Reply
Honored Contributor
Posts: 17,739
Registered: ‎03-09-2010
 

More and more, I am finding many people who as they enter their sixth decade, are finding new aches and pains that never existed before. Increasingly, many are finding something else that never existed before: diabetes. For most of these people, after a lifetime of enjoying reasonably healthy lives, seemingly out of nowhere, they are told they are now diabetic, and prescribed medication. Needless, to say, this comes as a shock!

However, consistent with many other changes in the body as we age, your body becomes more susceptible to diabetes.

Of course, seniors (those over 65) are not the only people to be affected by diabetes. According to the Centers for Disease Control and Prevention (CDC), over 30 million people in the United States have diabetes. The CDC also notes that 90 to 95% of cases involve type 2 diabetes. More than one-quarter of the US population aged 65 and older has diabetes, 1 including type 1 and 2, and approximately one-half of older adults have pre-diabetes. In this population, age-related insulin resistance and impaired pancreatic islet function increase the risk of developing the disease.

 

Many older people also have other conditions as well as diabetes, and this can complicate diabetes management. For example, high blood pressure or high levels of certain fats in the blood can speed up the progression of common complications of diabetes, such as kidney problems, eye problems, foot problems, and heart and blood vessel problems. People with diabetes whose blood glucose levels are high are more prone to infections than people with normal blood glucose levels.

People with poorly controlled diabetes are also at greater risk for dental problems. They’re more likely to have infections of their gums and the bones that hold their teeth in place, because diabetes can reduce the blood supply to the gums.

Not only that, but when we age, loss of teeth and poor dental health becomes more and more common. As a result, what we eat, and how we eat (along with age-related poorer appetite). We don’t, and can’t, chew like we used to. That means things like crunchy fruits and vegetables are off-limits. We end up gravitating towards softer chewy foods that tend to be more processed, and bad for our health in the long run.

A poor diet of soft and processed foods can have serious long-term effects, especially on the seniors or those with systemic health issues like heart disease and diabetes. Specifically, a poor diet can lead to either unhealthy weight loss or unhealthy weight gain, high blood pressure, high cholesterol, malnutrition, dehydration, jawbone loss, osteoporosis, stroke, and some cancers. Poor nutrition can also cause even more oral health issues, including gingivitis and tooth decay.

If we look, honestly, at all the things that go along with aging, we find that it makes sense that the risk of becoming diabetic increases as we get older. In addition to their many physical challenges, elderly diabetes patients often are socially isolated and have financial problems that negatively affect their care. They may forget to eat, be unable to afford medications or quality food, or skip medication doses to extend a prescription. They also may experience changes in taste and a lack of interest and ability to shop for food and prepare meals at home.

 

An additional concern with blood sugar being too high, is the danger of blood sugar dropping too low (hypoglycemia). This creates the conditions for many serious issues that wreak havoc in the lives of the elderly; particularly falls and fractures. Instead of, or in addition to, sweating and tremors, elderly diabetes patients should be taught to look for symptoms of hypoglycemia, such as dizziness, weakness, delirium, and confusion. Often, the low glucose will cause them to fall, resulting in a head injury and death.

There is good news! Despite the high rates of diagnosis, there are ways the disease may be delayed and even prevented. Your best options include regular exercise; losing 5 to 10% of your body weight if you’re overweight or obese; and reducing your intake of sugar and sweetened beverages. If we are all honest with ourselves, one or more of these risk factors is a part of who we are, and how we have grown accustomed to living. By losing just 5 to 7% of your body weight, you can slow the development of type 2 diabetes.

You may not be able to prevent diabetes entirely. But taking steps now may prevent related complications and improve your quality of life.

Remember, I’m not a doctor. I just sound like one.

Take good care of yourself and live the best life possible!

 
 

Glenn Ellis is a Research Bioethics Fellow at Harvard Medical School and author of “Which Doctor?” and “Information is the Best Medicine.” Ellis is an active media contributor on health equity and medical ethics.

 

Respected Contributor
Posts: 4,206
Registered: ‎08-08-2011

Re: Diabetes News 2020 winter

I was recently with a group of five other women friends (all in their 60s) and one was diagnosed with type two a couple years ago and three are in the prediabetic stage.  So the 60s does seem like a real turning point for the risk of diabetes. 

Honored Contributor
Posts: 17,739
Registered: ‎03-09-2010

Re: Diabetes News 2020 winter

Yes it seems to be @itsmagic  I was diagnosed at 66

Respected Contributor
Posts: 4,206
Registered: ‎08-08-2011

Re: Diabetes News 2020 winter

@cherry  You might have previously posted about this but have you been able to control it with low carb?  After speaking to my group of friends I took a hard look at all the sugar and carbs I’ve been eating throughout my lifetime and I’m committed to improving my diet in that regard. I know exercise is important too and I’ve added more walking. 

Honored Contributor
Posts: 17,739
Registered: ‎03-09-2010

Re: Diabetes News 2020 winter

No I needed medication ,but my thyroid doesnt work properly , and I think that is a contributor.

Honored Contributor
Posts: 17,739
Registered: ‎03-09-2010

Re: Diabetes News 2020 winter

[ Edited ]
January 1, 2020

 

Patients with diabetes are at risk for complications from vaccine-preventable diseases, making immunization especially critical. 

 

Diabetes can alter the immune system, making it more difficult for individuals to fight off infections. Additionally, conditions like influenza can increase blood glucose levels leading to serious complications. According to a study by the American Diabetes Association (ADA), adult vaccination rates in patients with diabetes are low. Vaccination rates for the 846 study participants included the following: influenza (17.6%), tetanus (18.6%), hepatitis B (8.6%), and pneumococcal (5.4%).1 Pharmacists can play an important role in administering vaccines and educating patients with diabetes on the importance of staying up-to-date on immunizations.

Recommended Vaccines

The CDC and ADA both recommend providing routine vaccinations for children and adults with diabetes. With flu season in full swing, it’s important for all patients 6 months of age and older to get an annual influenza vaccine. According to the CDC, there is elevated and even widespread flu activity across the country.2 Evidence demonstrates that influenza vaccination in patients with diabetes significantly reduces flu and diabetes-related hospital admissions.3

The CDC recommends routine administration of pneumococcal conjugate vaccine (PCV13 or Prevnar13) for all children younger than 2 years of age. All adults 65 years and older should receive the pneumococcal polysaccharide vaccine (PPSV23 or Pneumovax23) vaccine, and patients 19 to 64 years of age with diabetes should receive 1 dose. Individuals who received any doses of PPSV23 before age 65 should receive 1 final dose of the vaccine at 65 years or older.  Additionally, the last dose should be administered at least 5 years after the first PPSV23 dose.4  The Advisory Committee on Immunization Practices (ACIP) no longer recommends routine vaccination with PCV13 for all adults 65 years and older who do not have an immunocompromising condition.5 Pharmacists can download the CDC’s free PneumoRecs VaxAdvisor mobile app as a point-of-care resource for guidance on pneumococcal vaccination based upon a patient’s age, medical conditions, and immunization history.

According to a study published in Diabetes Research and Clinical Practice, individuals with diabetes have a higher risk of experiencing herpes zoster (shingles), making vaccination especially important in this population to prevent complications.6 Individuals 50 years of age and older should receive the recombinant zoster vaccine (RZV, Shingrix), which is recommended by ACIP as the preferred shingles vaccine. The vaccine is given as 2 doses separated by 2 to 6 months, and patients should receive RZV even if they have had shingles, previously received Zostavax, or have an unknown chickenpox history. The most common adverse effects include pain, redness, and swelling at the injection site.  Patients may also experience fever, muscle pain, and headache.

The CDC also recommends that all adults receive the tetanus, diphtheria, and pertussis (Tdap) vaccine once and a Td vaccine booster dose every 10 years. Additionally, all women should receive a Tdap vaccine during the 27th through 36th week of each pregnancy to pass on antibodies to the fetus to protect against pertussis. The CDC recommends hepatitis B vaccination for all unvaccinated adults with diabetes younger than 60 years of age as a 2- or 3-dose series. Individuals with diabetes have a higher risk of hepatitis B with transmission occurring from inappropriate use of blood glucose meters or infected needles (eg sharing lancets, improper equipment cleaning in nursing homes).7

References: 
  1. Feyizoğlu G, Karsli A, Oguz A. The alarming inadequacy of adult vaccination–vaccination rates in diabetic patients. Diabetes. 2018. Doi: https://doi.org/10.2337/db18-679-P
  2. CDC. Weekly US Influenza Surveillance Report. CDC’s website. https://www.cdc.gov/flu/weekly/index.htm.
  3. American Diabetes Association. Standards of Medical Care in Diabetes–2020. Diabetes Care. January 2020. https://care.diabetesjournals.org/content/diacare/suppl/2019/12/20/43.Supplement_1.DC1/DC_43_S1_2020....
  4. CDC. Pneumococcal Vaccine Recommendations. CDC’s website. https://www.cdc.gov/vaccines/vpd/pneumo/hcp/recommendations.html.
  5. Matanock A, Lee G, Gierke R, et al. Use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine among adults aged ≥65 years: Updated recommendations of the Advisory Committee on Immunization Practices. Morbidity and Mortality Weekly Report. 2019. https://www.cdc.gov/mmwr/volumes/68/wr/mm6846a5.htm
  6. Saadatian-Elahi M, Bauduceau B, Del-Signore C, et al. Diabetes as a risk factor for herpes zoster in adults: A synthetic literature review. Diabetes Res Clin Pract. 2019.  Doi: 10.1016/j.diabres.2019.107983. [Epub ahead of print]
  7. CDC. Diabetes and Hepatitis B. CDC’s website. https://www.cdc.gov/hepatitis/populations/diabetes.htm.
 
 
 
 
 
 
 
  •  
Honored Contributor
Posts: 17,739
Registered: ‎03-09-2010

Re: Diabetes News 2020 winter

Researchers discover process that may explain how Type 2 diabetes develops

Alice Walton | December 19, 2019
A new study helps to explain the mechanism by which pancreatic cells secrete high levels of insulin during the early stages of diabetes.

A central question in diabetes research is why cells of the pancreas, known as beta cells, initially over-secrete insulin. The prevailing theory was that the body may be in the process of becoming “deaf” to insulin, so beta cells secrete more to compensate. But isolated beta cells still over-secrete insulin, which exposes a gap in that theory.

In the new study, researchers set out to understand what other mechanism beyond insulin resistance (that is, the body becoming “deaf” to insulin) and high glucose levels might explain why diabetes develops. The scientists found that a pathway independent of glucose, but sensitive to fatty acids, appears to drive insulin secretion in the early stages of diabetes. 

The research team, led by Orian Shirihai, a professor of endocrinology and pharmacology at the David Geffen School of Medicine at UCLA and senior author of the study, used pre-diabetic mice to study the mechanisms by which insulin may be secreted in the absence of glucose. 

The team found that in beta cells from obese, pre-diabetic animals, a protein known as Cyclophilin D, or CypD, induced a phenomenon known as “proton leak,” and that this leak promoted insulin secretion in the absence of elevated glucose. The mechanism was dependent on fatty acids, which are normally incapable of stimulating insulin secretion in healthy animals.

Further, obese mice who lacked the gene for CypD did not secrete excess insulin. The team confirmed the same process was taking place in isolated human pancreas cells: In the presence of fatty acids at levels that would be typical in obese humans, the cells secreted insulin in the absence of elevated glucose.

The study was published in the American Diabetes Association’s journal Diabetes.

The results suggest new ways to prevent the development of insulin resistance and to treat diabetes, including halting its progression by blocking the proton leak in the beta cell.

The study’s first author is Evan Taddeo of the department of medicine, division of endocrinology, diabetes and hypertension, at the Geffen School. Marc Liesa, of UCLA, is a corresponding author. Other UCLA-affiliated authors are Nour Alsabeeh, Siyouneh Baghdasarian, Eleni Ritou, Karel Erion, Jin Li, Linsey Stiles and Marc Liesa. A full list of authors may be found in the journal article.

The work was funded by the National Institutes of Health; the UCLA Department of Medicine Chair; the UC San Diego/UCLA Diabetes Research Center; the Kuwait Foundation for the Advancement of Sciences, a fellowship from Kuwait University; and Janssen Research & Development.

Honored Contributor
Posts: 17,739
Registered: ‎03-09-2010

Re: Diabetes News 2020 winter

Medical
New research uncovers potential trigger for Type 2 diabetes

By Michael Irving
December 22, 2019

• Facebook
• Twitter
• Flipboard
• LinkedIn

 
New research may explain how Type 2 diabetes first begins
AndreyPopov/Depositphotos
View 1 Images
Research led by the University of California, Los Angeles (UCLA) has uncovered a new process that may help explain how Type 2 diabetes develops. In tests on live mice and human cells in the lab, the team found a new mechanism besides insulin resistance and high glucose levels that triggers pancreatic cells to begin overproducing insulin.


Type 2 diabetes is the form of the disease that’s usually a result of lifestyle choices, such as poor diet and not enough exercise. It involves a kind of vicious cycle of insulin – beta cells in the pancreas produce too much insulin, which causes the body to become resistant to it. That in turn means the beta cells could produce even more to compensate.

XYREM® (sodium oxybate) - See Full Prescribing Info
Prescription treatment website
Including Boxed Warning. Prescribers: find XYREM information and support here.
It was long thought that high glucose levels – most commonly caused by eating too much sugary and fatty foods – was the trigger for the beta cells to begin overproducing insulin. But it’s also been shown in the past that even beta cells isolated in a lab dish can over-secrete insulin, without glucose playing a part.

So the team on the new study investigated what else could be causing beta cells to overproduce insulin. In tests on obese, pre-diabetic mice, the researchers discovered a new, separate molecular pathway that can induce insulin secretion without glucose. Instead, the trigger appears to be fatty acids.


When levels of these fatty acids rose too high in the mice, a protein called Cyclophilin D (CypD) caused protons to “leak” into the mitochondria of the beta cells. This triggers them to boost production of insulin.

To check the mechanism, the team then engineered mice without the gene that codes for CypD, and found that their insulin stayed at regular levels.

The researchers also investigated whether the same mechanism could be occurring in humans, by testing human pancreas cells isolated in the lab. When exposed to high levels of fatty acids – levels found in obese humans – the cells began to produce more insulin. Again, there was no glucose present.


While it’s still early days for the research, the discovery could eventually lead to new types of diabetes treatment, such as preventing insulin resistance in pre-diabetic people.

The study was published in the journal Diabetes.

Source: UCLA

Honored Contributor
Posts: 17,739
Registered: ‎03-09-2010

Re: Diabetes News 2020 winter

Monday , January 13 2020

 

Issues to be aware of with diabetes and tattoos

A 29-year-old woman with insulin-dependent diabetes noted a painful erosion at the site of the tattoo which she had gotten 7 days before. A culture isolated staphylococcus aureus confirming the clinical impression of staph. This diagnosis was not entirely unexpected, since patients with diabetes mellitus are predisposed to staphylococcal infection. An oral cephalosporin cleared the cellulitis, leaving the tattoo a little distorted. The tattoo artist blamed the cellulitis on the patient’s failure to take proper care of the wound site. However, the lack of recurrent infections in the patient’s history indicates that she probably was not a carrier, and the infection grew from a new source.

Tattoos are very popular, especially with teens. But the tattoo application process and aftercare, which can be long, painful and stressful, can create some problems for our diabetes patients. Blood pressure and blood sugar levels can both rise while a tattoo is being applied, and high blood sugar levels can also complicate the healing process, increasing the risk of infection.

Other things to consider before getting a tattoo include:

Tattooist quality
The tattoo studio should be licensed and/or accredited. The patients can also research the company’s reputation, and hygiene and safety practices.

Safety and awareness
The tattooist should be informed of the patient’s diabetes so they can tailor both the procedure and aftercare information.

Placement
Certain areas should be avoided including those with poor circulation, such as:

• Buttocks
• Shins
• Ankles
• Feet
• Common insulin injection sites such as arms, abdomen and thighs.

Tattoos in these places usually take longer to heal, which can lead to complications (e.g. infection).

Other Risks

• Allergic reactions – reaction to the substances used in the inks and equipment.
• Skin infection – the tattooed area of skin may become infected if the studio and/or tattoo equipment is not clean or proper aftercare is not applied.
• Scarring – tattoo application can cause the formation of an oversized scar known as a keloid, which can be irritable and slightly painful.
• Blood-borne diseases – if the tattoo needle or ink has not been sterilized, there is a risk of blood-borne illnesses such as HIV and Hepatitis B or C.
• Wound healing – abnormally high levels of blood glucose could delay healing of the tattooed skin and increase the risk of infection.

If the patient feels unwell or sees any sign of infection after the tattoo has been completed, they should seek immediate help from their doctor or diabetes healthcare team. 
 
This guidance adapted from information found on the Diabetes UK website at http://www.diabetes.co.uk/tattoos-and-diabetes.html.
 
 



 

 

Honored Contributor
Posts: 17,739
Registered: ‎03-09-2010

Re: Diabetes News 2020 winter

Obesity, heart disease, and diabetes may be communicable

 
Credit: CC0 Public Domain

Non-communicable diseases including heart disease, cancer and lung disease are now the most common causes of death, accounting for 70 percent of deaths worldwide. These diseases are considered "non-communicable" because they are thought to be caused by a combination of genetic, lifestyle and environmental factors and can't be transmitted between people.

 

A new research paper in Science by a team of fellows in CIFAR's Humans and the Microbiome program throws this long-held belief into question by providing evidence that many diseases may be transmissible between people through microbes (including bacteria, fungi, and viruses) that live in and on our bodies.

"If our hypothesis is proven correct, it will rewrite the entire book on public health" says B. Brett Finlay, CIFAR Fellow and professor of microbiology at the University of British Columbia, who is lead author on the paper.

Connecting the dots

The authors base their hypothesis on connections between three distinct lines of evidence. First, they demonstrate that people with a wide range of conditions, from obesity and inflammatory bowel disease to type 2 diabetes and cardiovascular disease, have altered microbiomes. Next, they show that altered microbiomes, when taken from diseased people and put into animal models, cause disease. Finally, they provide evidence that the microbiome is naturally transmissible, for example: Spouses who share a house have more similar microbiomes than twins who live separately.

"When you put those facts together, it points to the idea that many traditionally non-communicable diseases may be communicable after all," says Finlay.

Eran Elinav, an author on the paper, CIFAR fellow, and professor at the Weizmann Institute of Science, sees the proposed connection between these points of evidence as an argument for thinking about disease more broadly. "This may represent new opportunities for interventions in some of the world's most common and bothersome diseases," he says. "We can now think about modulating environmental factors and the microbiome, not just about targeting the human host."

Interdisciplinary collaboration

CIFAR's Humans & the Microbiome program benefits from its international, interdisciplinary network of fellows, advisors and CIFAR Azrieli Global Scholars that includes microbiologists, anthropologists, immunologists, and geneticists, among others. Together they are discovering how microbes that live in and on us affect our health, development and even behavior.

"This paper provides a provocative new way to think about non-communicable diseases, with important implications for public health," says Alan Bernstein, President and CEO of CIFAR. "Ideas like this are a great example of what happens when top researchers from around the world work together in an environment of trust, transparency, and knowledge sharing."

The authors say the paper was a direct result of open and exploratory discussions at a CIFAR program meeting in March 2019.

"The idea developed from the integration of emerging biological data from animal models and from humans, coupled with critical insights with partners dealing with the same concepts, in other contexts, in anthropology and social sciences," says Elinav.

"It started as a thought experiment," says Finlay, "but then there was huge excitement when we started thinking about what there was evidence for. As the paper started coming together and new pieces of evidence from different specialties came in, discussions were flying around the table."

Next steps

While there is a lot of excitement about this hypothesis, the researchers are clear that much remains unknown about the mechanisms involved. "We still don't know in what cases transmission increases, or whether healthy outcomes can also be transmitted," says Maria Gloria Dominguez-Bello, an author on the paper, CIFAR fellow, and professor at Rutgers University. "We need more research to understand microbial transmission and its effects."

"We hope the paper will inspire further research into the mechanisms and extent of communicability." says Finlay. "We encourage researchers studying any disease to think about what effect microbes may be having."