QUOTE FOR WEDNESDAY:

“Unfortunately, there are currently no treatments for prion diseases, brain-wasting diseases that are invariably fatal. The most common human prion disease is Creutzfeldt-Jakob disease (CJD), better known as mad cow disease.  This disease is rare in humans.  Worldwide, there is an estimated one case of CJD diagnosed per million people each year, most often in older adults. There are 250 people who are inflicted with this in the U.S.”

The Center for Food Safety (https://www.centerforfoodsafety.org )

Part II MAD COW DISEASE=bovine spongiform encephalopathy (BS & in humans called Creutzfeldt-Jakob disease (vCJD).

        

Brain Results that were exposed to Mad Cow Disease making the brain a  spongy like appearance.  This is how it got the name BSE.

U.S. Drug and Food Administration states, “People can get a version of BSE called variant Creutzfeldt-Jakob disease (vCJD). As of December 4, 2017, 231 people worldwide are known to have become sick with vCJD according to the University of Edinburgh’s National CJD Research & Surveillance Unit. It is thought that they got the disease from eating food made from cows sick with BSE. Most of the people who have become sick with vCJD lived in the United Kingdom at some point in their lives. Only four lived in the U.S., and most likely, these four people became infected when they were living or traveling overseas.

Neither vCJD nor BSE is contagious. This means that it is not like catching a cold. A person (or a cow) cannot catch it from being near a sick person or cow. Also, research studies have shown that people cannot get BSE from drinking milk or eating dairy products, even if the milk came from a sick cow.”

Unfortunately, there are currently no treatments for prion diseases, brain-wasting diseases that are invariably fatal. The most common human prion disease is Creutzfeldt-Jakob disease (CJD), better known as mad cow disease.  This disease is rare in humans.

Symptoms of Creutzfeldt-Jakob disease (CJD) can resemble those of other dementia-like brain disorders, such as Alzheimer’s. But Creutzfeldt-Jakob disease usually progresses much more rapidly.

CJD captured public attention in the 1990s when some people in the United Kingdom developed a form of the disease — variant CJD (vCJD) — after eating meat from diseased cattle. However, “classic” Creutzfeldt-Jakob disease hasn’t been linked to contaminated beef.

Although serious, CJD is rare, and vCJD is the least common form. Worldwide, there is an estimated one case of CJD diagnosed per million people each year, most often in older adults.

Creutzfeldt-Jakob disease (CJD) is marked by rapid mental deterioration, usually within a few months. Initial signs and symptoms typically include:

  • Personality changes
  • Anxiety
  • Depression
  • Memory loss
  • Impaired thinking
  • Blurred vision or blindness
  • Insomnia
  • Difficulty speaking
  • Difficulty swallowing
  • Sudden, jerky movements

As the disease progresses, mental symptoms worsen. Most people eventually lapse into a coma, first dementia to death. Heart failure, respiratory failure, pneumonia or other infections are generally the cause of death. Death usually occurs within a year.

In people with the rarer vCJD, psychiatric symptoms may be more prominent in the beginning, with dementia — the loss of the ability to think, reason and remember — developing later in the illness. In addition, this variant affects people at a younger age than classic CJD does and appears to have a slightly longer duration — 12 to 14 months.

Creutzfeldt-Jakob disease & its variants belong to a broad group of human & Sanimal diseases known as transmissible spongiform encephalopathies (TSEs). The name derives from the spongy holes, visible under a microscope, that affect the brain tissue.

How its transmitted?  The risk of CJD is low. The disease can’t be transmitted through coughing or sneezing, touching, or sexual contact.

1-Heredity: 15 percent of people with CJD have a family history of the disease or test positive for a genetic mutation associated with CJD. This type is referred to as familial CJD.

2-Exposure to contaminated tissue. People who’ve received human growth hormone derived from human pituitary glands or who’ve had grafts of tissue that covers the brain (dura mater) may be at risk of iatrogenic CJD. .

3-The low risk of contracting vCJD from eating contaminated beef.

Regulating potential sources of vCJD

Most countries have taken steps to prevent BSE-infected tissue from entering the food supply, including:

  • Tight restrictions on importation of cattle from countries where BSE is common
  • Restrictions on animal feed
  • Strict procedures for dealing with sick animals
  • Surveillance and testing methods for tracking cattle health
  • Restrictions on which parts of cattle can be processed for food

 

QUOTE FOR TUESDAY:

“The word BSE is short but it stands for a disease with a long name, bovine spongiform encephalopathy. “Bovine” means that the disease affects cows, “spongiform” refers to the way the brain from a sick cow looks spongy under a microscope, and “encephalopathy” indicates that it is a disease of the brain. BSE is commonly called “mad cow disease.”

U.S. Food and Drug Administration (https://www.fda.gov)

Part I MAD COW DISEASE=bovine spongiform encephalopathy (BSE) & in humans called Creutzfeldt-Jakob disease (vCJD).

Mad Cow Disease (Spongiform Encephalopathy or BSE)

Mad cow disease, or bovine spongiform encephalopathy (BSE), is a disease that was first found in cattle. It’s related to a disease in humans called variant Creutzfeldt-Jakob disease (vCJD). Both disorders are universally fatal brain diseases caused by a prion. A prion is a protein particle that lacks DNA (nucleic acid). It’s believed to be the cause of various infectious diseases of the nervous system. Eating infected cattle products, including beef, can cause a human to develop mad cow disease.

What is mad cow disease?

Mad cow disease is a progressive, fatal neurological disorder of cattle resulting from infection by a prion. It appears to be caused by contaminated cattle feed that contains the prion agent. Most mad cow disease has happened in cattle in the United Kingdom (U.K.), a few cases were found in cattle in the U.S. between 2003 and 2006. There were 4 more reported up to 2018.  Feed regulations were then tightened.

In addition to the cases of mad cow reported in the U.K. (78% of all cases were reported there) and the U.S., cases have also been reported in other countries, including France, Spain, Netherlands, Portugal, Ireland, Italy, Japan, Saudi Arabia, and Canada. Public health control measures have been implemented in many of the countries to prevent potentially infected tissues from entering the human food chain. These preventative measures appear to have been effective. For instance, Canada believes its prevention measures will wipe out the disease from its cattle population by 2017.

What is variant Creutzfeldt-Jakob Disease (vCJD)?

Creutzfeldt-Jakob Disease (CJD) is a rare, fatal brain disorder. It causes a rapid, progressive dementia (deterioration of mental functions), as well as associated neuromuscular disturbances. The disease, which in some ways resembles mad cow disease, traditionally has affected men and women between the ages of 50 and 75. The variant form, however, affects younger people (the average age of onset is 28) and has observed features that are not typical as compared with CJD. About 230 people with vCJD have been identified since 1996. Most are from the U.K. and other countries in Europe. It is rare in the U.S., with only 4 reported cases since 1996.

What is the current risk of acquiring vCJD from eating beef and beef products produced from cattle in Europe?

Currently this risk appears to be very small, perhaps fewer than 1 case per 10 billion servings–if the risk exists at all. Travelers to Europe who are concerned about reducing any risk of exposure can avoid beef and beef products altogether, or can select beef or beef products, such as solid pieces of muscle meat, as opposed to ground beef and sausages. Solid pieces of beef are less likely to be contaminated with tissues that may hide the mad cow agent. Milk and milk products are not believed to transmit the mad cow agent. You can’t get vCJD or CJD by direct contact with a person who has the disease. Three cases acquired during transfusion of blood from an infected donor have been reported in the U.K. Most human Creutzfeldt-Jakob disease is not vCJD and is not related to beef consumption but is also likely due to prion proteins

The Risk of getting Mad Cow Disease in the US, based on CDC-Centers for Disease Prevention and Control show the following statistics:

On December 23, 2003, the U.S. Department of Agriculture (USDA) announced a presumptive diagnosis of the first known case of BSE in the United States. It was in an adult Holstein cow from Washington State. This diagnosis was confirmed by an international reference laboratory in Weybridge, England, on December 25. Trace-back based on an ear-tag identification number and subsequent genetic testing confirmed that the BSE-infected cow was imported into the United States from Canada in August 2001.

Because the animal was non-ambulatory (a “downer cow”) at slaughter, brain tissue samples were taken by USDA’s Animal and Plant Health Inspection Service as part of its targeted surveillance for BSE. However the animal’s condition was attributed to complications from calving. After the animal was examined by a USDA Food Safety and Inspection Service (FSIS) veterinary medical officer both before and after slaughter, the carcass was released for use as food for human consumption. During slaughter, the tissues considered to be at high risk for the transmission of the BSE agent were removed.

On December 24, 2003, FSIS recalled beef from cattle slaughtered in the same plant on the same day as the BSE positive cow.

On June 24, 2005, the USDA announced receipt of final results from The Veterinary Laboratories Agency in Weybridge, England, confirming BSE in a cow that had conflicting test results in 2004. This cow was from Texas, died at approximately 12 years of age, and represented the first endemic case of BSE by a cow in the United States.

On March 15, 2006, the USDA announced the confirmation of BSE in a cow in Alabama. The case was identified in a non-ambulatory (downer) cow on a farm in Alabama. The animal was euthanized by a local veterinarian and buried on the farm. The age of the cow was estimated by examination of the dentition as 10 years old.

It had no ear tags or distinctive marks; the herd of origin could not be identified despite an intense investigation.

In August 2008, several ARS investigators reported that a rare, genetic abnormality that may persist within the cattle population “is considered to have caused” BSE in this atypical (H-type) BSE animal from Alabama.

On April 24, 2012, the USDA confirmed a BSE case in a dairy cow in California. This cow was tested as part of the USDA targeted BSE surveillance at rendering facilities in the United States. The cow was 10 years and 7 months old and was classified as having the L-type BSE strain.

On July 18, 2017, the U.S. Department of Agriculture (USDA) announced the confirmation of the fifth case of bovine spongiform encephalopathy (BSE) in an 11-year-old cow in Alabama. The cow was found through USDA’s routine surveillance. The cow was found to be positive for an atypical (L-type) strain of BSE. Atypical BSE usually occurs in older cattle and seems to arise spontaneously in cattle populations.

On August 29, 2018 the U.S. Department of Agriculture (USDA) announced a confirmed atypical, H-type case of bovine spongiform encephalopathy (BSE) in a six year old mixed-breed beef cow in Florida. USDA reported that this animal never entered the food supply and at no time presented a risk to human health.

How does the cow even get Mad Cow Disease?

The parts of a cow that are not eaten by people are cooked, dried, and ground into a powder. The powder is then used for a variety of purposes, including as an ingredient in animal feed. A cow gets BSE by eating feed contaminated with parts that came from another cow that was sick with BSE. The contaminated feed contains the abnormal prion, and a cow becomes infected with the abnormal prion when it eats the feed. If a cow gets BSE, it most likely ate the contaminated feed during its first year of life. Remember, if a cow becomes infected with the abnormal prion when it is one-year-old, it usually will not show signs of BSE until it is five-years-old or older.

Learn more tomorrow in Part II on Mad Cow Disease.

 

 

QUOTE FOR THE WEEKEND:

“Approximately 36,000 units of red blood cells are needed every day in the U.S. Nearly 21 million blood components are transfused each year in the U.S. Although an estimated 38 percent of the U.S. population is eligible to donate blood at any given time, less than 10 percent of that eligible population actually do each year. The blood type most often requested by hospitals is type O (the universal donor).”


American Red Cross (www.redcross.org)

Why we need blood donor’s!

 

Why do we need blood donor’s?

We need to make sure that we have enough supplies of all blood groups and blood types to treat all types of conditions.

By giving blood, every donor helps us meet the challenge of providing life-saving products whenever and wherever they are needed.

The American Red Cross states the following facts:

  • Every two seconds someone in the U.S. needs blood.
  • Approximately 36,000 units of red blood cells are needed every day in the U.S.
  • Nearly 7,000 units of platelets and 10,000 units of plasma are needed daily in the U.S.
  • Nearly 21 million blood components are transfused each year in the U.S.
  • The average red blood cell transfusion is approximately 3 pints.
  • The blood type most often requested by hospitals is type O.
  • Nearly 21 million blood components are transfused each year in the U.S.
  • It is estimated that sickle cell disease affects 90,000 to 100,000 people in the U.S. About 1,000 babies are born with the disease each year. Sickle cell patients can require frequent blood transfusions throughout their lives.
  • The number of whole blood and red blood cell units collected in the U.S. in a year: 13.6 million
  • The number of blood donors in the U.S. in a year: 6.8 million
  • Although an estimated 38 percent of the U.S. population is eligible to donate blood at any given time, less than 10 percent of that eligible population actually do each year.
  • Blood cannot be manufactured – it can only come from generous donors.
  • Type O negative blood (red cells) can be transfused to patients of all blood types. It is always in great demand and often in short supply. Type O is the “Universal Blood Donor”
  • Type AB positive plasma can be transfused, it’s the “Universal Blood Recepient”.

This allows pt’s diagnosed with this illness to experience:

  • Bleeding due to lack of platelets
  • shortness of breath due to lack of RBC’s carrying oxygen (02) to the tissues of the body.
  • Dizziness again due to lack of 02 carried to the brain with anemic, & bleeding causing your B/P to be low (orthostatic b/p-changing your position anemic and blood dropping from the brain to cause dizziness) also.
  • cognitive impairment due to lack of 02 to the brain since RBC count is low in the body.
  • Bruising due to low platelets.
  • petachiae (small red/purple spots on the skin)
  • susceptibility to infections

Conditions for needing blood donors:

Aplastic anemia occurs when bone marrow stops making enough blood forming stem cells. In all three blood lines; red blood cells, white blood cells and platelets, patients with aplastic anemia have a low blood count. The bone marrow is found to be aplastic which means there is a low growth of blood forming stem cells.

Cancer of all types –  Where with or without the treatments of chemo or radiation in the end cancer itself kills all good cells that are created by our bone marrow.  Chemo or radiation kill the bad cells = cancer cells and good cells = RBCs, WBCs, Platelets.  So blood transfusion commonly needed in cancer patients.

Anemia– Lack of RBCs in the body.

Conditions causing bleeding in the body like GI bleed, hemmoragic stroke, endometriosis, hemophilia, and simple patients in the OR that bleed and need blood transfusions in the OR and ICU and even possibly on the Med/Surg or Telemetry unit.  I could go on with types of conditions the deciding factor that makes the doctor order the blood transfusion is obviously heavy bleeding occurring right in front of the surgeon’s or ER MDs eyes or checking the Complete Blood Count called a CBC looking at the hemoglobin (Hmg)-think of it at the fluids in the bloodstream and looking at the Hematocrit (Hct)-think of it as the solids in the bloodstream and if the Hg is critical 6-7 than one or two blood transfusions are ordered.

Treatments:

  • Treatments vary on a case by case basis. Age is often the determining factor for which treatment to use. Stem cell transplantation may be used for individuals younger than 30 years and who have a matched sibling donor=Blood Donor Needed.
  • Stem cell transplantation is a procedure which replaces defective bone marrow with healthy cells. Around 80% of patients make a complete recovery using stem cell transplantation.
  • For older patients with aplastic anemia, immune suppressing therapy with anti-thymocyte globulin(ATG) and cyclosporin is typically used. Around 70-80% of aplastic anemia patients respond to this treatment.

QUOTE FOR FRIDAY:

When diabetes is not controlled, too much sugar remains in the blood. Over time, this can damage organs, including the brain. Scientists are finding more evidence that could link Type 2 diabetes with Alzheimer’s disease, the most common form of dementia and the seventh leading cause of death in the United States.”

Alzheimer’s Association ( https://www.alz.org)

Diabetes increases your risk of Alzheimer’s dramatically.

If You Have Diabetes, Your Risk of Alzheimer’s Increases Dramatically

Diabetes is linked to a 65 percent increased risk of developing Alzheimer’s, which may be due, in part, because insulin resistance and/or diabetes appear to accelerate the development of plaque in your brain, which is a hallmark of Alzheimer’s. Separate research has found that impaired insulin response was associated with a 30 percent higher risk of Alzheimer’s disease, and overall dementia and cognitive risks were associated with high fasting serum insulin, insulin resistance, impaired insulin secretion and glucose intolerance.

A drop in insulin production in your brain may contribute to the degeneration of your brain cells, mainly by depriving them of glucose, and studies have found that people with lower levels of insulin and insulin receptors in their brain often have Alzheimer’s disease (people with type 2 diabetes often wind up with low levels of insulin in their brains as well). As explained in New Scientist, which highlighted this latest research:

What’s more, it encourages the process through which neurons change shape, make new connections and strengthen others. And it is important for the function and growth of blood vessels, which supply the brain with oxygen and glucose.

As a result, reducing the level of insulin in the brain can immediately impair cognition. Spatial memory, in particular, seems to suffer when you block insulin uptake in the hippocampus… Conversely, a boost of insulin seems to improve its functioning.

When people frequently gorge on fatty, sugary food, their insulin spikes repeatedly until it sticks at a high level. Muscle, liver and fat cells then stop responding to the hormone, meaning they don’t mop up glucose and fat in the blood. As a result, the pancreas desperately works overtime to make more insulin to control the glucose – and levels of the two molecules skyrocket.

The pancreas can’t keep up with the demand indefinitely, however, and as time passes people with type 2 diabetes often end up with abnormally low levels of insulin.”

Alzheimer’s Might be “Brain Diabetes”

BBA – Molecular Basis of Disease, Accepted manuscript. doi:10.1016/j.bbadis.2016.04.017

It’s becoming increasingly clear that the same pathological process that leads to insulin resistance and type 2 diabetes may also hold true for your brain. As you over-indulge on sugar and grains, your brain becomes overwhelmed by the consistently high levels of insulin and eventually shuts down its insulin signaling, leading to impairments in your thinking and memory abilities, and eventually causing permanent brain damage.

Regularly consuming more than 25 grams of fructose per day will dramatically increase your risk of dementia and Alzheimer’s disease. Consuming too much fructose will inevitably wreak havoc on your body’s ability to regulate proper insulin levels.

Although fructose is relatively “low glycemic” on the front end, it reduces the affinity for insulin for its receptor leading to chronic insulin resistance and elevated blood sugar on the back end. So, while you may not notice a steep increase in blood sugar immediately following fructose consumption, it is likely changing your entire endocrine system’s ability to function properly behind the scenes.

Additionally, fructose has other modes of neurotoxicity, including causing damage to the circulatory system upon which the health of your nervous system depends, as well as profoundly changing your brain’s craving mechanism, often resulting in excessive hunger and subsequent consumption of additional empty carbohydrate-based calories.

In one study from UCLA, researchers found that rats fed a fructose-rich and omega-3 fat deficient diet (similar to what is consumed by many Americans) developed both insulin resistance and impaired brain function in just six weeks.

Plus, when your liver is busy processing fructose (which your liver turns into fat), it severely hampers its ability to make cholesterol , an essential building block of your brain crucial to its health. This is yet another important facet that explains how and why excessive fructose consumption is so detrimental to your health.  Decreasing fructose intake is one of the most important moves you can take in decreasing the risk of Alzheimer’s disease in your lifetime.

 

QUOTE FOR THURSDAY:

“Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks. In most people with the disease—those with the late-onset type—symptoms first appear in their mid-60s. Early-onset Alzheimer’s occurs between a person’s 30s and mid-60s and is very rare. Alzheimer’s disease is the most common cause of dementia among older adults.”

National Institute on Aging    (https://www.nia.nih.gov)

What is actually Alzheimer’s Disease?

What structurally happens to the brain and what happens to the individual in brain thinking diagnosed with this disease:

Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks. In most people with the disease—those with the late-onset type—symptoms first appear in their mid-60s. Early-onset Alzheimer’s occurs between a person’s 30s and mid-60s and is very rare. Alzheimer’s disease is the most common cause of dementia among older adults.

The disease is named after Dr. Alois Alzheimer. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. Her symptoms included memory loss, language problems, and unpredictable behavior. After she died, he examined her brain and found many abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary, or tau, tangles).

These plaques and tangles in the brain are still considered some of the main features of Alzheimer’s disease. Another feature is the loss of connections between nerve cells (neurons) in the brain. Neurons transmit messages between different parts of the brain, and from the brain to muscles and organs in the body. Many other complex brain changes are thought to play a role in Alzheimer’s, too.

This damage initially appears to take place in the hippocampus, the part of the brain essential in forming memories. As neurons die, additional parts of the brain are affected. By the final stage of Alzheimer’s, damage is widespread, and brain tissue has shrunk significantly.

How many affected in the United States by Alzheimer’s Disease:

Estimates vary, but experts suggest that as many as 5.5 million Americans age 65 and older may have Alzheimer’s. Many more under age 65 also have the disease. Unless Alzheimer’s can be effectively treated or prevented, the number of people with it will increase significantly if current population trends continue. This is because increasing age is the most important known risk factor for Alzheimer’s disease.

Symptoms:

Memory problems are typically one of the first signs of Alzheimer’s, though initial symptoms may vary from person to person. A decline in other aspects of thinking, such as finding the right words, vision/spatial issues, and impaired reasoning or judgment, may also signal the very early stages of Alzheimer’s disease. Mild cognitive impairment (MCI) is a condition that can be an early sign of Alzheimer’s, but not everyone with MCI will develop the disease.

People with Alzheimer’s have trouble doing everyday things like driving a car, cooking a meal, or paying bills. They may ask the same questions over and over, get lost easily, lose things or put them in odd places, and find even simple things confusing. As the disease progresses, some people become worried, angry, or violent.

Alzheimer’s disease is not a normal part of aging.

Memory problems are typically one of the first warning signs of cognitive loss.

According to the National Institute on Aging, in addition to memory problems, someone with Alzheimer’s disease may experience one or more of the following signs:

  • Memory loss that disrupts daily life, such as getting lost in a familiar place or repeating questions.
  • Trouble handling money and paying bills.
  • Difficulty completing familiar tasks at home, at work or at leisure.
  • Decreased or poor judgment.
  • Misplaces things and being unable to retrace steps to find them.
  • Changes in mood, personality, or behavioral.