“There are known factors that can increase your risk of dementia. These include:
Center for Disease Control and Prevention – CDC (Reducing Risk for Dementia | Alzheimer’s Disease and Dementia | CDC)
Hall of Fame pitcher Tom Seaver, the star of the Miracle Mets 1969 World Series championship team, was diagnosed with dementia at age 74.
His family made the announcement Thursday through the Hall and said Seaver has retired from public life. He will continue to work at Seaver Vineyards, founded by the retired player and wife Nancy in 2002 on 116 acres at Diamond Mountain in the Calistoga region of California.
Seaver was diagnosed with Lyme disease in 1991, and it reoccurred in 2012 and led to Bell’s Palsy and memory loss, the New York Daily News reported in 2013.
Know this, Lyme disease also has the unique ability to bypass the body’s blood-brain barrier, a barrier which typically prevents foreign invaders from affecting the brain, allowing the disease to enter the nervous system accounting for Lyme’s many complex neurological symptoms. Antibiotic treatment protocols alone do not account for this invasion of the body’s nervous system through the blood-brain barrier and therefore are not likely to have lasting results. To effectively treat chronic Lyme disease, antibiotics need to also move past the blood-brain barrier.
Lyme related neurological symptoms are destructive and life-changing.
The struggle to find the right diagnosis is extremely draining for patients who are already facing depression, brain fog, memory loss, tremors, and other crippling symptoms.
Can this lead to Alzheimer’s disease or make it come quicker??
Art Shamsky, who hit .300 with 14 home runs that season for the Mets, details some of the health issues of other teammates as well, among other things, in “After the Miracle,” Newsday reported last week, March 6 on Fox News Channel.
Shamsky, 77, wrote that Seaver suffers from short-term memory loss that could stem from Lyme disease. Seaver, 74, apparently told Shamsky he contracted the disease in 1991 when he lived in Connecticut.
Bud Harrelson, another key player on the championship team, which defeated the Baltimore Orioles in the World Series, four games to one, had reportedly been making visits to Seaver regularly and told some members of the team to be prepared when they re-connected with the three-time Cy Young award winner.
“He can forget things that happened just a few minutes before,” Harrelson told Shamsky, according to Newsday. “And he repeats himself a lot. But when he gets his rest, he still has a lot of energy.”
Harrelson, 74, is having his own health struggles. The former Mets shortstop was diagnosed with Alzheimer’s disease in 2016. He opened up to CBS New York after 2016 and told the station he immediately stopped driving.
Dementia isn’t a specific disease. Instead, dementia describes a group of symptoms affecting memory, thinking and social abilities severely enough to interfere with daily functioning.
Though dementia generally involves memory loss, memory loss has different causes. So memory loss alone doesn’t mean you have dementia. So seeing a specialist who is a MD in Dementia is the expert to go to.
Alzheimer’s disease is the most common cause of a progressive dementia in older adults, but there are a number of causes of dementia. Depending on the cause, some dementia symptoms can be reversed.
Dementia symptoms vary depending on the cause, but common signs and symptoms include:
See a doctor if you or a loved one has memory problems or other dementia symptoms. Some treatable medical conditions can cause dementia symptoms, so it’s important to determine the underlying cause.
Dementia involves damage of nerve cells in the brain, which can occur in several areas of the brain. Dementia affects people differently, depending on the area of the brain affected.
Dementias are often grouped by what they have in common, such as the part of the brain that’s affected or whether they worsen over time (progressive dementias). Some dementias, such as those caused by a reaction to medications or vitamin deficiencies, might improve with treatment.
Types of dementias that progress and aren’t reversible include:
Some causes of dementia or dementia-like symptoms can be reversed with treatment. They include:
Many factors can eventually lead to dementia. Some factors, such as age, can’t be changed. Others can be addressed to reduce your risk.
You might be able to control the following risk factors of dementia.
Dementia can affect many body systems and, therefore, the ability to function. Dementia can lead to:
There’s no sure way to prevent dementia, but there are steps you can take that might help in slowing down the process of the disease. More research is needed, but it might be beneficial to do the following:
Mad Cow Disease has largely eradicated and does not pose much risk, atypical cases can still occur. Facts on Mad Cow Disease:
1-“Since 1996, evidence has been increasing for a causal relationship between the outbreak in Europe of a disease in cattle, called bovine spongiform encephalopathy (BSE, or “mad cow disease”), and a disease in humans, called “variant” Creutzfeldt-Jakob disease (vCJD).
Both disorders are invariably fatal brain diseases with unusually long incubation periods measured in years, and are caused by abnormally folded proteins in the brain called “prions” (pree-ons). ”
Cattle affected by BSE experience progressive degeneration of the nervous system. Signs usually don’t appear until about 3–6 years after initial infection.
The highest quality beef comes from animals that are under 36 months of age. Old cows produce highly acceptable beef if properly fattened and processed but know there is testing cows for it before making it food on our table.
Know this BSE belongs to a family of diseases known as transmissible spongiform encephalopathies that includes, among others, scrapie in sheep and goats; chronic wasting disease in deer, elk, and moose; and classic and variant Creutzfeldt-Jakob disease in people.”
1-Centers for Disease Control and Prevention-CDC (https://www.cdc.gov/prions/index.html)
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:
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.
Most countries have taken steps to prevent BSE-infected tissue from entering the food supply, including:
“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” meaning that it is a disease of the brain. BSE is commonly called “mad cow disease.
Cattle affected by BSE experience progressive degeneration of the nervous system. Signs usually don’t appear until about 3–6 years after initial infection.
Here’s what to look for:
After signs appear, the animal’s condition deteriorates until it dies. This usually takes anywhere from 2 weeks to 6 months.”
U.S.D.A. US Dept or Agriculture (https://www.aphis.usda.gov/livestock-poultry-disease/cattle/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.
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.
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 until May of 2023 in Chicago found in baby cow.
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 possibly older.
Learn more tomorrow in Part II on Mad Cow Disease.
“Your liver is the primary detoxification organ, and it handles the job in two phases. In the first phase, specialized enzymes chemically alter toxic substances through oxidation or reduction, essentially breaking them down into intermediate compounds. In the second phase, a different set of enzymes attaches those intermediates to molecules like glutathione or sulfate, making them water-soluble enough to be excreted through urine or bile.
The liver and gastrointestinal tract handle the bulk of this work, but they’re not alone. Your kidneys filter about 150 quarts of blood daily, pulling out waste products and excess substances. Your lungs expel volatile compounds with every breath. Your skin pushes some waste out through sweat. Your lymphatic system carries cellular debris toward filtration points throughout your body. This is a continuous, layered process that doesn’t need a reset button.”
Science Insights (https://scienceinsights.org/is-detoxing-good-for-you-what-science-actually-says/)
Detoxification is the body’s natural process of removing waste and toxins through the liver (the primary organ that does detoxifying), kidneys, lungs, skin, and digestive system. A structured detox, such as a short-term dietary reset or nutrient-rich cleanse, can support these organs by reducing the intake of processed foods, alcohol, & excess sugar, giving your body a “reset” and potentially improving overall health and energy levels.
Supports Digestion and Gut Health: A detox emphasizing whole foods, fiber, and hydration could definitely help the intestines eliminate waste more efficiently and reduce digestive discomfort.
Encourages Healthy Eating Habits: Periodic detoxes can help break cycles of overindulgence, that indirectly is making it easier to maintain a balanced nutrient-rich diet throughout the year.
May Reduce Toxin Load: While the body naturally detoxifies, reducing exposure to processed foods, alcohol, and the environmental toxins during a cleanse can lessen the burden on detox organs.
“Vaginal thinning of the wall or called vaginal atrophy (VA), though not as well-known as other things brought on by menopause—like hot flashes or night sweats—it’s estimated that over half of all post-menopausal women have VA.!”
Health Central (8 Signs You May Have Vaginal Atrophy)
What are the complications of vaginal atrophy (GSM)?Vaginal atrophy can affect your quality of life and your relationship with your partner(s). There are physical and emotional side effects of GSM. Physical symptoms like pain, burning, itching and leaking pee can disrupt all areas of your life. Emotional side effects are just as complicated as the physical side effects. If you’re experiencing symptoms of vaginal atrophy, you may lose interest in sex and intimacy or lose confidence in yourself. Please know that all of these feelings are normal and that your healthcare provider is there to help you.
A healthcare provider can diagnose vaginal atrophy based on your symptoms and a pelvic exam to look at your vagina and cervix. Classic signs of atrophy during a pelvic exam include:
While healthcare providers typically rely on examinations to diagnose atrophic changes or GSM, they may do the following tests to rule out other conditions:
It’s common to feel uncomfortable discussing symptoms of vaginal atrophy. Don’t feel ashamed to mention it to your healthcare provider if you think you have symptoms. There are several different treatment options available and most are successful in treating your symptoms.
Estrogen therapy and dehydroepiandrosterone (DHEA) are the only hormone therapies for vaginal atrophy.
Topical vaginal estrogen treats symptoms of vaginal atrophy without increasing levels of estrogen levels in your bloodstream. It’s available in a cream, a vaginal pill or a ring. Your healthcare provider can discuss each option with you and which may work best for you.
Also called systemic estrogen therapy, this type of hormone therapy may be helpful if you have other symptoms of menopause such as severe hot flashes. This is taken in higher doses that go to other cells of your body, not just to your vagina. If you’re more than 10 years past menopause or only have vaginal dryness, you’ll probably use local therapy. If you do need systemic hormone therapy, there are benefits, such as improved vaginal health, better sleep, fewer hot flashes and improved mood. You and your healthcare provider can discuss if systemic hormone therapy is right for you.
You and your healthcare provider will work closely together to come up with a treatment plan for vaginal atrophy. They’ll help you decide which plan is most effective based on your symptoms and the severity of them. Estrogen and DHEA therapy are considered to be the most effective. However, these therapies aren’t for everyone. There are several treatment options available that don’t involve hormones.
Lubricants and moisturizers treat vaginal dryness. This improves comfort during sex. Multiple brand names are available over the counter at your local grocery store.
Vaginal lubricants should be used during intercourse to reduce friction and pain with sex. They’re water, silicone or oil based. These products are very short-acting.
based on your health history and your situation. They’ll work with you to determine the most successful treatment plan. Keep in mind that many people find success combining treatments.
You don’t have to just “live with” vaginal atrophy. Even if you’re in menopause or postmenopausal, that doesn’t mean you should have to deal with UTIs, vaginal itching or painful sex. Treatment for GSM can be very successful. Don’t be afraid to try different treatments and work with your provider on a method that works best for you.
Vaginal atrophy can’t be cured, but you don’t have to live with the discomfort. With proper diagnosis and treatment, the symptoms can be managed.
Yes, it can. That’s why prompt treatment is important. The sooner you get treatment, the less likely it is that your vaginal atrophy will worsen. For example, the longer you go without estrogen, the dryer your vagina will become. Without treatment, your vaginal atrophy may get worse. Occasionally, atrophy can become so severe that it can significantly narrow your vaginal opening. This may make it harder to treat the atrophy if treatment is started too late.
Losing estrogen is part of your body’s natural aging process.
However, there are ways to keep vaginal atrophy from getting worse. Avoid vaginal irritants such as perfumes, dye, shampoo, detergents and douching.
Remember, regular sexual activity is good for vaginal atrophy because it increases blood flow to your vaginal tissue.
Vaginal atrophy can seriously affect your quality of life in general, not just your sex life. The pain, dryness, burning/itching, spotting, bleeding, urinary problems, UTIs and discharge can make you very uncomfortable and interfere with your daily living. One in 4 women report that vaginal atrophy has had a negative impact on other areas of their lives including their sleep, sexual health and general happiness.
Prioritize your sexual health as much as any other aspect of your health. Look to your healthcare provider for answers to any questions and concerns.
Even if you’re not in menopause, be sure to report any symptoms of dryness, pain, burning/itching, urinary problems, unusual spotting or bleeding or discharge to your healthcare provider.
If weeks go by and the over-the-counter moisturizers you’re using for dryness don’t work, you should see your healthcare provider.
Also, always see your healthcare provider for any symptoms that negatively impact your daily life.
Both vaginal atrophy and yeast infections can have symptoms of dryness, itching, redness and pain. However, lack of estrogen causes vaginal atrophy while a fungal infection causes a vaginal yeast infection. Consult with your healthcare provider regarding symptoms so that, together, you can determine what condition you have.
Vaginal atrophy is serious. It affects your quality of life with discomfort, frequent bathroom trips, frequent UTIs, burning, pain with sex and more. Fortunately, there are many treatments and your healthcare provider can help you find the best option for your symptoms.
Seek treatment. Don’t be afraid to have the conversation with your healthcare provider and with your partner(s). Always follow your healthcare provider’s instructions and do what you can to manage vaginal atrophy.