Toe Walking | AUTISM & SENSORY

Toe Walking | AUTISM & SENSORY
Toe Walking | AUTISM & SENSORY


What is toe walking? Tip toe walking can be confusing to some parents on what causes it and how to help it. For some, there’s an immediate concern about toe walking and autism. As always, never use my videos or ANY random internet platform to make a choice about your child. ALWAYS consult with a licensed professional.



Autism and Verbal Communication Challenges: When Speaking is Difficult

Autism and Verbal Communication Challenges
Autism and Verbal Communication Challenges


Do you remember a time when speaking became difficult for you? If speaking drains you and becomes tiring, you may be experiencing a challenge in verbal communication. It’s not only speaking that uses up energy. Even just thinking and forming the actual words in my head can already drain my energy when I’m feeling tired. For example, saying “Hello” out loud can be too difficult so I end up just “waving” instead. In this video, I share some verbal communication challenges that I have been experiencing and how I overcome them.

Insulin in the brain influences dopamins levels

Insulin-Dopamin Interaction


Intranasal insulin induces an increase in the [11C] raclopride binding potential in the striatum, which indicates a decrease in the synaptic dopamine level. © IDM

In the human brain, the hormone insulin also acts on the most important neurotransmitter for the reward system, dopamine. This was shown by researchers from the German Center for Diabetes Research (DZD) in Tübingen. Insulin lowers the dopamine level in a specific region of the brain (striatum *) that regulates reward processes and cognitive functions, among other things. This interaction can be an important driver of the brain’s regulation of glucose metabolism and eating behavior. The study has now been published in the Journal of Clinical Endocrinology & Metabolism.  

Worldwide, more and more people are developing obesity and type 2 diabetes. Studies show that the brain plays an important role in causing these diseases. Dopamine is the most important neurotransmitter for the reward system. The hormone insulin is released after eating and regulates the metabolism in the human body (homeostatic system). It is not yet known how these two systems interact. However, changes in these systems have been linked to obesity and diabetes. In the current study, researchers from the Institute of Diabetes Research and Metabolic Diseases (IDM) of Helmholtz Zentrum München at the University of Tübingen, a partner of the DZD, and Tübingen University Hospital (Innere IV, Director: Prof. Andreas Birkenfeld) examined how the two systems interact specifically in the reward center of the brain, the striatum.  

“Our eating behavior is regulated by the interaction between the reward system and homeostatic systems. Studies indicate that insulin also acts in dopamine-driven reward centers in the brain. It has also been shown that obesity leads to changes in the signaling of the brain that have a negative effect on the glucose metabolism in the whole body,” said first author Stephanie Kullmann. “We now wanted to decipher the interaction between the two systems in humans and find out how insulin regulates the dopamine system.” 

For this purpose, ten healthy, normal-weight men received insulin or a placebo via a nasal spray (randomized, placebo-controlled, blinded crossover study). When insulin is absorbed via the nose, it reaches the brain directly. To study the interaction between insulin and dopamine, the researchers used a unique measurement technique: they combined magnetic resonance imaging to assess functional brain activity and positron emission tomography to assess dopamine levels.   

Analysis of the study showed that the intranasal administration of insulin lowered dopamine levels and led to changes in the brain’s network structure. “The study provides direct evidence of how and where in the brain signals triggered after eating – such as insulin release and the reward system – interact,” said Professor Martin Heni, last author of the study, summarizing the results. “We were able to show that insulin is able to decrease dopamine levels in the striatum in normal-weight individuals. The insulin-dependent change in dopamine levels was also associated with functional connectivity changes in whoe-brain networks. Changes in this system may be an important driver of obesity and related diseases.” 

In further studies, the researchers want to investigate changes in the interaction of dopamine and insulin in obese or diabetic participants. These people often suffer from insulin resistance in the brain. The researchers therefore assume that this resistance prevents the normal insulin-induced regulation of dopamine levels in the reward center. In further steps, they want to restore the normal action of insulin in the brain by behavioral and/or pharmaceutical interventions. 

​​​​​​​UNH research finds venom of cone snail could lead to future diabetes treatments

Cone snail shell


Researchers at the University of New Hampshire have found that variants of this venom, known as cone snail insulin (Con-Ins), could offer future possibilities for developing new fast-acting drugs to help treat diabetics.

The tapered cone shell is popular among seashell collectors for its colorful patterns, but the smooth mottled shells are also home to the cone snail which is capable of spewing a potent insulin-like venom that can paralyze its prey. Researchers at the University of New Hampshire have found that variants of this venom, known as cone snail insulin (Con-Ins), could offer future possibilities for developing new fast-acting drugs to help treat diabetics.

“Diabetes is rising at an alarming rate and it’s become increasingly important to find new alternatives for developing effective and budget-friendly drugs for patients suffering with the disease,” said Harish Vashisth, associate professor of chemical engineering. “Our work found that the modeled Con-Ins variants, or analogs, bind even better to receptors in the body than the human hormone and may work faster which could make them a favorable option for stabilizing blood sugar levels and a potential for new therapeutics.”

In their study, recently published in the journal Proteins: Structure, Function, and Bioinformatics, researchers looked more closely at the cone snail venom which induces a hypoglycemic reaction that lowers blood sugar levels. Unlike insulin made in the body, the venom’s peptide sequence – which allows it to bind to human insulin receptors – is much shorter. To test whether it would still bind effectively, the researchers used sequences of the insulin-like peptides in the venom of the cone snail C. geographus as a template to model six different Con-Ins analogs. The newly created variants were made up of much shorter peptide chains than human insulin – lacking the last eight residues of the B-chain of the human insulin.

To study the stability and variability of the new Con-Ins structures, they conducted multiple independent computer simulations of each Con-Ins variant complex with human insulin receptor in a near-physiological environment (accounting for water solvent, salinity of solution, temperature and pressure). They found that each insulin complex remained stable during the simulations and the designed peptides bound strongly – even better than the naturally occurring human insulin hormone. The interactions were then compared with the human insulin receptor and it was determined that each Con-Ins variant exhibits few feasible residue substitutions in human insulin.

“While more studies are needed, our research shows that despite the shorter peptide sequences, the cone snail venom could be a viable substitute and we are hopeful it will motivate future designs for new fast-acting drug options,” said Biswajit Gorai, postdoctoral research associate and lead author.

The insulin-like venom released by certain cone snails can be highly dangerous causing a hypoglycemic shock that immobilizes fish and potential prey. C. geographus has the most toxic sting known among the species and there have been reports of human fatalities, especially to unsuspected divers who are not aware of the snail’s venom.

Long-term blood sugar history predicts risk of severe COVID-19 among diabetics

T2D and COVID-19


A long-term history of glycemic control better predicts risk of severe COVID-19 among type 2 diabetics than shorter-term measurements. CREDIT Rensselaer Polytechnic Institute

People with type 2 diabetes who contract COVID-19 are nearly 50% more likely to wind up in intensive care if they have poorly managed their blood sugar levels over the long-term than those with better long-term glycemic control, according to a study using anonymized health care data. The study, which looked at several potential impacts to COVID-19 severity among diabetics, also calculated a lower risk for patients using the common diabetes-control medication metformin, or a combination of metformin and insulin, or corticosteroids.

“We find that two- to three-year longitudinal glycemic levels better indicate the risk of COVID-19 severity than measurements which look at a shorter period of time,” said Deepak Vashishth, corresponding author, professor of biomedical engineering, and director of the Center for Biotechnology and Interdisciplinary Studies at Rensselaer Polytechnic Institute. “We hope these insights aid physicians in better treating and managing high-risk patients.”

Evaluation and management of COVID-19-related severity in people with type 2 diabetes” looked at records for more than 16,000 people with type 2 diabetes and COVID-19 between 2017 and 2020, and was published in BMJ Open Diabetes Research & Care.

Type 2 diabetes patients are unable to regulate the amount of the sugar glucose in their bloodstream without medication and managing their diet. Chronic high blood-sugar levels, typically tracked as the percentage of hemoglobin A1c (HbA1c) found in the blood, can damage a variety of functions, including the circulatory, nervous, and immune systems.

Poor glycemic control creates a reaction that causes molecules known as advanced glycation end-products (AGEs) to accumulate, deteriorating the quality of bone over time, and Vashishth, an expert in bone, researches the impact of diabetes on bone. At the time the SARS-CoV-2 pandemic began, his research team was investigating whether measurements of longitudinal glycemic control – measures of blood-sugar levels averaged over two to three years – could provide a more accurate predictor of bone fracture risk among diabetics than the current standard predictor, which relies on measurements of bone mineral density.

AGEs are known to contribute to increased oxidant stress and inflammation, which are risk factors in COVID-19 and other respiratory illnesses. The team reasoned that the same longitudinal glycemic control measurement they were testing as a predictor of bone fracture risk might be useful in predicting the severity of COVID-19, said Bowen Wang, first author and a doctoral student in Vashishth’s lab.

Wang divided the records of type 2 diabetic patients in the study into two groups, those with “adequate” longitudinal glycemic control ranging from 6 to 9%, and those with “poor” glycemic control of 9% or above over two to three years. His analysis of the two groups revealed that those with poor glycemic control were 48% more likely to require treatment in an intensive care unit. By another measure, a 1% increase in longitudinal HbA1c is directly associated with a 12% increase in the risk of landing in the ICU.

Other statistically significant findings showed that diabetics who were taking metformin when they contract COVID-19 face a 12% lower risk of visiting the ICU, those on metformin and insulin have an 18% lower risk, and those prescribed corticosteroids have a 29% lower risk.

“People knew that diabetes was a risk factor for COVID-19-related outcomes, but not all diabetic patients are the same. Some people have a longer history of diabetes, some have more severe diabetes, and that has to be accounted for,” said Wang. “What this study does is to better stratify the level of diabetes within the population, so diabetic patients aren’t treated as a single population without any differences among them.”

Vashishth and Wang were joined on the research by Benjamin S. Glicksberg and Girish N. Nadkarni at the Icahn School of Medicine at Mount Sinai. Their work was supported by a grant from the National Institutes of Health.