Study: Effects of Type I Diabetes on a Young Child's Brain
I'm posting chunks from a recent study that can be found on Diabetes Care (American Diabetes Association) and blurbs from a corresponding article about the study, from Reuters Health. Study text is in the left column, Reuters on the right.
I don't believe that this information should lead you to more worry (Though it likely will) but I do believe that the parents of young children, who live with type I diabetes, should be aware of the study findings. These articles are not fun to read for many reasons, but I found them to be full of the kind of information that helps me to (hopefully) avoid long-term complications for Arden.
If you are currently struggling with BGs or generally feeling down about type I - seriously - bookmark this and save it for a better day - even though you'll likely not find much of the information surprising, it is a somber reminder. My thoughts, are as always, with you and your families. - Scott
Links to the complete articles are included below, at the end of each column.
“While many children may not show overt complications from these differences in neural structure, some do have difficulties with processing speed, memory, learning, and complex cognitive functions”
Alterations in White Matter Structure in Young Children With Type 1 Diabetes
Study Objective: To investigate whether type 1 diabetes affects white matter (WM) structure in a large sample of young children.
Results: Between-group analysis showed that children with type 1 diabetes had significantly reduced axial diffusivity (AD) in widespread brain regions compared with control subjects. Within the type 1 diabetes group, earlier onset of diabetes was associated with increased radial diffusivity (RD) and longer duration was associated with reduced AD, reduced RD, and increased fractional anisotropy (FA). In addition, HbA1c values were significantly negatively associated with FA values and were positively associated with RD values in widespread brain regions. Significant associations of AD, RD, and FA were found for CGM measures of hyperglycemia and glucose variability but not for hypoglycemia. Finally, we observed a significant association between WM structure and cognitive ability in children with type 1 diabetes but not in control subjects.
Conclusions: These results suggest vulnerability of the developing brain in young children to effects of type 1 diabetes associated with chronic hyperglycemia and glucose variability.
The entire study can be found here, it includes a significant introduction, an outline of research design and methods, as well as a description of the participants, CGM use in the study, data analysis and much more.
Chronic hyperglycemia, glucose variability may affect children's brains
By Lorraine L. Janeczko
NEW YORK (Reuters Health)
"Chronic hyperglycemia and glucose variability could impact the brains of young children with type 1 diabetes, new research suggests."
"In what the authors call the largest study to date investigating white matter structure in young children with type 1 diabetes, diabetic children had widespread and significant differences in their white matter microstructure compared with nondiabetic controls."
"Compared to controls, children with type 1 diabetes had significantly reduced axial diffusivity (AD) in their frontal, temporal, parietal, and occipital lobes. Earlier diabetes onset was associated with increased radial diffusivity (RD), and longer duration was associated with reduced AD, reduced RD, and increased fractional anisotropy (FA) (all P<0.05)."
"While many children may not show overt complications from these differences in neural structure, some do have difficulties with processing speed, memory, learning, and complex cognitive functions which can be associated with poor neuronal function," she said.
"I believe that these effects could be improved with good glycemic control, although an empirical investigation would help to answer this question. It seems that in the quest to prevent hypoglycemia in children with diabetes, there has been an increase in hyperglycemia in many children. It may be the case that a balance needs to be struck between the two extremes, perhaps with better methods of glucose monitoring."
Link between Type I Diabetes and Coxsackie B Virus
I found this article particularly interesting because Arden was diagnosed with the Coxsackie virus prior to her diagnosis with type I diabetes. I was wondering how many of you also saw Coxsackie before type I?
The following is from The Scotsman.
A SPECIFIC virus family has been implicated in the development of Type 1 diabetes, raising the prospect of vaccinations against the disease. -
- by JOHN VON RADOWITZ
Scientists are encouraged by data from two studies that show a clear link between the condition and group B coxsackieviruses, which are known to damage insulin-producing cells in the pancreas.
The potential breakthrough relates to type 1 diabetes which affects around 400,000 people in the UK, 29,000 of whom are children.
Researchers believe that, in time, it may be that with screening and a vaccine, they could prevent a proportion of diabetes.
Type 1 diabetes is an autoimmune disease caused by the body’s defences destroying insulin-producing beta cells. But what triggers the extreme immune reaction in the first place has been an unanswered question.
Suspicion has fallen on enteroviruses, one of the most common infective agents in humans. They include the virus responsible for the common cold, as well as those responsible for polio and viral meningitis.
The new study narrowed the diabetes culprit down to one particular enterovirus population known as group B coxsackieviruses.
The remainder of this article a valuable read and can be found here.
Why does basketball make Arden's BG rise?
Arden brings the ball down the court, passes and looks for a rebound. (video)
Last week during Arden's quarterly Endo appointment I brought up an issue that I had identified but couldn't figure out. I explained to our nurse practitioner that when Arden exercises her BG falls. Riding a bike, running around, recess at school, really all of the her physical activities decrease her BG... except sports.
I, of course, am aware that activity can cause a decline in BG but our issue didn't seem to be following that "rule". It took me a while to be able to see past the expectation that physical exertion would decrease Arden's blood glucose level. Inexplicably, I was having trouble with her BGs actually going up during basketball games and practices this winter. When I finally thought back, I realized that I saw similar BG trends last summer during softball.
Our NP asked about Arden's level of competitiveness, as she spoke I began to understand what she was getting at...
Arden is a very competitive little girl, when it counts. That is to say that if she goes out back with her brother to shoot baskets her BG falls from the activity as you may expect but when she is in a game, when there is a score being kept and winners and losers are recorded - Arden's BGs go up.
I explained to our NP that Arden entered her last basketball game with a BG of 125 and that by the end of the game, just one hour later with no food or carbs in her system, her BG was 220 and climbing. I was bolusing during the game, which was nerve wracking when you consider that the expectation is that there will be a fall from the activity.
The NP described to me that this is a phenomenon that they generally see with boys, then she turned to Arden and said, "so, you like to win huh?". Apparently it's common for very competitive people to access their flight or flight response (also known as 'the stress response') during a sporting competition. Their desire to win is so strong that they feel the game on a different level. Adrenaline is released and their body prepare to battle as if they are fighting for their lives.
Next week when we arrived at the gym. I am going bolus as if Arden was about to consume a 15 carb juice box (the ones we use for low BGs). I'm confident that the insulin begins to act it will find a rising BG to tussle with, if I'm wrong... we'll just drink the juice. I'll report back and let you know what happens... Never a dull moment with type I diabetes.
Pathway to Stop Diabetes
Image courtesy of Pathways to Stop Diabetes
The American Diabetes Association has just announced an initiative called Pathways to Stop Diabetes. Here is a brief snippet from their website about the program's intentions.
We realize that it takes more than natural talent for young researchers to realize their full potential. It takes comprehensive support every step of the way. To make the career commitment to diabetes research attractive, fulfilling and rewarding, Pathway to Stop Diabetes will provide that support in every way.
I think that it's very exciting to see such a large organization thinking about research in a different way. It's also encouraging to see that program financially backed so significantly by pharma companies. I hope you can take a few minutes to learn more about Pathway.
If you are a brilliant young scientist, are raising one or know a young researcher that may be interested in being at the forefront of discovery. Please consider diabetes research as your field of focus. Pathway offers researchers mentoring, grants and much more. Who knows, maybe you're the next Frederick Banting, MD.
More blurbs from the Pathway to Stop Diabetes website:
"Our vision is simple yet revolutionary: find a new generation of brilliant scientists at the peak of their creativity, then provide them with the freedom, autonomy, and financial and professional resources to set them on the road to breakthrough discoveries."
"Diabetes research is critically underfunded. Twice as many Americans have diabetes as have cancer. Diabetes is over 20 times more prevalent than HIV/AIDS. Yet National Institutes of Health (NIH) funding for diabetes is 1/5 that of cancer and 1/3 that of AIDS. On a per-person-affected basis, diabetes funding is a rounding error in comparison. This difference has persisted for decades." - more
Arden's Day wishes the Pathway program a very successful (but hopefully short) life!
Be well,
Scott
Alzheimer's and insulin resistance
This is an old article from Time Health but it raises interesting points about insulin's effect on Alzheimer's and I thought it was worth sharing.
When the body refuses to make insulin, the condition is called type 1 diabetes; when the body mismanages the hormone, it's known as type 2. Now, scientists report new evidence linking insulin to a disorder of the brain: when the brain prevents the hormone from acting properly, the ensuing chemical imbalance may help trigger Alzheimer's disease. The correlation is so strong that some researchers are calling Alzheimer's disease "type 3" diabetes.
In the body, insulin helps convert food into cellular energy. But the brain has other uses for insulin, namely as a means to learn and make new memories. Here's how it works: At synapses, the spaces across which brain cells communicate and where memories are conceived, neurons reserve special parking spots just for insulin. When the hormone pulls in, a connection is made that enables new memories to form. Since new memory formation is one of the first things to go awry in people with early stages of the disease, this insulin-initiated process may hold the key to decoding the mystery of Alzheimer's.
In August, a team of scientists at Northwestern University were the first to show why the brain's "memory function" fails in the face of an insulin shortage. The group's prior research had already pinpointed the culprit: toxic proteins called amyloid beta-derived diffusible ligands (ADDLs, for short), which are known to pile up in the brains of people with Alzheimer's. Scientists also knew that Alzheimer's patients' brains have lower levels of insulin and are insulin resistant. But what the Northwestern team discovered is the molecular mechanism behind that resistance: when ADDLs bind to neurons at synapses, they obliterate the receptors that are normally reserved for insulin. Without those parking spaces on the brain cells' surface, insulin has no place to connect, and memory fails.
"We now understand that the function of insulin at those synapses is to modulate and influence the underlying cellular structure of memories," says William Klein, professor of neurobiology and physiology at Northwestern University and a co-author of the study published online by the FASEB Journal. "What we have here is a striking phenomenon that may ultimately explain why the brains of people with Alzheimer's disease are insulin resistant and how that ties into memory."
Researchers hope these findings will help shape future research in Alzheimer's therapy — perhaps in the development of drugs that can make brain cells' insulin receptors more responsive to the hormone, or in the application of type 2 diabetes drugs, which address insulin resistance, to Alzheimer's.
The notion that Alzheimer's disease might be a neuroendocrine disorder, akin to diabetes, isn't entirely new; it first showed up in the scientific literature roughly 20 years ago, but the idea petered out. In 2005, Suzanne la Monte, a neuropathologist at Brown University Medical School, revisited the idea. Based on two of her discoveries — that the brain makes its own insulin and that Alzheimer's disease depletes insulin — she coined the disease process "type 3" diabetes.
Still, referring to Alzheimer's disease as "type 3" diabetes is controversial, especially within the diabetes community. Alzheimer's disease is a complication of diabetes, not a unique form of the disease, says Dr. Sue Kirkman, vice president of clinical affairs for the American Diabetes Association. "Nevertheless," she says, "this is primarily a semantic argument."
The terminology aside, both diseases share many traits and risk factors, including high cholesterol, high blood pressure, and metabolic disorders. So, de la Monte sees the semantic "splitting of hairs" as a good thing. "People are arguing about small parts of the bigger story," she says. "At the end of the day, these conversations will help us to better understand both diabetes and Alzheimer's disease."