408-854-1883 starts at $30 per hr home care

http://reference.medscape.com/calculator/aac-aha-cardiovascular-risk-ascvd

Connie’s comments: Diet such as sugar consumption, low potassium, lack of exercise, insomia, stress, environmental toxins and genetics are not added in this equation (heart disease risk formula).

Personal Data – The term “Personal Data” refers to any PHR Data that is linked to the consumer as an individual person, computer, or device such as names, health conditions, and other identifiers. …

Source: Patient Health Records – PHR

• Personal Data – The term “Personal Data” refers to any PHR Data that is linked to the consumer as an individual person, computer, or device such as names, health conditions, and other identifiers. For example, Personal Data would include results from a laboratory report even if the name and other information is deleted.
• Statistical Data – The term “Statistical Data” refers to PHR Data that is BOTH 1) de-identified according to the process set out in the HIPAA Privacy Rule, and 2) grouped in the aggregate by category or subset of people. For example, Statistical Data may show the average age A personal health record (PHR) is an electronic application used by patients to maintain and manage their health information in a private, secure, and confidential environment.

PHR

• Are managed by patients
• Can include information from a variety of sources, including health care providers and patients themselves
• Can help patients securely and confidentially store and monitor health information, such as diet plans or data from home monitoring systems, as well as patient contact information, diagnosis lists, medication lists, allergy lists, immunization histories, and much more
• Are separate from, and do not replace, the legal record of any health care provider
• Are distinct from portals that simply allow patients to view provider information or communicate with providers
• Properly designed and implemented, PHRs can help patients manage their health information and become full partners in the quest for good health.of diabetic PHR users.

Motherhealth is partnering with Kony, named a Gartner Mobile Application Development Platform Magic Quadrant Leader for the fourth year in a row.  We are inviting all doctors and consumers to help define the new mobile outpatient application to help reduce chronic care cost. Email motherhealth@gmail.com
https://www.indiegogo.com/projects/cancer-riskfactor-and-doctor-video-chat-mobile-app-medicine#/

Accelerating Health Information Exchange (HIE)

 

New research from a large international team of scientists offers a more complete picture of the genes responsible for type 2 diabetes, demonstrating that previously identified common alleles share…

Source: Fatty liver gene and Type 2 Diabetes

New research from a large international team of scientists offers a more complete picture of the genes responsible for type 2 diabetes, demonstrating that previously identified common alleles shared by many in the world are the biggest culprits—not the less common variants some scientists had hypothesized might play a large role in who gets the disease.

The researchers also identified a novel variant specific to East Asians through their study that analyzed the genes of individuals from five ethnic groups, making this the largest multi-ethnic genetic sequencing study published to date.

Their findings are reported in the July 11 issue of Nature.

Led by researchers at the University of Michigan School of Public Health, the Wellcome Trust Centre for Human Genetics at the University of Oxford, the Broad Institute of MIT and Harvard, and the Massachusetts General Hospital, more than 300 scientists from 22 countries used DNA from 120,000 individuals to pinpoint genes and their variants, which influence the disease that impacts 10 percent of the world’s population.

A variant TM6SF2 gene causes susceptibility to nonalcoholic fatty liver disease due to impaired very low density lipoprotein (VLDL) production14.[21]

TM6SF2 inhibition was associated with reduced secretion of TG-rich lipoproteins (TRLs) and increased cellular TG concentration and lipid droplet content, whereas TM6SF2 overexpression reduced liver cell steatosis. TM6SF2 is a regulator of liver fat metabolism with opposing effects on the secretion of TRLs and hepatic lipid droplet content.

“Our study has taken us to the most complete understanding yet of the genetic architecture of type 2 diabetes,” said Michael Boehnke, the Richard G. Cornell Distinguished University Professor of Biostatistics, director of the Center for Statistical Genetics at the U-M School of Public Health and one of three senior authors of the study. “With this in-depth analysis we have obtained a more complete picture of the number and characteristics of the genetic variants that influence type 2 diabetes risk.”

Through the collaboration that combined two research projects—GoT2D and T2D-GENES—researchers identified more than a dozen genetic regions that harbor variants that influence risk to type 2 diabetes. The majority of these were common variants, found in all human populations, and most had previously been detected by other genome-wide association studies.

The team identified a novel association between type 2 diabetes and a variant in the gene PAX4, present only in individuals from East Asia, including Korea, China and Singapore. They also demonstrated that variants in the gene TM6SF2, previously linked to hepatic steatosis (commonly known as “fatty liver”), influences risk of type 2 diabetes.

The researchers completed whole genome sequencing of more than 2,600 people and exome sequencing of 13,000, complemented with genome- or exome-wide array genotyping of 111,000 people. Exomes are the portion of the genome that code for proteins.

Type 2 diabetes is a major threat to global public health as deaths from the disease continue to rise rapidly, along with its complications including blindness, kidney failure, heart attack, stroke and amputation. Type 2 is the most common form of the diabetes; it impacts the body’s ability to regulate glucose (or sugar). In addition to its genetic components, environment and behavior play major roles in who gets the disease, with obesity, excessive stress and an inactive lifestyle among the contributors. Combined with other risk factors such as smoking, high cholesterol and high blood pressure, people with type 2 diabetes have a much higher risk of cardiovascular disease.

http://medicalxpress.com/news/2016-07-team-explores-genetic-architecture-diabetes.html

In 2015, total federal revenues in fiscal year 2015 are expected to be $3.18 trillion.2 These revenues come from three major sources: Income taxes paid by individuals: $1.48 trillion, or 47% of all…

Source: 2015 Federal Taxes collected

In 2015, total federal revenues in fiscal year 2015 are expected to be $3.18 trillion.² These revenues come from three major sources:

1. Income taxes paid by individuals: $1.48 trillion, or 47% of all tax revenues.
2. Payroll taxes paid jointly by workers and employers: $1.07 trillion, 34% of all tax revenues.
3. Corporate income taxes paid by businesses: $341.7 billion, or 11% of all tax revenues.

There are also a handful of other types of taxes, like customs duties and excise taxes that make up much smaller portions of federal revenue. Customs duties are taxes on imports, paid by the importer, while excise taxes are taxes levied on specific goods, like gasoline. This pie chart below shows how much each of these revenue sources is expected to bring in during fiscal year 2015.

On another note, Trump used $8M of donated campaign money to pay himself.

https://affectiva.github.io/youtube-demo/

Post by @momdancer40.

Source: Save the day, vote

Stress may counteract the beneficial effects of a healthful diet, a study in Molecular Psychiatry suggests. The study, a double-blinded randomized trial, looked at 58 women who first ate a meal hig…

Source: Stress may counteract the beneficial effects of a healthful diet

Stress may counteract the beneficial effects of a healthful diet, a study in Molecular Psychiatry suggests.

The study, a double-blinded randomized trial, looked at 58 women who first ate a meal high in saturated fats, the kind found in meat and butter. Then, one to two weeks later, the women ate a meal low in saturated fats. The only difference between the meals was in the ratio of saturated fats to unsaturated. In all other respects — number of calories, types of food, and amounts of fat, carbohydrate and protein — they were identical.

Before each meal, the women completed several well-validated questionnaires assessing symptoms of depression over the past week and the number of daily stressors in the past 24 hours. Researchers took blood samples before and after each meal.

Among women who had low levels of stress, markers of inflammation tended to be higher after eating the meal containing high levels of saturated fat than after the low saturated fat meal.

But for women who had high levels of stress, those differences disappeared — they had high levels of inflammation even after the meal that was low in saturated fats.

“The surprise here is that stress made the healthier-fat meal look like the saturated-fat meal,” said the lead author, Janice K. Kiecolt-Glaser, a professor of psychiatry at Ohio State University. “Stress is doing things with the metabolism that we really didn’t know about before.”

---

Depression, stress and diet can all alter inflammation. This double-blind, randomized crossover study addressed the impact of daily stressors and a history of major depressive disorder (MDD) on inflammatory responses to high-fat meals. During two separate 9.5 h admissions, 58 healthy women (38 breast cancer survivors and 20 demographically similar controls), mean age 53.1 years, received either a high saturated fat meal or a high oleic sunflower oil meal. The Daily Inventory of Stressful Events assessed prior day stressors and the Structured Clinical Interview for DSM-IV evaluated MDD. As expected, for a woman with no prior day stressors, C-reactive protein (CRP), serum amyloid A (SAA), intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) were higher following the saturated fat meal than the high oleic sunflower oil meal after controlling for pre-meal measures, age, trunk fat and physical activity.

But if a woman had prior day stressors, these meal-related differences disappeared—because the stressors heightened CRP, SAA, sICAM-1 and sVCAM-1 responses to the sunflower oil meal, making it look more like the responses to the saturated fat meal. In addition, women with an MDD history had higher post-meal blood pressure responses than those without a similar history. These data show how recent stressors and an MDD history can reverberate through metabolic alterations, promoting inflammatory and atherogenic responses.

---

Adherence to a Mediterranean-type diet can reduce the risk for depression, cardiovascular disease, type 2 diabetes and total mortality.1, 2, 3, 4 Reduced inflammation may be the cornerstone for the Mediterranean diet’s benefits.5, 6, 7, 8

The central fat source in the Mediterranean diet, olive oil, appears to be a key anti-inflammatory dietary component.8, 9 Indeed, a meta-analysis concluded that olive oil interventions lowered C-reactive protein (CRP) and interleukin 6 (IL-6) compared with control conditions.9 The major dietary fatty acids in the North American diet are palmitic acid, a saturated fatty acid found in meat and dairy products, and the monounsaturated oleic acid, the main fatty acid in olive oil, and many vegetable oils.10

Saturated fatty acids trigger proinflammatory signaling pathways.11 For example, palmitic acid activated toll-like receptor 4, leading to nuclear transcription factor-κB signaling and increased gene expression of IL-6, IL-8, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) in contrast, the monounsaturated palmioleate did not have inflammatory sequelae.11 A meal made with butter, a rich source of saturated fatty acids, activated nuclear transcription factor-κB in peripheral blood mononuclear cells and also increased sICAM-1 concentrations, but a meal with olive oil, a rich source of oleic acid, did not.12 Palmitate-stimulated monocytes also fuel ICAM-1 expression in endothelial cells via an IL-1 signaling pathway.13

High saturated fat meals raise adhesion molecule concentrations while monounsaturated fat meals lower concentrations.

For example, high palmitate milkshakes boosted sICAM-1 levels while olive oil milkshakes decreased sICAM-1.14 Similarly, a high-palmitic fatty acid oil breakfast heightened post-meal sICAM-1 and sVCAM-1, but a refined olive oil breakfast lowered their concentrations.  Postprandial sICAM-1 levels were amplified by a 12-week high saturated fat diet and reduced by a monounsaturated fat diet.

These meal-related differences are important because adhesion molecules play a central role in the development of atherosclerosis and diabetes.

Plasma sICAM-1 reflects a more generalized inflammatory process, while sVCAM-1 appears to be a better indicator of plaque burden.

In healthy people sICAM-1 serves as a more reliable prognostic indicator of cardiovascular disease than sVCAM-1, but sVCAM-1 better predicts cardiovascular events among patients with atherosclerotic disease than sICAM-1.17, 18, 19 Furthermore, adhesion molecules and inflammation are associated with an increased risk of hypertension and and monounsaturated fat interventions have reduced blood pressure.

Elevated sICAM-1 levels also predict type II diabetes.

For example, data from the Nurses’ Health Study showed that sICAM-1 independently predicted incident diabetes.21 In a large population-based prospective, sICAM-1 levels were higher among those participants who developed diabetes than in those who did not.20

In addition to these dietary fat influences, depression and stressors can also boost nuclear transcription factor-κB signaling, thus augmenting inflammation and increasing adhesion molecule concentrations.

For example, sICAM-1 levels were higher among all 18 physicians following an academic oral presentation compared with their own values 2 h earlier, as well as their data from parallel assessments obtained on a control day.

Comparisons of 22 patients who developed post-traumatic stress disorder following a myocardial infarction and 22 who did not develop post-myocardial infarction post-traumatic stress disorder showed that those with post-traumatic stress disorder had higher concentrations of sICAM-1 and sVCAM-1 at rest, as well as following a trauma-specific interview than their post-traumatic stress disorder-free counterparts.

Among patients who had experienced a recent acute coronary syndrome, sICAM-1 levels were higher among those with major depression than those who did not meet criteria.

Young adults with major depression had higher levels of sICAM-1 than nondepressed controls,34 and heightened sICAM-1 concentrations have also been found in healthy adults with elevated depressive symptoms.35, 36, 37, 38

People with a history of depression experience more major and minor stressors than those without a similar history, and past depression can also boost emotional reactivity to stressors.

Thus a mood disorder history could act synergistically with stress through multiple pathways.

http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2016149a.html