than $10k price with low mileage. Use the savings for 50% of the down payment and do a loan for the balance which you will budget to pay within 4 months. You then will never have to pay monthly car payments for the next 3 to 6 years. Live simply and within your means.
One tax team who tells you that they can help you lower your IRS bills said that there are two hardship programs, one is called Currently Not Collectable status and the other is called Partial Pay Installment Agreement.
It is better that you do it yourself , to negotiate with the IRS directly for a payment plan you can afford and to explain your financial hardships as they do not have this program when you chat with the IRS online.
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Summary: Major depressive disorder has been linked to at least 22 distinct diseases, including asthma, coronary heart disease, and an increased risk of E. coli infection.
Source: University of South Australia
Major depressive disorder – referred to colloquially as the ‘black dog’ – has been identified as a genetic cause for 20 distinct diseases, providing vital information to help detect and manage high rates of physical illnesses in people diagnosed with depression.
Assessing risk factors between depression* and 925 diseases, a study from the Australian Centre for Precision Health at the University of South Australia found a causal relationship between depression and a range of respiratory, heart and digestive diseases including: asthma, coronary heart disease, high cholesterol, oesophagitis, gastroenteritis, E. coli infections, and urinary system disorders.
UniSA researcher, Anwar Mulugeta, says understanding the relationship between depression and other diseases can reduce the incidence of comorbidities – the presence of one or more additional conditions occurring with a primary condition – and improve the lives of millions of people worldwide.
“Data shows that people living with serious mental diseases, like depression, have much higher rates of physical illness than those in the general population,” Mulugeta says.
“But until now, these studies have been complicated by the possibility of other confounding factors, or even reverse causation where the physical condition is assumed to cause depression.
“This research puts the ‘chicken and egg’ conundrum to rest, showing that depression causes disease, rather than only the other way around.
“Importantly, this research signals that an individual diagnosed with depression should now also be screened for a defined set of possible comorbidities, enabling much better clinical management and significantly improved outcomes.”
Published in Molecular Psychiatry, the study is the first to use MR-PheWAS analyses to screen for a causal link between depression and a range of diseases. MR-PheWAS is a method that uses genetic data to explore causal associations between a risk factor (depression) and a range of disease outcomes. In this study, researchers assessed data from 337,536 UK Biobank participants to confirm the range of diseases affected by depression.
This study was led by Professor Elina Hyppönen, Director of the Australian Centre for Precision Health, who says appreciating the link between depression and distinct comorbidities has important implications for individuals, practitioners and policymakers.
“Today, nearly half of the population is estimated to experience a mental health condition in their lifetime,” Prof Hyppönen says.
“Understanding the connections between depression and other diseases is critical to ensure people with depression receive the support they require. The more we can look at the individual patient as a whole, the better their outcomes are likely to be.
“Our results suggest that it is important to look beyond the obvious, and that we need to screen and effectively manage depression-related comorbidities if we want to minimise the longer-term negative implications on health.
“It’s also important to focus on diet and encourage healthy lifestyles in this context. It was concerning to see that depression was associated with multiple inflammatory and even haemorrhagic gastro-intestinal complications, which may be due to side effects from medications used to treat depression, or even due to the greater occurrence of e-coli infections, both of which could be prevented.
“Through this study we provide critical evidence to help navigate the complexities of depression and its comorbidities, with the ultimate goal of delivering customer-centric treatment strategies for people suffering from this debilitating disease.”
Notes:
* Depression is a common illness with more than 300 million people affected worldwide. It is the leading cause of ill health and disability worldwide, with more than half of the costs of depression directly or indirectly related to comorbidities. The economic burden of depression in Australia is more than $9.1 billion each year.
Source:
University of South Australia
Media Contacts:
Annabel Mansfield – University of South Australia
Image Source:
The image is in the public domain.
Original Research: Closed access
“Association between major depressive disorder and multiple disease outcomes: a phenome-wide Mendelian randomisation study in the UK Biobank”. Anwar Mulugeta, Ang Zhou, Catherine King & Elina Hyppönen.
Molecular Psychiatry. doi:10.1038/s41380-019-0486-1
Abstract
Association between major depressive disorder and multiple disease outcomes: a phenome-wide Mendelian randomisation study in the UK Biobank
Depression affects all aspects of an individual’s life but evidence relating to the causal effects on health is limited. We used information from 337,536 UK Biobank participants and performed hypothesis-free phenome-wide association analyses between major depressive disorder (MDD) genetic risk score (GRS) and 925 disease outcomes. GRS–disease outcome associations passing the multiple-testing corrected significance threshold (P < 1.9 × 10−3) were followed by Mendelian randomisation (MR) analyses to test for causality. MDD GRS was associated with 22 distinct diseases in the phenome-wide discovery stage, with the strongest signal observed for MDD diagnosis and related co-morbidities including anxiety and sleep disorders. In inverse-variance weighted MR analyses, MDD was associated with several inflammatory and haemorrhagic gastrointestinal diseases, including oesophagitis (OR 1.32, 95% CI 1.18–1.48), non-infectious gastroenteritis (OR 1.25, 95% CI 1.06–1.48), gastrointestinal haemorrhage (OR 1.26, 95% CI 1.11–1.43) and intestinal E.coli infections (OR 3.24, 95% CI 1.74–6.02). Signals were also observed for symptoms/disorders of the urinary system (OR 1.36, 95% CI 1.19–1.56), asthma (OR 1.23, 95% CI 1.06–1.44), and painful respiration (OR 1.28, 95% CI 1.14–1.44). MDD was associated with disorders of lipid metabolism (OR 1.22, 95% CI 1.12–1.34) and ischaemic heart disease (OR 1.30, 95% CI 1.15–1.47). Sensitivity analyses excluding pleiotropic variants provided consistent associations. Our study indicates a causal link between MDD and a broad range of diseases, suggesting a notable burden of co-morbidity. Early detection and management of MDD is important, and treatment strategies should be selected to also minimise the risk of related co-morbidities.
Oct 21, 2014 – I suggest that major depression may result from a parasitic, bacterial, ….. Mind-
Apr 19, 2016 – Major depressive disorder (MDD) is typified by markers known to be influenced by the microbiome. For example, depression-associated …
Oral health is an essential part of psychological well-being and overall health in older adults. Poor oral health is associated with decreased quality of life, depression, hypertension, and cognitive decline. Two Rutgers studies, co-authored by Darina Petrovsky, Bei Wu, and Weiyu Mao, and published in the Journal of the American Geriatrics Society, explored the relationship between poor oral health and cognitive decline and the effects of perceived stress and social support on dry mouth among older Chinese Americans.
Researchers interviewed more than 2,700 Chinese Americans aged 60 and older and found that nearly 50 percent of study participants reported experiencing tooth symptoms, 25.5 percent reported dry mouth. In the first study, those who reported tooth symptoms experienced declines in cognition and episodic memory, often precursors to dementia. In the second study, the researchers found that stress increased symptoms of dry mouth, leading to poorer overall oral health.
“Racial and ethnic minorities are particularly vulnerable to the negative consequences of poor oral health,” said XinQi Dong, director of Rutgers University’s Institute for Health, Health Care Policy and Aging Research. “Minorities have less access to preventive dental care that is further exacerbated by language barriers and low socioeconomic status. Older Chinese Americans are at particular risk for experiencing oral health symptoms due to lack of dental insurance or not visiting a dental clinic regularly.”
According to Dong, the increasing oral health disease burdens among older Chinese immigrants point to the need for investigations of psychosocial factors due to the current emphasis on physical diseases and health behaviors in oral health.
“Efforts must be made to increase social support to alleviate stress and the resulting dry mouth issues reported by our study participants,” Dong continued. “These efforts can help preserve older adults’ health and well-being and limit cognitive decline.”
Key findings:
“These studies demonstrate the importance of examining immigrant oral health outcomes later in life to understand the specific type of outcomes of different cultural groups,” said Dong. “The studies further serve as a call to action for policymakers to develop programs aimed at improving oral health preventative and dental care services in this high-risk population. Darina Petrovsky, first author, added, “Examining current oral health practices among older Chinese Americans is crucial for developing culturally-tailored interventions to promote oral health and ultimately mitigate cognitive decline.”
“Poor oral health is a top concern among older Chinese Americans. In our study, the prevalence rate of dry mouth is followed by diabetes and heart disease. Our findings demonstrate the importance of studying the linkage between stress and dry mouth in this vulnerable population.” said author Weiyu Mao, Assistant Professor, School of Social Work, University of Nevada, Reno.
“Support from family and friends could be protective against dry mouth symptoms in relation to stress; however, the potential overload of such support could be detrimental to oral health outcomes among older Chinese Americans.” Mao continued. “Intervention strategies need to expand beyond the common risk factors, such as health conditions and health behaviors, and account for the psychosocial determinants, including stress and social support, to better promote oral health and reduce oral health disparities in this population.”
“Our research raises critical awareness for dental and healthcare providers of the role of perceived stress in dry mouth symptoms,” added Dong. “Working collaboratively, dental, and healthcare providers can better identify oral health symptoms as risk factors of cognitive decline in this fast-growing vulnerable population. The primary focus should include promoting optimal oral health and improving the quality of life.”
Source:
Rutgers
Media Contacts:
Jacquelyn Goss – Rutgers
Image Source:
The image is in the public domain.
Original Research: Open access
“Oral Health Symptoms and Cognitive Function Among US Community‐Dwelling Chinese Older Adults”. Darina V. Petrovsky PhD, RN, Bei Wu PhD, Weiyu Mao PhD, MSW, MPhil, XinQi Dong MD, MPH.
Journal of American Geriatrics Society. doi:10.1111/jgs.15748
Abstract
Oral Health Symptoms and Cognitive Function Among US Community‐Dwelling Chinese Older Adults
BACKGROUND/OBJECTIVES
Limited research is available on the relationship between oral health symptoms and cognitive function among community‐dwelling US Chinese older adults. The purpose of this study was to examine the associations between tooth/gum symptoms and changes in cognitive function.
DESIGN
Two‐wave epidemiological study.
SETTING
Population Study of Chinese Elderly in Chicago (PINE).
PARTICIPANTS
US Chinese older adults (N = 2713; mean age = 72.6 y; 58.4% women).
MEASUREMENTS
We selected self‐reported oral (tooth and gum) symptoms as independent variables. To examine changes in cognitive function (wave 2: Baseline), we chose the following three domains: episodic memory (East Boston Memory Test); executive function (Symbol Digit Modalities Test); and working memory (Digit Span Backwards). In addition, we assessed global cognitive function by constructing a composite measure.
RESULTS
At baseline, 1297 participants (47.8%) reported having teeth symptoms, and 513 participants (18.9%) reported having gum symptoms. Adjusting for sociodemographic and health‐related characteristics, participants who reported having teeth symptoms at baseline experienced their global cognition decrease by 0.07 units (estimate = −0.07; p = .003) and their episodic memory decrease by 0.07 units (estimate = −0.07; p = .026). Participants who reported having teeth symptoms at baseline experienced a faster rate of decline in global cognition for every additional year (estimate = 0.02; p = .047). However, this effect disappeared once we adjusted for all covariates (estimate = 0.02; p = .069). We found no significant relationship between baseline gum symptoms and change of cognitive function.
CONCLUSION
Having teeth symptoms was associated with a decline in cognitive function among US Chinese older adults. Developing policy measures aimed at ameliorating health and improving cognition in this high‐risk fast‐growing population in the United States would need to include oral health preventive and dental care services. J Am Geriatr Soc 67:S532–S537, 2019.
In a small pilot study, the researchers identified several distinct gut microbiome signatures – the chemicals produced by bacteria – in study participants with mild cognitive impairment (MCI) but not in their counterparts with normal cognition, and found that these bacterial signatures correlated with higher levels of markers of Alzheimer’s disease in the cerebrospinal fluid of the participants with MCI.
Through cross-group dietary intervention, the study also showed that a modified Mediterranean-ketogenic diet produced changes in the gut microbiome and its metabolites that correlated with reduced levels of Alzheimer’s markers in the members of both study groups.
The study appears in the current issue of EBioMedicine, a journal published by The Lancet.
“The relationship of the gut microbiome and diet to neurodegenerative diseases has recently received considerable attention, and this study suggests that Alzheimer’s disease is associated with specific changes in gut bacteria and that a type of ketogenic Mediterranean diet can affect the microbiome in ways that could impact the development od dementia,” said Hariom Yadav, Ph.D., assistant professor of molecular medicine at Wake Forest School of Medicine, who co-authored the study with Suzanne Craft, Ph.D., professor gerontology and geriatric medicine at the medical school and director of Wake Forest Baptist Health’s Alzheimer’s Disease Research Center.
The randomized, double-blind, single-site study involved 17 older adults, 11 with diagnosed MCI and six with normal cognition. These participants were randomly assigned to follow either the low-carbohydrate modified Mediterranean-ketogenic diet or a low-fat, higher carbohydrate diet for six weeks then, after a six-week “washout” period, to switch to the other diet. Gut microbiome, fecal short-chain fatty acids and markers of Alzheimer’s, including amyloid and tau proteins, in cerebrospinal fluid were measured before and after each dieting period.
The study’s limitations include the subject group’s size, which also accounts for the lack of diversity in terms of gender, ethnicity and age.
“Our findings provide important information that future interventional and clinical studies can be based on,” Yadav said. “Determining the specific role these gut microbiome signatures have in the progression of Alzheimer’s disease could lead to novel nutritional and therapeutic approaches that would be effective against the disease.”
Funding: The research was supported by grant P30 AG049638 and award R01 AG055122 from the National Institute on Aging, Department of Defense grant W81XWH-18-1-0118, National Center for Advancing Translational Sciences grant UL1 TR001420 and a grant from the Hartman Family Foundation.
Source:
Wake Forest Baptist Medical Center
Media Contacts:
Marguerite Beck – Wake Forest Baptist Medical Center
Image Source:
The image is in the public domain.
Original Research: Open access
“Modified Mediterranean-ketogenic diet modulates gut microbiome and short-chain fatty acids in association with Alzheimer’s disease markers in subjects with mild cognitive impairment”. Ravinder Nagpal, Bryan J. Neth, Shaohua Wang, Suzanne Craft, Hariom Yadav.
EBioMedicine. doi:10.1016/j.ebiom.2019.08.032
Abstract
Modified Mediterranean-ketogenic diet modulates gut microbiome and short-chain fatty acids in association with Alzheimer’s disease markers in subjects with mild cognitive impairment
Background
Alzheimer’s disease (AD) prevalence is increasing, but its etiology remains elusive. Gut microbes can contribute to AD pathology and may help identifying novel markers and therapies against AD. Herein, we examine how the gut microbiome differs in older adults with mild cognitive impairment compared to cognitively normal counterparts, and whether and how a modified Mediterranean-ketogenic diet (MMKD) alters the gut microbiome signature in association with cerebrospinal fluid (CSF) AD biomarkers.
Methods
A randomized, double-blind, cross-over, single-center pilot study of MMKD versus American Heart Association Diet (AHAD) intervention is performed on 17 subjects (age: 64.6 ± 6.4 yr), of which 11 have mild cognitive impairment, while 6 are cognitively normal. Subjects undergo MMKD and AHAD intervention for 6-weeks separated by 6-weeks washout periods. Gut microbiome, fecal short-chain fatty acids (SCFAs), and markers of AD in CSF including amyloid β (Aβ)-40 and Aß-42, total tau, and phosphorylated tau-181 (tau-p181) are measured at before and after diet interventions.
Findings
At baseline, subjects with normal vs. impaired cognition show no notable difference in microbiome diversity but several unique microbial signatures are detected in subjects with mild cognitive impairment. Proteobacteria correlate positively with Aβ-42: Aβ-40 while fecal propionate and butyrate correlates negatively with Aβ-42 in subjects with mild cognitive impairment. Several bacteria are differently affected by the two diets with distinct patterns between cognitively normal and impaired subjects. Notably, the abundance of Enterobacteriaceae, Akkermansia, Slackia, Christensenellaceae and Erysipelotriaceae increases while that of Bifidobacterium and Lachnobacterium reduces on MMKD, while AHAD increases Mollicutes. MMKD slightly reduces fecal lactate and acetate while increasing propionate and butyrate. Conversely, AHAD increases acetate and propionate while reducing butyrate.
Interpretation
The data suggest that specific gut microbial signatures may depict the mild cognitive impairment and that the MMKD can modulate the gut microbiome and metabolites in association with improved AD biomarkers in CSF.
One common physiological phenomenon that is involved both in infectious and in malignant processes is the reduction in appetite: disease anorexia. An increase in plasma levels of leptin with inflammation is thought to be involved in this process. However, from an evolutionary perspective, in certain cases, it would be more adaptive for an internal parasite to stimulate the appetite of the host instead of causing its suppression.
We tested whether a parasitic infection with the larvae of the helminth parasite Taenia taeniaformis affects the levels of appetite-regulating proteins, such as leptin, ghrelin and neuropeptide-Y (NPY) in wild yellow-necked mouse (Apodemus flavicollis). We found that infected mice had lower plasma levels of leptin and increased levels of NPY than the uninfected subjects. Ghrelin levels were not associated with the occurrence of the parasites; however, these levels strongly correlated with the levels of NPY. This study suggests a possible manipulation by parasitic larvae of appetite regulation in infected subjects.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3440990/
Scientists at The University of Texas at Dallas have found evidence suggesting that resistance to the “hunger hormone” ghrelin in the brain is linked to the cognitive impairments and memory loss associated with Alzheimer’s disease (AD).
The findings, based on observations of postmortem brain-tissue samples from Alzheimer’s patients and on experiments with a mouse model of AD, also suggest a possible treatment strategy for the incurable neurodegenerative disorder that affects about 5.8 million older adults in the United States.
The research was published Aug. 14 as the cover article in the journal Science Translational Medicine.
“This is a proof-of-concept study, but we are very encouraged by the results,” said Dr. Heng Du, associate professor of biological sciences at UT Dallas and corresponding author of the study.
Produced in the stomach, ghrelin sends signals to the brain that regulate energy balance and body weight. Often called the hunger hormone, it plays a role in appetite and meal initiation. But ghrelin also has been implicated in learning and memory.
The hippocampus region of the brain — crucial to learning, memory and emotions — is one of the first to suffer cell death and damage in Alzheimer’s disease due to a toxic buildup of protein fragments called amyloid beta.
In a healthy hippocampus, ghrelin binds with proteins called ghrelin receptors, which combine with similarly activated receptors for the neurotransmitter dopamine. The two receptors then form a protein complex that helps maintain communication between brain cells and, ultimately, memory.
In the new study, Du and his colleagues found that amyloid beta binds to ghrelin receptors in the hippocampus, blocking their ability to combine with dopamine receptors.
“Our hypothesis is that this dissociation between ghrelin and dopamine receptors may be what is affecting cognition in Alzheimer’s patients,” Du said. “As the brain loses the function of ghrelin receptors due to amyloid beta, the body tries to compensate by increasing the production of ghrelin and the number of ghrelin receptors. But the amyloid prevents the receptors from functioning.”
Du likened the condition to insulin resistance found in individuals with type 2 diabetes. In that disease, insulin receptors malfunction.
“To compensate, patients in the early stages of type 2 diabetes produce more insulin to bind insulin receptors,” Du said. “But they become insulin-resistant. No matter how much insulin your body produces, the insulin receptors are unable to activate the downstream biochemical reactions needed to transport glucose from blood into cells.
“Similarly, based on our findings, Alzheimer’s might be linked to ghrelin resistance.”
Du said the new findings help explain why a recent clinical trial of a compound called MK0677 — designed to activate ghrelin receptors in the brain — proved unable to slow the progression of Alzheimer’s.
To test a different approach in their mouse model of AD, Du’s team gave the mice MK0677 and another compound — SKF81297 to activate dopamine receptors — at the same time.
“When we gave these compounds simultaneously, we saw improved cognition and memory in the AD mice, and lesions in the hippocampus were reduced,” Du said. “Activating both receptors at the same time was key; it restored the receptors’ ability to form complexes. When this happens, we suspect the ghrelin receptor becomes protected and can no longer bind to amyloid beta.
Connie’s notes: Many Parkinson’s and Alzheimer’s clients of Motherhealth caregivers love ice cream in the middle of the night. They are hungry at night.
As a caregiver, I observed that many seniors never had a massage and are left home alone. They have aches and pains and never learned how to massage their own bodies.
We train Motherhealth caregivers, 408-854-1883 , in massaging seniors to offer caring hands that can help them heal and feel loved.
We use ginger, coconut oil, essential oils of eucalyptus and rosemary mixed in apricot or almond oil.
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The MIND vs. the Mediterranean Diet
Signs of the preactive and active phase of dying, medications for terminally ill
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Circadian clock alters response to diet and changes to gut microbiome
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Nitric Oxide Dump Exercise with nose breathing to lower blood pressure and thin blood
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Slimy veggies, saluyot and okra fight cancer
We are gathering interested investors who wanted to provide affordable senior housing in the bay area.
Those with better FICO scores and those passive investors are welcome.
We will consider modular and senior safe building spaces.
Your suggestions are welcome. Email Connie at motherhealth@gmail.com , subject: affordable senior housing investing in the bay area. Motherhealth LLC
Motherhealth Inc 501c3 is seeking car donations for senior home care. Email motherhealth or snail mail at PO Box 3138 Saratoga CA 95070 or text 408-854-1883
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