A long childhood feeds the hungry human brain

A five-year old’s brain is an energy monster. It uses twice as much glucose (the energy that fuels the brain) as that of a full-grown adult, a new study led by Northwestern University anthropologists has found.

The study helps to solve the long-standing mystery of why human children grow so slowly compared with our closest animal relatives.

It shows that energy funneled to the brain dominates the human body’s metabolism early in life and is likely the reason why humans grow at a pace more typical of a reptile than a mammal during childhood.

Results of the study will be published the week of Aug. 25 in the journal Proceedings of the National Academy of Sciences.

"Our findings suggest that our bodies can’t afford to grow faster during the toddler and childhood years because a huge quantity of resources is required to fuel the developing human brain," said Christopher Kuzawa, first author of the study and a professor of anthropology at Northwestern’s Weinberg College of Arts and Sciences. "As humans we have so much to learn, and that learning requires a complex and energy-hungry brain."

Kuzawa also is a faculty fellow at the Institute for Policy Research at Northwestern.

The study is the first to pool existing PET and MRI brain scan data — which measure glucose uptake and brain volume, respectively — to show that the ages when the brain gobbles the most resources are also the ages when body growth is slowest. At 4 years of age, when this “brain drain” is at its peak and body growth slows to its minimum, the brain burns through resources at a rate equivalent to 66 percent of what the entire body uses at rest.

The findings support a long-standing hypothesis in anthropology that children grow so slowly, and are dependent for so long, because the human body needs to shunt a huge fraction of its resources to the brain during childhood, leaving little to be devoted to body growth. It also helps explain some common observations that many parents may have.

"After a certain age it becomes difficult to guess a toddler or young child’s age by their size," Kuzawa said. "Instead you have to listen to their speech and watch their behavior. Our study suggests that this is no accident. Body growth grinds nearly to a halt at the ages when brain development is happening at a lightning pace, because the brain is sapping up the available resources."

It was previously believed that the brain’s resource burden on the body was largest at birth, when the size of the brain relative to the body is greatest. The researchers found instead that the brain maxes out its glucose use at age 5. At age 4 the brain consumes glucose at a rate comparable to 66 percent of the body’s resting metabolic rate (or more than 40 percent of the body’s total energy expenditure).

"The mid-childhood peak in brain costs has to do with the fact that synapses, connections in the brain, max out at this age, when we learn so many of the things we need to know to be successful humans," Kuzawa said.

"At its peak in childhood, the brain burns through two-thirds of the calories the entire body uses at rest, much more than other primate species," said William Leonard, co-author of the study. "To compensate for these heavy energy demands of our big brains, children grow more slowly and are less physically active during this age range. Our findings strongly suggest that humans evolved to grow slowly during this time in order to free up fuel for our expensive, busy childhood brains."

Google unveils ‘smart contact lens’ to measure glucose levels

Google has said it is testing a “smart contact lens” that can help measure glucose levels in tears. It uses a “tiny” wireless chip and a “miniaturised” glucose sensor embedded between two layers of lens material. The firm said it is also working on integrating tiny LED lights that could light up to indicate that glucose levels have crossed certain thresholds. But it added that “a lot more work” needed to be done to get the technology ready for everyday use. “It’s still early days for this technology, but we’ve completed multiple clinical research studies which are helping to refine our prototype,” the firm said in a blogpost. “We hope this could someday lead to a new way for people with diabetes to manage their disease.” (via BBC News - Google unveils ‘smart contact lens’ to measure glucose levels)

15 Things to Remember When Living With a Diabetic

Diabetes does not only affect the patient, but it has a profound impact on the nearest and dearest around them. My partner, Ms YoYo, has been living with type 1 diabetes for the last 15 years. During our time together, I have learnt some key points about living with a diabetic person, which I have collated below. Hopefully, my experience can also help the others, who are affected by diabetes.

  1. Learn how to use the Glucagon kit. Hopefully you’ll never have to use it, but just in case, it’s worth knowing how it works and what you should do if she is unconscious.
  2. Remind her to check the sugar levels regularly.
  3. Learn to count the carbs; it should not be just down to her to do this.
  4. When she is injecting insulin in a public place and other people are staring at her when she’s doing this, stare back at them disapprovingly.
  5. If she is acting in a strange way or saying weird things to you, never take it personally. Most often it’s the ’sugar levels talking’.
  6. 9 out of 10 times it is indeed the sugar levels talking. Learn to recognise this, so that when she is actually telling you off about something, you know she’s serious and you should take notice and act accordingly.
  7. Check her feet regularly for any cuts or bleeding wounds.
  8. Learn to recognise a hypo so that you can provide food and support to treat it.
  9. Never ask her if she should eat whatever she wants to eat, be it an ice cream, a cake or some sweets. Managing diabetes is a full time job and she deserves a treat occasionally. You’ll deal with the high sugar levels later.
  10. Never tell her that you know exactly how she feels, because you don’t. Only another type 1 diabetic can know how she feels.
  11. Put her needs ahead of your own. No matter how much you want to go out, to the cinema, or for a walk, if her sugar levels disagree, it will not happen.
  12. Remember to have fun. Living with diabetes is tough and at times depressing, but little things in life can cheer you up such as cinema, a concert, art show, or simply a day out.
  13. Learn how to use the glucose meter. Pricking your finger occasionally will help you remind of what diabetics go through on a daily basis (and you can also check that you are not a diabetic).
  14. Don’t panic. We have all been stuck in a traffic jam with nothing to eat in the car when a hypo strikes, counting down the miles to the nearest service station. Stay calm and keep a cool head.
  15. Love your diabetic unconditionally.

I hope you have found these tips useful, and if you have something to add to the list, please let me know. You can also follow our journey on Twitter.


Mr YoYo


Nucleic acids and proteins are the most important macromolecules for our purposes, so this discussion of carbohydrates will be relatively short. There are just a few key things you need to know.

Carbohydrates are the most abundant macromolecules on Earth, and are composed of monosaccharides (simple sugars). Two monosaccharides (monomers) make up a disaccharide (polymer), joined by a glycosidic link—a covalent bond that forms (you guessed it) through a dehydration reaction. An example of a disaccharide is sucrose—ordinary sugar. Many monosaccharides make up a more complex polysaccharide, whose structure and function is determined by the sequence of monomers and the positions of the bonds between them. It’s important to note that in carbohydrates, polymers don’t have to be linear—they can branch out.

There are many different classes of carbohydrates that serve many functions—they can protect proteins, provide cell recognition, store energy…and in particular, they’re the main fuel for cellular work, and they can create strong, flexible structures like cell walls and cartilage.

The most common monosaccharide—and the most important for this series—is glucose, a six-carbon sugar that is of central importance to life. We’ll talk about how it’s synthesised later on (hint: it involves plants!).

Glucose ‘control switch’ in the brain key to both types of diabetes

Researchers at Yale School of Medicine have pinpointed a mechanism in part of the brain that is key to sensing glucose levels in the blood, linking it to both type 1 and type 2 diabetes. The findings are published in the July 28 issue of Proceedings of the National Academies of Sciences.

“We’ve discovered that the prolyl endopeptidase enzyme — located in a part of the hypothalamus known as the ventromedial nucleus — sets a series of steps in motion that control glucose levels in the blood,” said lead author Sabrina Diano, professor in the Departments of Obstetrics, Gynecology & Reproductive Sciences, Comparative Medicine, and Neurobiology at Yale School of Medicine. “Our findings could eventually lead to new treatments for diabetes.”

The ventromedial nucleus contains cells that are glucose sensors. To understand the role of prolyl endopeptidase in this part of the brain, the team used mice that were genetically engineered with low levels of this enzyme. They found that in absence of this enzyme, mice had high levels of glucose in the blood and became diabetic.

Diano and her team discovered that this enzyme is important because it makes the neurons in this part of the brain sensitive to glucose. The neurons sense the increase in glucose levels and then tell the pancreas to release insulin, which is the hormone that maintains a steady level of glucose in the blood, preventing diabetes.

“Because of the low levels of endopeptidase, the neurons were no longer sensitive to increased glucose levels and could not control the release of insulin from the pancreas, and the mice developed diabetes.” said Diano, who is also a member of the Yale Program in Integrative Cell Signaling and Neurobiology of Metabolism.

Diano said the next step in this research is to identify the targets of this enzyme by understanding how the enzyme makes the neurons sense changes in glucose levels. “If we succeed in doing this, we could be able to regulate the secretion of insulin, and be able to prevent and treat type 2 diabetes,” she said.

Targeting cancer’s sweet tooth

Ludwig researchers have elucidated a key mechanism by which cancer cells change how they metabolize glucose to generate the energy and raw materials required to sustain runaway growth.

Published online in Cell Metabolism, the Ludwig Cancer Research study also reveals how the aggressive brain cancer glioblastoma harnesses the mechanism to resist targeted therapies that should disrupt this capability—known as the Warburg effect—and suggests how such resistance might be overcome. In detailing the molecular circuitry of the phenomenon, the researchers uncover several possible targets for new drugs that might disrupt cancer cell metabolism to destroy tumors.

"Cancer and other fast-growing cells extract energy from glucose using a process that ordinarily kicks in only when oxygen is in short supply," explains Ludwig scientist Paul Mischel, MD, who is based at the University of California, San Diego School of Medicine. "This allows them to thread the needle: they get the energy they need from glucose but also retain the carbon-based building blocks for molecules like lipids, proteins and DNA, which dividing cells need in large quantities."

More at EurekAlert

FIGURE 1 | Glucose metabolism in mammalian cells. From the following article: Why do cancers have high aerobic glycolysis? Robert A. Gatenby & Robert J. Gillies. Nature Reviews Cancer 4, 891-899 (November 2004)  doi:10.1038/nrc1478

Watch on taryngilliganhealth.tumblr.com

13:45-14:30- explains it all!

This is for followers who heckle Becca for her gummy worms after her work outs! 

Freaking workout noobs… It’s science guys…

The role of lactate in boosting memory

Everyone knows that neurons are the key to how the brain operates. But it turns out they aren’t the only stars in the show; neighboring cells called astrocytes are quickly gaining increasing respect for the critical role they play in memory and learning. EPFL scientists have recently outlined the molecular mechanics of this process in an article published in Proceedings of the National Academy of Sciences (PNAS). Lactate produced by the star-shaped astrocytes accelerates the memorization process. This result, surprising until very recently, opens up new possibilities for treating cognitive and memory disorders, as well as psychiatric conditions such as depression.

Our brains are greedy, gobbling up as much as 25% of our daily energy consumption. Neurons and astrocytes thrive on glucose. Neurons use it to protect themselves from the buildup of toxic products resulting from their activity. Astrocytes, which are glial cells (as opposed to neurons), manufacture lactate; this was long thought to be a byproduct of glucose metabolism, and then as a simple energy source for neurons.

In 2011, research published in the journal Cell by EPFL’s Laboratory of Neuroenergetics and Cellular Dynamics in collaboration with a U.S. team unveiled the critical role of lactate. “In vivo, when the transfer of lactate from astrocytes to neurons is blocked, we found that the memorization process was also blocked,” explains EPFL professor Pierre Magistretti, head of the lab. “We thus knew that it was an essential fuel for that process.”

Focusing their attention on the molecular mechanism, the scientists discovered that lactate provides more than just energy. It acts as a moderator of one type of glutamate receptor (NMDA receptors), the nervous system’s primary neurotransmitter. This glutamate receptor is involved in the memorization process, and the research demonstrates that lactate gives them what amounts to a turbo-boost. “Glutamate lets you drive in first gear; with lactate, you can shift into fourth and travel at 100 km/h,” says Magistretti.

Palliating cognitive deficits
The scientists did their initial research in vitro. They exposed mice neurons to various substances and measured their effect on the expression of genes involved in memory. Glucose and pyruvate (another glucose derivative) didn’t have any effect. A lactate supplement, on the other hand, triggered the expression of four genes involved in cerebral plasticity that are essential to memorization.

They followed this work with in vivo studies, which confirmed their results. They administered lactate into the brains of living mice, and then extracted the tissues and measured gene expression. Once again, the expression of genes involved in cerebral plasticity increased significantly.

Could we take lactate supplements and develop encyclopedic memory? Magistretti’s lab has just received a grant to study the effects of artificial lactate supplementation. “We have identified a series of molecules that can make astrocytes produce more lactate. Now the idea is to see in vivo if we can mitigate cognitive deficits and memory disorders.” In addition, since conditions such as depression are often accompanied by cognitive problems, “lactate could also have an antidepressant effect,” says Magistretti, who also conducts research at the National Center for Competence in Research Synapsy, dedicated to the understanding of the synaptic basis of psychiatric disease.

Quercetin alleviates high glucose-induced Schwann cell damage by autophagy

It is believed that hyperglycemia leads to increased aldose reductase activity and polyol metabolism in Schwann cells, and the resultant abnormal metabolites cause the organelle’s damage and morphological changes such as swelling and vacuolation. Autophagy can remove the damaged organelles, but also provide the materials for cell survival under stressful conditions. Quercetin can reverse high glucose-induced inhibition of neural cell proliferation. Quercetin is also implicated in the mechanism underlying the reduction of apoptosis through autophagy induction. Whether or not quercetin protects Schwann cells through autophagy pathways remains unclear. Dr. Ling Qu and co-workers from Peking Union Medical College Hospital, Peking Union Medical College, China Academy of Medical Sciences, China show that under high glucose conditions, there are fewer autophagosomes in immortalized rat RSC96 cells and primary rat Schwann cells than under control conditions, the proliferative activity of both cell types is signifcantly impaired, and the expression of Beclin-1 and LC3, the molecular markers for autophagy, is significantly lower. After intervention with quercetin, the autophagic and proliferative activity of both cell types is rescued. These results, published in the Neural Regeneration Research (Vol. 9, No. 12, 2014), suggest that quercetin can alleviate high glucose-induced damage to Schwann cells by autophagy.

Article: “Quercetin alleviates high glucose-induced Schwann cell damage by autophagy” by Ling Qu1, Xiaochun Liang1, Bei Gu2, Wei Liu1 (1 Department of Traditional Chinese Medicine, Peking Union Medical College Hospital, Peking Union Medical College, China Academy of Medical Sciences, Beijing, China; 2 Cell Center, Institute of Basic Medical Science, Peking Union Medical College, China Academy of Medical Sciences, Beijing, China) Qu L, Liang XC, Gu B, Liu W. Quercetin alleviates high glucose-induced Schwann cell damage by autophagy. Neural Regen Res. 2014;9(12):1195-1203.

Medicinal oil reduces debilitating epileptic seizures associated with Glut 1 deficiency, trial shows

Two years ago, the parents of Chloe Olivarez watched painfully as their daughter experienced epileptic seizures hundreds of times a day. The seizures, caused by a rare metabolic disease that depleted her brain of needed glucose, left Chloe nearly unresponsive, and slow to develop.

Within hours, treatment with an edible oil dramatically reduced the number of seizures for then-4-year-old Chloe, one of 14 participants in a small UT Southwestern Medical Center clinical trial.

“Immediately we noticed fewer seizures. From the Chloe we knew two years ago to today, this is a completely different child. She has done amazingly well,” said Brandi Olivarez, Chloe’s mother.

For Chloe and the other trial participants who suffer from the disease called Glut1 deficiency (G1D), seizure frequency declined significantly. Most showed a rapid increase in brain metabolism and improved neuropsychological performance, findings that suggested the oil derived from castor beans called triheptanoin, ameliorated the brain glucose-depletion associated with this genetic disorder, which is often undiagnosed.

“This study paves the way for a medical food designation for triheptanoin, thus significantly expanding therapeutic options for many patients,” said Dr. Juan Pascual, Associate Professor of Neurology and Neurotherapeutics, Physiology, and Pediatrics at UT Southwestern and lead author of a study on the findings, published in JAMA Neurology.

For the estimated 38,000 Americans suffering from this disease, the only proven treatment has been a high-fat ketogenic diet, which only works for about two-thirds of patients. In addition, this diet carries long-term risks, such as development of kidney stones and metabolic abnormalities.

Based on the results of this trial, triheptanoin appears to work as efficiently as the ketogenic diet; however, more research needs to be done before the oil is made available as a medical food therapy, researchers said.

“Triheptanoin byproducts produced in the liver and also in the brain refill brain chemicals that we found are preferentially diminished in the disorder, and this effect is precisely what defines a medical food rather than a drug,” said Dr. Pascual, who heads UT Southwestern’s Rare Brain Disorders Program, maintains an appointment in the Eugene McDermott Center for Human Growth and Development, and holds The Once Upon a Time Foundation Professorship in Pediatric Neurologic Diseases.

The oil, approved for use in research only, is an ingredient in some cosmetic products and is added to butter in some European countries. It is not commercially available in the U.S. for clinical use.

Triheptanoin’s success as an experimental treatment for other metabolic diseases, along with preclinical success in G1D mice, led Dr. Pascual and his trial collaborator, Dr. Charles Roe, Clinical Professor of Neurology and Neurotherapeutics, to first conceive the idea and then launch this trial for G1D patients. The 14 pediatric and adult patients in the study consumed varying amounts of the oil, based on their body weight, four times a day. Given the trial’s success, Dr. Pascual plans further research to refine the optimal dosage toward the goal of facilitating medical food designation of triheptanoin as a new G1D treatment.

While some trial participants reported mild stomach upset as a side effect, for Chloe the oil has been a miracle medicine without negative effects. Her parents, Brandi and Josh Olivarez of Waco, Texas, continue to be amazed by her progress.

“Before, she was having so many seizures a day that she couldn’t even talk. Now she sings all the time, she can eat whatever she wants, and her speech is greatly improved. She still has some learning delays, but has come a long way,” said Mrs. Olivarez.

Many Glut1 patients suffer from movement disorders that limit their physical capabilities, but that does not appear to be the case with Chloe. As for the seizures, she still has minor ones occasionally, but they are not debilitating.

“She is now able to run a solid mile without stopping. This would not have been possible without the oil,” Mrs. Olivarez said. “Before, she had almost no muscle tone, was lethargic and had a very wide gait due to trying to balance herself while walking, which was very tiring for her.”

To better understand this disease, UT Southwestern established a patient-completed registry to track G1D incidence and what treatments work or do not work for those registered.

Diabetes Awareness
  1. Diabetes cannot be always managed with only diet and exercise.
  2. Many diabetics are insulin dependent.
  3. There are many types of diabetes such as Type 1, 2, 3 and gestational diabetes
  4. Most diabetics are injecting themselves up to 5/6 times a day, just to stay alive.
  5. Diabetes is not caused by eating too much sugar; in fact type one diabetes is thought to be an  auto immune disease but the real cause is not known. It could be from a virus, no one knows.
  6. Diabetes cannot be controlled just by avoiding sugar. Remember sugar is not  found only in chocolate and sweets, it is in everyday food such as rice, vegetables, fruits - in fact onions have more sugar than an apple.
  7. Diabetes is not an easy to manage illness. In many cases, it requires continuous calculations of carbs, exercise and insulin amounts.
  8. Without sugar vital organs such as the brain and kidneys die. So, everyone needs continuous levels of sugar supplied to these vital organs.
  9. Diabetes kills and also over the time it can deteriorate and be linked to many life threatening illnesses.
  10. Diabetes is hard work because we constantly need to measure and inject ourselves to find this optimal balance while trying not to get too high or too low. Both are dangerous for the body.
  11. Diabetics need to manage this illness in many cases with little or no help from others, starting from day one. In many cases, they have a blood measurement device and insulin but that’s it. No blood sensors or closed loop insulin mechanisms, hence they can go up and down like a yoyo sometimes.
  12. Not all diabetics are like often described in the media sugar junkies.
  13. Diabetes happens when the body cannot turn food into energy and feed the cells. So, no matter how much they eat their cells are starving unless there is sufficient insulin supply to the body.

Let’s hope that one day there is a cure for this illness. In the meantime, we just have to keep going and keep raising awareness. Next time the media paints a wrong picture about the illness, or if you see a ‘diabetes joke’ you can hopefully comprehend better how a bit more is involved in the cause and management of diabetes.

You can follow us on Twitter and also visit our website.