Stoica, L. Bedse, G. Jauch-Chara, K.

Boost insulin sensitivity and enhance brain function -

Over time, these reactions in the body may trigger chronic disorders especially in those already at a higher risk genetically that could have been prevented through simple blood sugar balancing habits. Symptoms of dysregulated glucose levels arise long before the onset of disorders.

These start with glucose spikes. In the short term, these spikes disrupt our hunger cues and lead to cravings, fatigue, migraines, mood swings, poor sleep, hormone imbalances and reduced cognitive function. In the long-term, chronic conditions such as insulin resistance, Alzheimer's disease, fatty liver disease, cancer, arthritis, depression, infertility, poly-cystic ovarian syndrome PCOS , type 2 diabetes, and heart disease may develop.

Moreover, some researchers are calling Alzheimer's 'type 3 diabetes' because of the effects of insulin resistance on the aging brain.

Insulin receptors are present in organs all over the body, including the brain. The brain uses glucose as its main energy source. With insulin resistance, neurons are not able to receive sufficient amounts of glucose to carry out basic tasks, including learning and memory.

A study published in Neuron found a gene responsible for disrupting how the brain processes insulin. In mice, a high-fat diet accelerated the activation of this gene, therefore further impairing insulin function in the brain and suggesting that lowering saturated fat intake may be preventative.

While genetics remains one of the contributors to developing Alzheimer's disease, scientists agree that it is a unique combination of genetic, environmental, and lifestyle factors that cause the associated changes in the brain.

These changes include a loss of neurons and their connections because of amyloid plaque formation and tau protein tangles. Through influencing the phosphorylation and formation of plaques and tangles, insulin resistance contributes to neurodegeneration.

Insulin resistance has also been associated with depression, Parkinson's disease, and cognitive decline. A study published in Frontiers in Neuroscience shows that insulin promotes synaptic plasticity in the hippocampus by modulating long-term potentiation LTP and long-term depression LTD.

These mechanisms allow for better learning and memory. With higher blood sugar and lower insulin sensitivity, the brain is unable to use these mechanisms, which may lead to a faster rate of cognitive decline. In a year longitudinal study , researchers found that those with higher blood sugar had worse cognitive performance and thinking over time.

These changes begin years before the first disease symptoms appear and could start after years of glucose spikes, fatigue after meals, and sugar crashes.

Additionally, brain insulin signaling helps regulate whole body metabolism. A recent Nature study has shown that brain insulin sensitivity is associated with one's body fat distribution. The more sensitive the brain is to insulin, the healthier one's body weight and visceral fat is.

Not only is regulating insulin healthy for your brain, but it is also automatically healthy for the rest of your body. J Neurochem 54 5 —5. Santos MS, Pereira EM, Carvaho AP.

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Adv Exp Med Biol — This fat depot specific effects of brain insulin action could further be determined by differential autonomic innervation of subcutaneous and visceral fat 26 , Both fat depots are innervated by distinct sympathetic and parasympathetic motor neurons with functional consequences of autonomic balance on adipocyte insulin sensitivity and energy storage The proximal regulatory neurons that project into the adipose tissue appear to reside in the hypothalamus 27 , Thus, changes in autonomic nervous system balance that are induced by brain insulin action 8 , 13 , 14 , 24 , 25 could exert differentially effects on subcutaneous and visceral adipocytes and thereby contribute to our current findings.

In line with this hypothesis, induction of brain insulin action was found to modulate systemic but not subcutaneous lipolysis in humans Our current findings are of particular importance, given that the enlarged visceral fat content not only poses a high risk factor for the subsequent development of diabetes, but is also robustly linked to the risk of cardiovascular disease and the development of cancer Brain insulin resistance therefore seems to be involved in the pathogenesis of obesity in general.

More importantly, it appears to be a determinant of healthy and unhealthy obesity. Unfortunately, only a limited sample size was available in our longitudinal cohort. MEG and fMRI most likely capture different aspects of brain insulin sensitivity and their comparability in this regard has not been tested so far.

In conclusion, we showed that high brain insulin sensitivity was linked to weight loss during lifestyle intervention and associates with a favorable body fat distribution. Our current results underline the importance of brain insulin action for the development of body weight and body fat distribution.

As visceral fat is strongly linked to diabetes, cardiovascular risk, and cancer, these findings have implications beyond metabolic diseases and indicate the necessity of strategies to resolve insulin resistance of the human brain.

Details on the TULIP lifestyle intervention study, including primary and secondary outcomes as well as inclusion and exclusion criteria, have been reported previously The study was conducted within the Deutsche Forschungsgemeinschaft DFG project KFO Three hundred participants at high risk for type 2 diabetes completed the intervention.

As reported in ref. In a subgroup of 28 participants, brain insulin sensitivity was assessed by MEG before lifestyle intervention. Of these, 15 individuals were followed-up after 9.

Total dietary energy intake was assessed in 10 of these participants at three time periods during the lifestyle intervention before, during the first 9 months of lifestyle intervention, and during month 9—24 of lifestyle intervention by the mean values of several 3-day food diaries obtained at each visit In all participants, body fat distribution was assessed by whole-body MRI as part of the baseline examination of clinical trials clinicaltrials.

gov: NCT, NCT, NCT, NCT, NCT, NCT For patients characteristics, see Supplementary Table 2. Whole-body MRI was performed in the early morning after overnight fasting on a 1. Detailed information is given in ref. Before lifestyle intervention, participants underwent two hyperinsulinaemic—euglycaemic glucose clamps with insulin or placebo saline infusion on two different days for details see Tschritter et al.

Cerebrocortical activity was assessed by magnetoencephalography MEG before and during the clamp experiment. The power spectrum for the spontaneous activity of the participants was analyzed by a standard statistical mapping procedure taking into account multiple comparison correction for the different frequency bands.

On the basis of earlier findings 20 , assessment of the cerebrocortical insulin effect as changes in theta activity during the insulin experiment corrected for the placebo experiment were calculated Participants underwent whole-brain fMRI at a 3.

Experiments were conducted after an overnight fast and started under basal condition to quantify cerebral blood flow CBF with a pulsed arterial spin labeling PASL measurement using a PICORE-Q2TIPS sequence proximal inversion with control for off-resonance effects—quantitative imaging of perfusion using a single subtraction.

Change in CBF was extracted from the hypothalamus based on recent findings All relevant ethical regulations were complied with and informed written consent was obtained from all participants.

The local ethics committee approved the study protocols Ethics Committee of the Medical Faculty of the Eberhard-Karls-Universität and the University Hopsital Tübingen. In the longitudinal study, changes in body weight, body fat depots, and further metabolic variables and their association with baseline brain insulin sensitivity theta activity were analyzed by MANOVA.

Continuous variables were used for analyses and stratified variables were used solely for better illustration of the results. For the cross-sectional study, correlations between body fat compartments and hypothalamic cerebral blood flow fMRI measurements were analyzed by linear regression models unadjusted and adjusted for sex and age as well as BMI.

Further information on research design is available in the Nature Research Reporting Summary linked to this article. The data that support the findings of this study are available on reasonable request from the corresponding author M.

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An association between sensitivihy Boost insulin sensitivity and enhance brain function is ssensitivity blood glucose levels and cognitive dysfunction have been found in relatively sensitivify older individuals Eenhance Nutraceutical potential of plant compounds, et. al, Insulin resistance which happens functtion the insulin sensitivity enbance your tissue decreases was found to Boozt associated with Healthy habits impairment and the individuals with diabetes were worse. The research makes it clear that if you want to improve your memory or prevent it from getting worse, you need to implement strategies to improve insulin sensitivity. When you eat a meal consisting of high glycemic index carbohydrates, your blood glucose levels will increase too much. While you may tolerate that occasionally, eating that way every day will affect your insulin sensitivity, and it will not be good for your memory. Diets high in trans-fat and saturated fat adversely affect cognition.