Keep Track Of Your Activity And Diet
Although there are a several rules outlined above for optimal brain health, we are all different. The way you respond to certain foods is unique to you. So keep track of what you eat, how often you eat it, and how you feel after eating it. Something that can can give someone brain fog can be what gives you an extra boost of cognitive functionality.
Cant Face Food In The Morning
Some people find they just cant tolerate food first thing in the morning perhaps because they have their last meal of the day quite late at night or they dont find typical breakfast foods appealing, or because food first thing in the morning turns their stomach.If its hard for you to eat food first thing in the morning, you might like to try:
- reducing the size of your meals in the evening and eating them earlier so youre hungry in the morning
- investigating some new recipes and stocking your cupboards with some different types of foods to increase your breakfast appetite
- switching your breakfast to morning tea or mid-morning snack time instead perhaps try some of the portable breakfast ideas listed above so youve got healthy options ready to go when you feel ready for your mid-morning breakfast.
Glucose Content Reflects The Balance Between Transport And Consumption
The steady-state brain glucose concentration is a sensitive indicator of the ability of the BBB to transport glucose relative to the rate of glucose consumption, Tmax/CMRglc. The observed linear relationship between plasma and brain glucose is consistent with the need to take into account the reversibility of the transport process . The apparent Km of glucose transport, Kt, is of the order of 5 mM. Decreased electrical activity and thus decreased energy metabolism result in increased brain glucose concentrations yet a sizable concentration gradient is maintained at isoelectricity, implicating considerable net glucose uptake and thus substantial energy metabolism not related to signaling ). Increases in luminal glucose transporter result in an increase in the maximal transport capacity of the BBB, the consequence of which is an accordingly increased brain glucose content, suggesting that the luminal membrane is the major rate-determining step for glucose entry into the brain ).
Figure 3. Schematic of glucose transport across the bloodâbrain barrier, depicting the steady-state situation and showing the reversible MichaelisâMenten kinetic expression for transport . Standard MichaelisâMenten kinetics neglect the effect of product concentration on reaction velocity , and expressions for the transport rates are derived by assuming zero product concentration .
Jia Yao, Roberta Diaz Brinton, in, 2012
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Neuronal Mitochondria Have Heterogeneous Subcellular Localization
Neurons have the highest energy demands, and mitochondria are the power plants of all cells, producing ~16 times more ATP per molecule of glucose oxidized than glycolysis. Glycolytic and oxidative fluxes are tightly coupled in whole brain of awake resting humans and synaptosomes isolated from guinea pig cerebral cortex . Mitochondria have a major, but not exclusive, role in the brain’s energy budget, and they also have other important functions, including biosynthetic capability, calcium sequestration, and generation of ROS. Anatomical localization and density of mitochondria is heterogeneous at the regional, cellular, and subcellular levels.
Absence of mitochondria in about half of presynaptic structures complicates the simplified schematic presentations of presynaptic energetics, glutamateglutamine cycling, and conversion of glutamine into glutamate by mitochondrial enzyme glutaminase . There must be some reliance on other precursors for glutamate, selective local dependence on glycolysis, and/or substantial ATP-PCr diffusion between spine heads or varicosities and dendritic or axonal shafts . Presynaptic glutamate transporters are present on neurons , but their contributions to neurotransmission are debated and they are thought to have a minor role in glutamate uptake compared with astrocytes .
Viii Nutritional Therapy For Brain Disorders
Nutritional treatment for specific brain disorders has been a clinically accepted practice for decades, and new approaches have promising outcomes for diverse patient groups. Metabolic therapy involves provision of supplemental substrates . These compounds provide oxidative fuel, supplement deficiencies, and supply anaplerotic precursors, and they differ in their ability to fulfill different metabolic needs. For example, -hydroxybutyrate is a source of acetyl CoA and oxidative energy but cannot serve as a precursor for the anaplerotic pathway via PC, whereas pyruvate supplementation serves both functions.
One of the best examples of nutrient therapy is use of a ketogenic or high-fat diet for patients with intractable epilepsy . Use of ketogenic diets has been extended to include patients with PDH deficiency and glucose transporter GLUT1 deficiency . Ketone esters that enter brain more readily have been given as dietary supplements, resulting in better cognitive and physical performance in rats and improved energy metabolism with aging in an Alzheimer disease mouse model .
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Glucose Uptake In The Brain How Are Neurons And Astrocytes Fed
Dependence of the brain on glucose as its obligatory fuel derives mainly from the blood-brain barrier , and its selective permeability for glucose in the adult brain. Glucose cannot be replaced as an energy source but it can be supplemented, as during strenuous physical activity when blood lactate levels are elevated or during prolonged starvation when blood levels of ketone bodies are elevated and BBB monocarboxylic acid transporter levels are upregulated. Because entry of neuroactive compounds into brain is highly restricted by the BBB, these compounds must be synthesized from glucose within the brain. The BBB and its transport properties sharply contrast with muscle and liver that do not have tight junctions between their vascular endothelial cells and have different transporter levels for various compounds, enabling these organs to metabolize glucose, monocarboxylic acids, fatty acids, amino acids, and ketone bodies.
Sugar Creates A Dangerous Cycle Of Insulin Resistance
Poor insulin control appears to be a risk factor for Alzheimers disease. When you eat food, carbohydrates, starches and sugar in your food are broken down into another type of sugar called glucose. As your body digests the food, the stomach and small intestine absorb the sugar and send it into your bloodstream.
The hormone insulin pulls sugar from the bloodstream and gives it to cells in the organs and muscles. This gives your cells energy.
If your blood sugar levels are too high your body releases more insulin. So, insulin is trying to give MORE sugar to cells. Your cells will try to protect themselves from the powerful effect of insulin by becoming insulin resistant.
The pancreas is the large gland that creates the hormone insulin. It responds to this resistance by releasing more insulin, which starts a dangerous cycle.
Eating sugary and high-carbohydrate foods causes high blood sugar. The body tries to control this onslaught of sugar by pumping out a lot of insulin quickly. This is an “insulin spike.”
Over time, high insulin causes cells to become resistant to insulin. Insulin resistance leads to higher blood sugar levels. High blood sugar levels cause more insulin to be released. Another dangerous pattern emerges.
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Glucose Metabolism And The Regulation Of Cell Death
Glucose metabolism is evolutionarily linked to the regulation of cell death ,3a), and this link is tightly controlled in a similar fashion in many cell types, arguing for a universal role of co-regulated metabolic and apoptotic pathways. Neurons and cancer cells are among the cell types that rely almost exclusively on glucose metabolism for energy generation, and recent evidence suggests that these cells can use similar mechanisms to adapt to substrate deprivation and promote survival .
The connection between glucose metabolism and cell death
Hexokinase II , a hypoxia-regulated HK isoform in the brain, has been demonstrated to control neuronal survival depending on the metabolic state .3). HKII restricts or inhibits apoptosis in a variety of different cell types depending on whether or not it is bound to mitochondria , and on the availability of glucose . Furthermore, the capacity of HKII to phosphorylate glucose is involved in sensing the metabolic state of the cell . In addition, HKII elicits its antiapoptotic function through a molecular interaction with PEA15/PED . HKII activity protects against neuronal cell death after hypoxia and in the presence of oxidative stress . However, HKII increases neuronal cell death under glucose deprivation, thereby functioning as a molecular switch that regulates neuronal survival depending on the metabolic state. Importantly, the capacity of HKII to phosphorylate glucose and its interaction with PEA15 both mediate this effect .
Glucose Is The Main Obligatory Substrate For Energy Metabolism In Adult Brain
Brain glucose metabolism exhibits large regional variations at rest and is profoundly affected by local brain activation , demonstrating a strong link between energy metabolism and brain function . Brain glucose concentration is constant across brain regions despite large metabolic differences between white and gray matter and among different brain nuclei, indicating close linkage of glucose supply and demand. Cerebral blood flow differs with respect to the brain region, consistent with differences in regional resting metabolic activity . However, brain glucose concentrations can change acutely, consistent with the facilitative nature of glucose transport, and are higher when metabolism is reduced . Brain glucose can become rate limiting during metabolic extremes, e.g., during the earliest stages of profound activation or during hypoglycemia. Nevertheless, even when the intracellular concentration of glucose approaches the Km of hexokinase , significant facilitated transport of glucose into brain still occurs in vivo because CBF increases , possibly regulated by adenosine and K+-ATP channels . Glycogen is the only endogenous fuel store that can provide significant amounts of energy in periods during which the local supply of glucose does not meet metabolic demand .
Rebecca A. Simmons, in, 2017
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Evidence Of A Role For The Brain In Normal Glucose Homeostasis
There is little question about the brains ability to influence key determinants of glucose homeostasis in response to input from humoral signals, including glucose and other nutrients , and nutritionally relevant hormones . What remains uncertain is the extent to which such effects participate in day-to-day glucoregulation. Studies that use loss-of-function strategies are perhaps most useful in this regard, but the interpretation of such data is often confounded by associated changes of food intake and body weight, by off-target effects , or by compensatory adaptations triggered by the experimental intervention. Beyond these concerns, the impact of brain-directed interventions on circulating glucose levels is often seemingly negated by adjustments of islet function. Together, these observations raise the possibility that although the brain can affect glucose homeostasis, day-to-day control of blood glucose levels does not require its active participation. Clearly, new approaches that can tease apart the contributions of brain and islet to overall control of glucose homeostasis are needed.
High Blood Sugar Can Cause A Stroke
Insulin resistance affects the flow of blood to the brain. When brain cells dont get enough blood, brain function suffers. A decrease in blood flow can lead to mini-strokes. High blood sugar levels can also make the blood vessels weak, like old leaky pipes. Strokes are one of the factors in developing dementia.
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How To Fuel Your Brain And Body With Lasting Energy
Clearly, sugar is a nightmare when it comes to brain function. But luckily, theres an alternative that will get your brain the energy it needs without all the negative side effectsand thats ketones.
Ketones set the stage for brain health and function both directly by serving as super fuels for brain cells, as well as by triggering expression of our DNA that allows us to create chemicals that actually enhance the growth of new brain cells as well as their connection to each other, says Perlmutter.
A high-fat, lower-carbohydrate diet gives the brain more efficient fuel than a diet heavy in carbs and sugars . For example, a study found that a ketogenic diet produced enhanced mitochondrial gene expression in the hippocampus, the area of the brain responsible for learning and memory. Pretty smart.
Whats more, eating more quality fats helps you feel more satisfied, without the effects of sugar on the brain you get from a high-carb meal . Ketones actually help curb cravings while keeping you fueledone of the big benefits of the keto diet.
By and large, a diet that favors sugar and carbs is a diet that steers a person away from burning fat. And thats really threatening for brain function. Burning fat, and not sugar, is the ideal scenario for brain functionality, says Perlmutter.
Now that weve covered what sugar does to your body and brain, are you ready to kick your sweet tooth to the curb? Find out how to detox from sugar.
Macrophage Atp Generation And O2 Consumption Rates
Macrophages are known to have a large oxidative capacity and their O2 consumption rates are similar to those of sheep heart and rat liver in vitro as calculated by using original data from Krebs, Johnson and Karnovsky. Additionally, calculated ATP generation rates for isolated and incubated macrophages in vitro and cultured macrophages, taking into account oxygen utilized by the NADPH oxidase of these cells. The ATP generation rate in the presence of both glucose and glutamine was 930 nmol/, based on known pathways of metabolism. Glucose contributed 62% and glutamine 38% to the energy requirement of the cell. Because the ATP concentration of the macrophage is 7 nmol/mg protein , then the total ATP concentration of the cell must have been turned over at least 2 times/min. The macrophage, when studied over longer periods , had a similar dependency on these fuels in which glucose contributed 68% and glutamine 32% to the energy needs of the cell. The major difference in metabolism between freshly isolated cells and cultured cells is that a greater proportion of glutamine carbon is fully oxidized in culture thus the overall rate of glutamine utilization is lower .
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What Is Brain Health And Why Is It Important
Yongjun Wang and colleagues discuss the definition of brain health and the opportunities and challenges of future research
The human brain is the command centre for the nervous system and enables thoughts, memory, movement, and emotions by a complex function that is the highest product of biological evolution. Maintaining a healthy brain during ones life is the uppermost goal in pursuing health and longevity. As the population ages, the burden of neurological disorders and challenges for the preservation of brain health increase. It is therefore vital to understand what brain health is and why it is important. This article is the first in a series that aims to define brain health, analyse the effect of major neurological disorders on brain health, and discuss how these disorders might be treated and prevented.
You Need To Make Sure You Eat The Right Sugar Though
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Most of us know that we need to cut down on sugar – doing so can lower your blood pressure, decrease your risk of heart attack and make you less likely to develop dementia.
But according to a physician who specialises in brain health, sugar can have beneficial effects on our brain.
Sugar is vital for your brain health – which is the biggest guzzler of the sweet stuff in your body, Dr Drew Ramsay wrote for Well + Good.
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Effects Of Glucose On Cognition
Blood glucose is normally 45.5 mmol/1 and is controlled by a series of hormonal mechanisms. When it falls below 2.2 mmol/1, hypoglycaemia occurs . Hypoglycemia occurs when the uptake of glucose by the tissues including the brain, exceeds the rate of supply from the liver and/or meals. The decline in glucose, occurring in both mild and severe hypoglycaemia, impairs cognitive performance. The threshold for impairment of cognitive tasks has been found to be within a range of 2.2 to 2.8 mmol/l . However, some individuals maintained normal performance at below 2.2 mmol/l, and others showed disruption of function at 4 mmol/l. suggesting that glycaemic control and glucose tolerance may be more critical to cognitive function than absolute blood glucose levels . There is substantial evidence however, that higher baseline levels of blood glucose can facilitate cognitive performance . Cognitive disruption at higher glucose levels occurs in non-diabetics whose symptoms of hypoglycaemia are relieved by food intake . Subjective effects of neuroglycopenia include negative mood and attenuated arousal but not all individuals will be aware of their hypoglycaemic status.
Pariyarath Sangeetha Thondre, in, 2013
Astrocytic Energetics Is Complex And Integrated With Neuronal Activity
Astrocytic filopodial movements respond to synaptic activity, with spontaneous extension and retraction in brain slices . These activities may be driven, in part, by glutamate release from neurons and astrocytic receptor activation because application of glutamate to cultured astrocytes induces Ca2+ waves and filopodial extension involving actin , increasing ATP utilization for actin polymerizationdepolymerization and for restoration of calcium homeostasis. Actin cycling during filopodial movement may be powered by glycolysis because GAPDH and other glycolytic enzymes bind to F-actin in other circumstances , and enzyme-actin filament complexes occur in synaptosomes, postsynaptic densities, and muscle . Spontaneous, wide-spread Ca2+ waves through astrocytic networks also occur, and can be independent of or accompanied by changes in neuronal network activity rather than being caused by changes in electrical-stimulationevoked neuronal activity . Re-establishing Ca2+ homeostasis includes its ATP-dependent uptake into ER that is preferentially fueled by glycogenolysis , with a secondary influence on glucose utilization.
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What Happens When The Brain Runs On Ketones
Ketones are burned using different pathways and enzymes than sugar, causing a cascade of effects that improve brain health. Lets go over some of the ways that ketone bodies benefit the brain:
Whether you want to boost brain function, prevent neurodegenerative disease, or reduce the severity of a brain-related issue, the ketogenic diet one of the best ways to do it. By using the ketogenic diet to enter ketosis, you provide your body and brain with a more efficient fuel source that decreases inflammation and neuronal damage, improves brain cell growth and function, and regulates your brains neurotransmitters.
As an added bonus, you will be eating highly-satiating, healthy foods that will help you eat fewer calories, improve health, and lose fat rapidly. This is what makes the ketogenic diet a win-win for many people, especially those with neurological conditions.