Holidays are meaningful, fun, and enjoyable for many people. Yet, it’s easy to make a big production out of them when we try and accomplish too many holiday “to-dos.” Cue the cooking marathon, never-ending errands, perfectly orchestrated family pictures, Instagram-worthy homemade meals, … should I say more? Planning out the “perfect” holiday season while navigating chronic illness can become overwhelming. In fact, chronic illness is emotionally and physically taxing any day of the year, so adding to it the pressure of checking off every holiday “must-do” can lead to undue pain, fatigue, and symptoms flare. Below are 7 ideas and tips to reclaim the fun of this holiday season and alleviate some of the stress.

1. Set boundaries

Setting boundaries can be as easy as saying NO! “I appreciate the invitation but I won’t be able to attend”, “I love that you’re hosting this event, I’ll pass this year. Hope you have a fun time!” And give yourself permission to turn down invitations without justifying yourself if you don’t want to. Limit the number of events that you will attend. Identify the ones you really want to be part of, whether you’re hosting or attending, and RSVP no to the other ones. And before attending a party, it can be helpful to have an idea of how much time you plan on spending there. Know your limits! If you know from experience that you become fatigued and your pain increases significantly after one hour of mingling, standing, or being in a loud environment, give yourself permission to leave at the 55-minute mark. It can also help to share a “code word” with your partner or a friend giving you a ride. This way, they know that when you say “blue cheese” it’s time to leave!

2. Prioritize the things that bring you most joy and meaning

Be wise about how you spend your time, energy (and even money)! Prioritize activities, events, experiences that bring you joy or meaning. Ditch those that you don’t particularly care about. It’s okay if your list of “must-do holiday things” looks different from that of your next-door neighbor or even from your list from the previous year.

3. Simplify your life as much as possible

Some holiday experiences or items may be important to you, yet you’d rather not be in charge of planning or executing them. For instance, you may enjoy nicely wrapped gifts but wrapping gifts for hours increases your pain. You enjoy eating a traditional thanksgiving meal but can’t stand for hours cooking in the kitchen. Delegate! Find support to make the holiday season meaningful without having to be the one in charge of all the logistics. And allow yourself to take off your list all the activities and items that you’ve been doing but that don’t really bring you or your family much joy or meaning. It’s not rare that we find ourselves doing things out of habit only to realize that it’s not something that speaks to our values.

4. Self-care

Now is the time to double-up on self-care! The holiday season is without an ounce of a doubt one of the most stressful and busy time of year. Holidays are physically, emotionally, financially taxing. It’s important to be even more intentional about making time for your needs and prioritize your body and mind. And if you don’t enjoy the holidays, it can also be difficult to go through this season. So taking care of yourself and reaching out for support might be much needed.

5. Pace yourself

Pacing is an important aspect of living with chronic illness. The holidays should be no exception. While your schedule might be more packed than usual and your to-do list might run longer, try as much as possible to plan errands and events in a way that allows for resting and recovery. The key word here is to plan!

6. Keep up with your routine

Make a list of your non-negotiable health routines and plug them into your schedule before planning anything else. Then, you can schedule other events and errands around your routines, as much as possible.

7. Create traditions that are meaningful to you and your family

Creating fun traditions that are meaningful for you and your family AND respect your health needs is especially important. One family for instance started a new tradition for Thanksgiving, when each family member would order in their favorite food, and they would then share a meal in bed, picnic style, and it made for great memories! You can also plan on having a virtual Friendsgiving, which allows you to rest as needed and turn down the volume when you need to take a break. As we enter this holiday season, take some time to reflect on what you want this season to look like and how you can focus on the most meaningful experiences without adding too much physical and emotional stress

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Eliminating old, dysfunctional cells in human fat also alleviates signs of diabetes, researchers from UConn Health report. The discovery could lead to new treatments for Type 2 diabetes and other metabolic diseases.

The cells in your body are constantly renewing themselves, with older cells aging and dying as new ones are being born. But sometimes that process goes awry. Occasionally damaged cells linger. Called senescent cells, they hang around, acting as a bad influence on other cells nearby. Their bad influence changes how the neighboring cells handle sugars or proteins and so causes metabolic problems.

Type 2 diabetes is the most common metabolic disease in the US. About 34 million people, or one out of every 10 inhabitants of the US, suffers from it, according to the Centers for Disease Control and Prevention (CDC). Most people with diabetes have insulin resistance, which is associated with obesity, lack of exercise and poor diet. But it also has a lot to do with senescent cells in people’s body fat, according to new findings by UConn Health School of Medicine’s Ming Xu and colleagues. And clearing away those senescent cells seems to stop diabetic behavior in obese mice, they report in the 22 November issue of Cell Metabolism. Ming Xu, assistant professor in the UConn Center on Aging and the department of Genetics and Genome Sciences at UConn Health, led the research, along with UConn Health researchers Lichao Wang and Binsheng Wang as major contributors.

Alleviating the negative effects of fat on metabolism was a dramatic result, the researchers said. If a therapy worked that well in humans, it would be a game-changing treatment for diabetes.

Xu and his colleagues tested the efficacy of a combination of experimental drugs, dasatinib and quercetin. Dasatinib and quercetin had already been shown to extend lifespan and good health in aged mice. In this study, they found these drugs can kill senescent cells from cultures of human fat tissue. The tissue was donated by individuals with obesity who were known to have metabolic troubles. Without treatment, the human fat tissues induced metabolic problems in immune-deficient mice. After treatment with dasatinib and quercetin, the harmful effects of the fat tissue were almost eliminated.

“These drugs can make human fat healthy, and that could be great,” says Xu. “The results were very impressive and cleared the route for potential clinical trials.”

Xu and his colleagues at UConn Health and the Mayo Clinic are now pursuing using the dasatinib and quercetin combination in clinical trials to see if the drugs can improve Type 2 diabetes in human patients. “Although these preclinical results were very promising, large scale clinical trials are absolutely critical to examine the efficacy and safety of these drugs in humans before clinical use”, emphasized Xu.

The research team is also focusing on a previously unexplored senescent cell population. These senescent cells express high levels of p21, a cyclin-dependent kinase inhibitor, and one of the key markers for cellular senescence. By using a newly developed mouse model, Xu’s team demonstrated that clearance of these senescent cells once every month is effective for both slowing down the development of diabetes and alleviating developed diabetic symptoms in obese mice. Xu says previous research has focused on different cell markers, but that the effects of clearing away cells highly expressing p21 was so marked on alleviating diabetes that this marker should get more attention.   

Just about everyone knows that exercise is good for you. Some people can even rattle off reasons it keeps your muscles and joints strong, and how it fights off certain diseases. But how many people can tell you the story of why and how physical activity was built into human biology? 

A team of evolutionary biologists and biomedical researchers from Harvard are taking a run at it (sometimes literally) in a new study published in PNAS. The work lays out evolutionary and biomedical evidence showing that humans, who evolved to live many decades after they stopped reproducing, also evolved to be relatively active in their later years.  

The researchers say that physical activity later in life shifts energy away from processes that can compromise health and toward mechanisms in the body that extend it. They hypothesize that humans evolved to remain physically active as they age—and in doing so to allocate energy to physiological processes that slow the body’s gradual deterioration over the years. This guards against chronic illnesses such as cardiovascular disease, type 2 diabetes, and even some cancers. 

“It’s a widespread idea in Western societies that as we get older, it’s normal to slow down, do less, and retire,” said Harvard evolutionary biologist Daniel E. Lieberman, the paper’s lead author. “Our message is the reverse: As we get older, it becomes even more important to stay physically active.” 

The research team, which includes Aaron Baggish and I-Min Lee from Harvard Medical School, believes the paper is the first detailed evolutionary explanation for why lack of physical activity as humans age increases disease risk and reduces longevity. 

Baggish, 47, who also serves as team cardiologist for the New England Patriots and U.S. Soccer, and Lieberman, 57, are longtime running buddies and often discussed the ideas that went into the paper during 5-to-10-mile morning runs. 

The study uses humans’ ape cousins as a jumping off point. The researchers point out that apes, which usually live only about 35 to 40 years in the wild and rarely survive past menopause, are considerably less active than most humans, suggesting that there was selection in human evolution not just to live longer but also to be more physically active. 

“We evolved basically from couch potatoes,” said Lieberman, who has twice observed wild chimpanzees in Tanzania and been surprised by how much of their day is spent “sitting on their butts, digesting.” 

This is especially jarring when contrasted against contemporary hunter-gatherers, who average about 135 minutes of moderate to vigorous physical activity a day. That level of movement—about six to ten times more than average Americans—may be one of the keys to why hunter-gatherers who survive childhood tend to live about seven decades, approximately 20 years past the age at which humans generally stop having children. Fossil evidence indicates that these extended lifespans were common by 40,000 years ago, contrary to the belief that human lifespans until recently were short. 

The team emphasized that the key health benefit of physical activity is to extend the human healthspan, which is defined as the years of life spent in good health. 

Researchers examined two pathways by which lifelong physical activity reallocates energy to improve health. The first involves dealing excess energy away from potentially harmful mechanisms, like excess fat storage. The team also identified how physical activity allocates energy to repair and maintenance processes. The paper shows that besides burning calories, physical activity is physiologically stressful, causing damage to the body at the molecular, cellular, and tissue levels. The body’s response to this damage, however, is essentially to build back stronger.  

This includes repairing tears in muscle fibers, repairing cartilage damage, and healing microfractures. The response also causes the release of exercise-related antioxidants and anti-inflammatories, and enhances blood flow. In the absence of physical activity, these responses are activated less. The cellular and DNA repair processes have been shown to lower the risk of diabetes, obesity, cancer, osteoporosis, Alzheimer’s, and depression. 

“The key take-home point is that because we evolved to be active throughout our lives, our bodies need physical activity to age well. In the past, daily physical activity was necessary in order to survive, but today we have to choose to exercise, that is do voluntary physical activity for the sake of health and fitness,” Lieberman said.  

The research team, which includes the graduate students Timothy Kistner and Daniel Richard, hope the study makes that message harder to ignore.  

Physical activity levels have been decreasing worldwide as machines and technology replace human labor. A recent study from Lieberman’s lab showed that Americans are engaging in less physical activity than they did 200 years ago.  

The researchers’ advice? Get out of your chair and get in some exercise.  

“The key is to do something, and to try to make it enjoyable so you’ll keep doing it,” Lieberman said. “The good news is that you don’t need to be as active as a hunter-gatherer. Even small amounts of physical activity — just 10 or 20 minutes a day —substantially lower your risk of mortality.” 

Intestinal stem cells in green, cell division in red. CREDIT Helmholtz Munich / Anika Böttcher

The intestine is essential for maintaining our energy balance and is a master at reacting quickly to changes in nutrition and nutrient balance. It manages to do this with the help of intestinal cells that among other things are specialized in the absorption of food components or the secretion of hormones. In adult humans, the intestinal cells regenerate every five to seven days. The ability to constantly renew and develop all types of intestinal cells from intestinal stem cells is crucial for the natural adaptability of the digestive system. However, a long-term diet high in sugar and fat disrupts this adaptation and can contribute to the development of obesity, type 2 diabetes, and gastrointestinal cancer.

The molecular mechanisms behind this maladaptation are part of the research field of Heiko Lickert and his group at Helmholtz Munich and the Technical University of Munich. The scientists assume that intestinal stem cells play a special role in maladaptation. Using a mouse model, the researchers investigated the effects of a high-sugar and high-fat diet and compared it with a control group.

From high-calorie diet to increased risk of gastrointestinal cancer
“The first thing we noticed was that the small intestine increases greatly in size on the high-calorie diet,” says study leader Anika Böttcher. “Together with Fabian Theis’ team of computational biologists at Helmholtz Munich, we then profiled 27,000 intestinal cells from control diet and high fat/high sugar diet-fed mice. Using new machine learning techniques, we thus found that intestinal stem cells divide and differentiate significantly faster in the mice on an unhealthy diet.” The researchers hypothesize that this is due to an upregulation of the relevant signaling pathways, which is associated with an acceleration of tumor growth in many cancers. “This could be an important link: Diet influences metabolic signaling, which leads to excessive growth of intestinal stem cells and ultimately to an increased risk of gastrointestinal cancer,” says Böttcher.

With the help of this high-resolution technique, the researchers have also been able to study rare cell types in the intestine, for example, hormone-secreting cells. Among their findings, they were able to show that an unhealthy diet leads to a reduction in serotonin-producing cells in the intestine. This can result in intestinal inertia (typical of diabetes mellitus) or increased appetite. Furthermore, the study showed that the absorbing cells adapt to the high-fat diet, and their functionality increases, thus directly promoting weight gain.

Important basic research for non-invasive therapies
These and other findings from the study lead to a new understanding of disease mechanisms associated with a high-calorie diet. “What we have found out is of crucial importance for developing alternative non-invasive therapies,” says study leader Heiko Lickert, in summarizing the results. To date, there is no pharmacological approach to prevent, stop or reverse obesity and diabetes. Only bariatric surgery causes permanent weight loss and can even lead to remission of diabetes. However, these surgeries are invasive, non-reversible and costly to the healthcare system. Novel non-invasive therapies could happen, for example, at the hormonal level through targeted regulation of serotonin levels. The research group will examine this and other approaches in subsequent studies.