The brain is the complex organ responsible for controlling most of the body's functions and processes. It is the center of the nervous system and plays a vital role in cognition, emotion, memory, sensory processing, motor control, and coordination. Comprising billions of neurons and glial cells, the brain consists of various interconnected regions, each with specific functions and responsibilities. The cerebral cortex, divided into four lobes (frontal, parietal, temporal, and occipital), is responsible for higher-level cognitive functions, such as reasoning, language, and perception. The brainstem regulates essential functions such as heart rate, breathing, and sleep-wake cycles. The cerebellum coordinates movement and balance, while the limbic system is involved in emotions and memory. Despite its relatively small size compared to the rest of the body, the brain is incredibly complex and remains one of the least understood organs in the human body.
The brain can be affected by various disorders, including:
These disorders can significantly impact a person's quality of life and may require various treatments, including medications, physical therapy, surgery, and lifestyle modifications, depending on the severity and underlying causes.
Overall, the dysregulation of insulin and metabolic processes seen in hyperinsulinemia, insulin resistance, and metabolic syndrome can impact brain health and contribute to the development or exacerbation of various neurological disorders.We are prepared to provide grants for online attendance at a range of conferences/courses.
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Associated with cognitive decline, neuroinflammation, and an increased risk of stroke.
Increases the risk of vascular dementia, Alzheimer's disease, and cognitive impairment due to impaired cerebral blood flow and insulin resistance.
Attention-Deficit/Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder characterized by persistent patterns of inattention, hyperactivity, and impulsivity that significantly impact functioning and development. ADHD symptoms typically manifest in childhood and may persist into adolescence and adulthood.
In summary, while ADHD primarily affects brain function and is considered a neurodevelopmental disorder, metabolic factors such as insulin resistance, hyperinsulinemia, and metabolic syndrome can potentially influence disease presentation and management. Understanding the interactions between ADHD and metabolic abnormalities is important for developing comprehensive treatment strategies that address both the neurodevelopmental and metabolic aspects of the condition, ultimately improving outcomes and quality of life for individuals affected by ADHD.
The World Federation of ADHD International Consensus Statement: 208 Evidence-based conclusions about the disorder
https://pubmed.ncbi.nlm.nih.gov/33549739/
"People with ADHD are at increased risk for obesity, asthma, allergies, diabetes mellitus, hypertension, sleep problems, psoriasis, epilepsy, sexually transmitted infections, abnormalities of the eye, immune disorders,
and metabolic disorders"
August 2023
In conclusion, KD improved typical behavioral performance of ADHD with hyperactivity and impulsivity in SHR. Additionally, KD significantly activated the DRD1/cAMP/PKA/DARPP32 pathway in SHR. The richness and diversity of gut microbiota were altered in SHR after KD treatment, with significant changes in Ruminococcus_gauvreauii_group, Bacteroides, Bifidobacterium, and Blautia at the genus level. KD-induced gut microbiota were enriched in amino acid metabolism- and sugar-related pathways. These results give novel insights into the mechanism of KD in ADHD treatment.
Alzheimer's disease is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and eventual loss of ability to perform daily
In summary, while Alzheimer's disease primarily affects brain function and is considered a neurodegenerative disorder, metabolic factors such as insulin resistance, hyperinsulinemia, and metabolic syndrome can potentially influence disease progression and management. Understanding the interactions between Alzheimer's disease and metabolic abnormalities is important for developing comprehensive treatment strategies that address both the neurodegenerative and metabolic aspects of the condition, ultimately improving outcomes and quality of life for individuals affected by Alzheimer's disease.
"There are no cures for Alzheimers' disease and Parkinson's Disease and current treatments are limited to symptom management. "
" Given the link between metabolic dysfunction in obesity and neurodegeneration, dietary interventions are a logical approach
" In a single-phase, assessor-blinded, two-period randomized crossover trial, participants diagnosed with AD (n=26) were randomized into a ketogenic diet (29% protein, 6% carbohydrates and 58% fat) or a low fat diet (19% protein, 62% carbohydrates and 11% fat) for 12 weeks."
" lthough motor and nonmotor symptoms were improved in both diet groups, the ketogenic urinary problems, pain, fatigue, daytime sleepiness, and cognitive impairment were lower in the ketogenic group. "
Multiple pieces of evidence here for seed oils in AD progression.
Oxidized LA is a primary source of the DNA damage measure used. HNE is a toxin from seed oils that induces mitochondrial dysfunction, reduced ATP, and beta-amyloid production. RLIP and glutathione are both part of HNE detoxifying system, both are impaired by high levels of HNE.
H/T @tuckergoodrich on X
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The role of RLIP76 in oxidative stress and mitochondrial dysfunction:
Evidence based on autopsy brains from Alzheimer's disease patients
Our study strongly suggests the feasibility of a VLCKD in the treatment of a group of women with self-reported binge eating and food addiction symptoms. After a maintenance low-calorie diet, the patients experienced a reduction of food addiction and/or binge eating symptoms.
The patients showed a weight loss associated only with fat mass, while their muscle mass was preserved and their metabolic health improved.
Having a feasible nutritional approach to limit overeating and food addiction symptoms may help healthcare professionals find a reliable treatment to favor weight loss. In this view, a ketogenic diet may be a novel therapy for people with addictive-like eating disorders, helping to lower the sensation of hunger and craving.
This pilot study described the possibility of assessing a ketogenic protocol in patients with food addiction and\or binge eating, in the absence of other pathologies, where other interventions have failed. Future research to explore the role of nutritional ketosis in addiction symptoms in humans is needed.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by persistent deficits in social communication and interaction, as well as restricted, repetitive patterns of behavior, interests, or activities. While the exact causes of autism are not fully understood, a combination of genetic, environmental, and neurobiological factors is believed to contribute to its development.
Here's how autism spectrum disorder relates to metabolic factors:
In summary, while autism primarily affects brain development and function and is considered a neurodevelopmental disorder, metabolic factors such as insulin resistance, hyperinsulinemia, and metabolic syndrome can potentially influence disease progression and management. Understanding the interactions between autism spectrum disorder and metabolic abnormalities is important for developing comprehensive treatment strategies that address both the neurodevelopmental and metabolic aspects of the condition, ultimately improving outcomes and quality of life for individuals affected by autism.
"She's lost weight, cleared her head, and feels more stable”. She also uses these ketogenic metabolic therapies with kids with ADHD and Autism to normalize their blood sugar and mood and stabilize them so they can improve in other ways as well.
The mission of The Johnson Center for Child Health and Development is to advance the understanding of childhood development through clinical care, research, and education.
http://www.johnson-center.org/
Part one of this webinar is in the heading
The mission of The Johnson Center for Child Health and Development is to advance the understanding of childhood development through clinical care, research, and education.
Behavioral disorders encompass conditions affecting behavior, emotions, and social interactions, including ADHD, ODD, and conduct disorder. While their causes vary, genetic, environmental, and neurobiological factors play significant roles. Metabolic factors like insulin resistance and metabolic syndrome, though not direct causes, may influence brain function and neurotransmitter systems involved in these disorders. Additionally, they are associated with inflammation, oxidative stress, and hormonal dysregulation, which can exacerbate symptoms. Addressing metabolic abnormalities through lifestyle changes and medications may improve treatment outcomes for behavioral disorders, necessitating comprehensive strategies considering both neurological and metabolic aspects.
"Behavioural inflexibility is a symptom of neuropsychiatric and neurodegenerative disorders such as Obsessive-Compulsive Disorder, Autism Spectrum Disorder and Alzheimer's Disease, encompassing the maintenance of a behaviour even when no longer appropriate. Recent evidence suggests that insulin signalling has roles apart from its regulation of peripheral metabolism and mediates behaviourally-relevant central nervous system (CNS) functions including behavioural flexibility. Indeed, insulin resistance is reported to generate anxious, perseverative phenotypes in animal models, with the Type 2 diabetes medication metformin proving to be beneficial for disorders including Alzheimer's Disease. Structural and functional neuroimaging studies of Type 2 diabetes patients have highlighted aberrant connectivity in regions governing salience detection, attention, inhibition and memory "
Food addiction (FA) is loosely defined as hedonic eating behavior involving the consumption of highly palatable foods (ie, foods high in salt, fat, and sugar) in quantities beyond homeostatic energy requirements. FA shares some common symptomology with other pathological eating disorders, such as binge eating. Current theories suggest that FA shares both behavioral similarities and overlapping neural correlates to other substance addictions. Although preliminary, neuroimaging studies in response to food cues and the consumption of highly palatable food in individuals with FA compared to healthy controls have shown differing activation patterns and connectivity in brain reward circuits including regions such as the striatum, amygdala, orbitofrontal cortex, insula, and nucleus accumbens. Additional effects have been noted in the hypothalamus, a brain area responsible for regulating eating behaviors and peripheral satiety networks. FA is highly impacted by impulsivity and mood. Chronic stress can negatively affect hypothalamic–pituitary–adrenal axis functioning, thus influencing eating behavior and increasing desirability of highly palatable foods. Future work will require clearly defining FA as a distinct diagnosis from other eating disorders.
Bipolar disorder is a mood disorder characterized by manic and depressive episodes. While its precise causes are complex, metabolic factors like insulin resistance and metabolic syndrome may influence its development and severity:
Neurological Manifestations:Bipolar disorder involves disruptions in neurotransmitter systems. Metabolic factors like insulin resistance may affect neurotransmitter balance, potentially contributing to bipolar symptoms.
Inflammation and Oxidative Stress:Metabolic syndrome is linked to inflammation and oxidative stress, implicated in bipolar disorder. These factors can disrupt neuronal function and exacerbate mood dysregulation.
Hormonal Dysregulation: Bipolar disorder involves hormonal abnormalities, and metabolic factors may exacerbate this dysregulation, contributing to mood instability.
Addressing metabolic abnormalities through lifestyle changes and medications may improve treatment outcomes for bipolar disorder, considering its interactions with metabolic factors. Understanding these connections is crucial for comprehensive treatment strategies and better outcomes.
Bipolar disorder is a mood disorder characterized by manic and depressive episodes. While its precise causes are complex, metabolic factors like insulin resistance and metabolic syndrome may influence its development and severity:
Neurological Manifestations:Bipolar disorder involves disruptions in neurotransmitter systems. Metabolic factors like insulin resistance may affect neurotransmitter balance, potentially contributing to bipolar symptoms.
Inflammation and Oxidative Stress:Metabolic syndrome is linked to inflammation and oxidative stress, implicated in bipolar disorder. These factors can disrupt neuronal function and exacerbate mood dysregulation.
Hormonal Dysregulation: Bipolar disorder involves hormonal abnormalities, and metabolic factors may exacerbate this dysregulation, contributing to mood instability.
Addressing metabolic abnormalities through lifestyle changes and medications may improve treatment outcomes for bipolar disorder, considering its interactions with metabolic factors. Understanding these connections is crucial for comprehensive treatment strategies and better outcomes.
Cognitive decline refers to a gradual worsening of cognitive abilities, often associated with aging or neurodegenerative disorders like Alzheimer's disease. Metabolic factors, including insulin resistance, hyperinsulinemia, and metabolic syndrome, play a role in cognitive decline:
Neurological Manifestations: Metabolic factors are implicated in the pathogenesis of cognitive decline, affecting brain function and contributing to neurodegeneration, particularly in Alzheimer's disease and vascular dementia.
Vascular Dysfunction: Metabolic syndrome increases the risk of cerebrovascular disease, damaging brain blood vessels and leading to reduced blood flow and cognitive impairment.
Inflammation and Oxidative Stress: Metabolic syndrome is linked to inflammation and oxidative stress, which contribute to neuroinflammation, synaptic dysfunction, and neurodegeneration in cognitive decline.
Treatment Considerations: Addressing metabolic abnormalities like insulin resistance and metabolic syndrome may improve treatment outcomes for cognitive decline. Lifestyle changes and medications targeting metabolic syndrome can help manage cognitive decline by addressing vascular risk factors and reducing inflammation.
Understanding the relationship between metabolic factors and cognitive decline is crucial for developing effective treatment strategies that address both cognitive and metabolic aspects of the condition, ultimately improving outcomes and quality of life for affected individuals.
"The peri-menopausal transition is a tipping point for female brain aging. From the metabolic perspective, the process begins with decline in glucose metabolism and increase in insulin resistance, followed by a compensatory mechanism to use fatty acids and ketone bodies as an auxiliary fuel source’ Wang et al
TCR reduces brain insulin resistance and inflammation. If carbohydrate intake is sufficiently reduced ketone bodies can provide an alternative fuel source for the brain, further supporting cognitive function.
82-Year-Old woman reverse cognitive decline with keto.
She has seen amazing benefits to her cognitive function once starting a keto diet. Her brain function has improved tremendously using diet alone ! This is just emerging in the scientific literature and was previously thought to be impossible using diet alone.
Ketogenic protocols are unequal in regard to ketosis. KD and IF require constant adherence to establish ketosis as opposed to MCT, which can trigger ketosis in a matter of minutes [41]. Future research should determine the ideal feasible method and sub-method (e.g., time-restricted IF vs. alternate-day IF), or minimum-effective-dose of MCT and composition (i.e., C8 vs. C10) that can produce cognitive advantages. Novel methods, such as MCT-supplemented IF or KD-combined IF [39], are worth examining. Moreover, the identification of the minimum ketosis threshold that can produce favorable cognitive outcomes, regardless of method, is essential for clinical relevance. We wish to emphasize that molecular and neurophysiological explanations are highly valued at this point with respect to their research potential, and acknowledge that mechanistic research may have promise in bolstering the evidence within this context and is needed to advance ketogenic use to manage cognitive decrements.
Dementia is a broad term used to describe a decline in cognitive function severe enough to interfere with daily life. It is characterized by memory loss, impaired judgment, difficulty communicating, and other cognitive deficits. Alzheimer's disease is the most common cause of dementia, accounting for approximately 60-70% of cases, followed by vascular dementia, Lewy body dementia, and other less common types.
Neurological Manifestations: Dementia primarily affects brain function and is characterized by the progressive loss of neurons and synaptic connections. While the exact mechanisms underlying dementia vary depending on the specific type, metabolic factors have been implicated in the pathogenesis of certain types of dementia, including Alzheimer's disease and vascular dementia. Insulin resistance, for example, may impair neuronal insulin signalling and contribute to neurodegeneration and cognitive decline.
Vascular Dysfunction: Metabolic factors are associated with vascular dysfunction and an increased risk of cerebrovascular disease, including stroke and small vessel disease. Vascular risk factors can damage blood vessels in the brain, leading to reduced cerebral blood flow, hypoperfusion, and ischemia, which may contribute to the development or exacerbation of vascular dementia. Additionally, metabolic abnormalities associated with insulin resistance and hyperinsulinemia may exacerbate vascular dysfunction and increase the risk of cerebrovascular events in individuals with dementia.
Inflammation and Oxidative Stress: Metabolic factors are associated with chronic low-grade inflammation and oxidative stress, which have been implicated in the pathogenesis of dementia. Inflammatory cytokines and oxidative damage can contribute to neuroinflammation, synaptic dysfunction, and neurodegeneration in dementia. Additionally, inflammatory markers may be elevated in individuals with dementia, suggesting a link between metabolic abnormalities and neuroinflammatory processes in the disorder.
Developing comprehensive treatment strategies that address both the cognitive and metabolic aspects of the condition, ultimately improving outcomes and quality of life for individuals affected by dementia.
Management of cardiometabolic health may be a key component of dementia prevention. Yet, with metabolic changes owing to both aging and potential underlying chronic diseases, including dementia, studies in older persons have been discordant, and there is no clear consensus on the strategy to use for their management in late adulthood for the purpose of delaying or preventing dementia onset. Most previous studies have examined risk factors individually and did not formally model trajectories over a long time prior to dementia. By modeling concurrently the trajectories of main cardiometabolic risk factors in prodromal dementia in a large prospective cohort, we provide evidence that BMI declines several years before dementia diagnosis and might indicate preclinical disease, whereas BP, specifically DBP, is consistently lower among future dementia cases, which may reflect both underlying disease and a causal association between low BP and dementia. Finally, elevated glucose levels over the course of older adulthood were higher among those who eventually developed dementia and may thus represent a risk factor for dementia.
Whether confirmed and extended to other populations, these findings emphasizing blood glucose control, low BP, and weight loss as key components of cardiovascular health management for primary and secondary prevention of dementia in older persons may have important implications for preventive care practice in geriatric populations.
Depression is a mental health disorder characterized by persistent feelings of sadness, changes in appetite or sleep patterns, fatigue, and difficulty concentrating. While its exact cause is complex, metabolic factors like insulin resistance and inflammation may play a role. These factors can affect neurotransmitter balance, trigger neuroinflammatory pathways, and disrupt hormonal regulation, potentially contributing to depression. Addressing metabolic abnormalities through lifestyle changes and medications may help optimize depression management. Understanding the link between depression and metabolic factors is crucial for developing effective treatment strategies.
Glioblastoma is an aggressive type of brain cancer that originates in the glial cells, which are supportive cells in the brain. It is the most common and deadliest form of primary brain tumor in adults. Glioblastomas are highly malignant and infiltrative, making complete surgical removal challenging and leading to a high rate of recurrence.
Here's how glioblastoma relates to metabolic factors:
Tumor Metabolism: Glioblastoma cells exhibit altered metabolism compared to normal brain cells, a phenomenon known as the Warburg effect. This metabolic shift involves increased glucose uptake and glycolysis, even in the presence of oxygen (aerobic glycolysis), leading to the generation of energy and metabolic intermediates necessary for rapid tumor growth and proliferation. Insulin resistance and hyperinsulinemia may influence tumor metabolism by providing additional glucose and growth-promoting signals to glioblastoma cells, potentially exacerbating tumor progression.
Inflammation and Immune Dysregulation: Metabolic syndrome is associated with chronic low-grade inflammation and immune dysregulation, which may contribute to tumor growth and progression in glioblastoma. Inflammatory mediators released from adipose tissue in metabolic syndrome can create a pro-inflammatory microenvironment that promotes tumor cell proliferation, angiogenesis (formation of new blood vessels), and metastasis. Additionally, immune dysfunction associated with metabolic syndrome may impair the anti-tumor immune response, allowing glioblastoma cells to evade immune surveillance and promote tumor progression.
Treatment Implications: While surgical resection, radiation therapy, and chemotherapy are standard treatments for glioblastoma, addressing underlying metabolic abnormalities such as insulin resistance and metabolic syndrome may be important for optimizing treatment outcomes. Some medications used to manage metabolic syndrome, such as certain antidiabetic agents or anti-inflammatory drugs, may have adjunctive benefits in glioblastoma treatment by targeting metabolic pathways or modulating the tumor microenvironment. Additionally, lifestyle modifications such as regular physical activity, weight management, and dietary changes may help improve metabolic health and potentially enhance the effectiveness of conventional glioblastoma therapies.
Case Reports
Logan Sneed had a glioblastoma removed and turned to a ketogenic diet to keep it from growing back. Even though doctors said he only had 1-10 years to live, he's seen the exact opposite. The tumor hasn't grown back at all and he is thriving more than ever. He's building muscle and becoming a huge influencer in the space !
" I am a Brain Cancer survivor that was diagnosed with a stage 4 Glioblastoma Brain Tumor March 26th, 2016. I have been through brain surgery, radiation, and chemotherapy. I have grown in numerous ways mentally, physically, and emotionally. The day my life changed was the day that I began the Ketogenic diet. Doctors told me nothing would help this. Might as well give up. "
Huntington's disease (HD) is a progressive neurodegenerative disorder caused by a genetic mutation in the huntingtin gene. While it primarily affects the central nervous system, metabolic factors like insulin resistance and metabolic syndrome can exacerbate disease progression through various pathways. Metabolic abnormalities such as alterations in glucose metabolism and inflammation have been observed in HD patients, contributing to neurodegeneration. Addressing underlying metabolic abnormalities through lifestyle changes and medications may optimize treatment outcomes and improve quality of life for individuals with HD. Understanding the interplay between HD and metabolic factors is crucial for developing comprehensive treatment strategies to manage the condition effectively.
Huntington's disease (HD) is a progressive, fatal neurodegenerative disorder with limited treatment options. Substantial evidence implicates mitochondria dysfunction in brain and skeletal muscle in the pathogenesis of HD. Metabolic strategies, such as fasting and ketogenic diets, theoretically enhance brain and muscle metabolism and mitochondria function, which may improve the clinical symptoms of HD. We report the case of a 41-year-old man with progressive, deteriorating HD who pursued a time-restricted ketogenic diet (TRKD) for 48 weeks. Improvements were measured in his motor symptoms (52% improvement from baseline), activities of daily living (28% improvement), composite Unified HD Rating Scale (cUHDRS) score (20% improvement), HD-related behavior problems (apathy, disorientation, anger, and irritability improved by 50-100%), and mood-related quality of life (25% improvement). Cognition did not improve. Weight remained stable and there were no significant adverse effects. This case study is unique in that a patient with progressive, deteriorating HD was managed with a TRKD, with subsequent improvements in his motor symptoms, activities of daily living, cUHDRS score, most major HD-related behavior problems, and quality of life. Our patient remains dedicated to his TRKD, which continues to provide benefit for him and his family. .
Insomnia, a sleep disorder characterized by difficulty falling or staying asleep, is influenced by metabolic factors such as insulin resistance, hyperinsulinemia, and metabolic syndrome. These factors disrupt circadian rhythms, hormone balance, and may contribute to sleep-disordered breathing. Psychological factors like stress and depression, often linked to metabolic abnormalities, can also exacerbate insomnia. Treatment involves addressing metabolic issues through lifestyle changes and cognitive-behavioral therapy for insomnia (CBT-I) alongside conventional approaches. Understanding the interplay between metabolic factors and insomnia is crucial for effective treatment and improved sleep outcomes.
The prevalence of insomnia (symptoms) is 39% (95% confidence interval, 34-44) in the T2D population and may be associated with deleterious glycemic control.
Metabolic factors like insulin resistance, hyperinsulinemia, and metabolic syndrome can influence migraine susceptibility, severity, and management:
Neurological Manifestations:Metabolic abnormalities may affect neuronal excitability and neurotransmitter signalling pathways involved in migraine pathogenesis.
Inflammatory and Vascular Mechanisms:Metabolic syndrome is associated with inflammation and endothelial dysfunction, exacerbating vascular abnormalities and neuroinflammation linked to migraine attacks.
Hormonal Influence: Insulin resistance and metabolic syndrome can impact oestrogen metabolism and hormone signalling, potentially affecting migraine susceptibility, especially in women.
Addressing metabolic abnormalities through lifestyle changes and medications may optimize migraine management, reducing attack frequency and severity.
Understanding the interplay between metabolic factors and migraine is crucial for developing tailored treatment approaches, improving outcomes, and enhancing quality of life for migraine sufferers.
"The problem can be resolved by avoiding a high carbohydrate diet and by adding a sufficiently increased amount of salt to consumed water to increase blood volume, to provide enough sodium for the brain under any circumstance, so it can continuously support those important action potentials. "
Mitochondria play a vital role in supporting brain health and functionality. Within neurons, mitochondria are responsible for providing the energy necessary for various neuronal processes, including neurotransmission, synaptic plasticity, and axonal transport. Additionally, mitochondria regulate cellular processes critical for brain function, such as calcium homeostasis, oxidative stress response, and apoptosis.
Dysfunction in these cellular powerhouses due to poor dietary choices can lead to impaired neuronal function and compromised brain integrity. This dysfunction may contribute to cognitive decline, neurodegenerative diseases (such as Alzheimer's and Parkinson's), and mood disorders. Nutrient-dense foods support optimal mitochondrial function, while processed foods may compromise brain health.
Prioritizing a diet rich in whole foods is essential for preserving mitochondrial health and reducing the risk of brain disorders. By nourishing the brain with essential nutrients, individuals can help maintain cognitive function, support mood regulation, and reduce the risk of neurodegenerative diseases. This underscores the critical role of dietary choices in supporting brain health and overall cognitive function.
Dr. Palmer’s clinical practice has focused on helping people suffering from treatment-resistant mental illnesses, including mood disorders, psychotic disorders, and personality disorders. Most recently, his research interests have turned to the areas of metabolism, metabolic disorders, and their connection to mental disorders. He is focused on combining and understanding epidemiological data, basic science research, and clinical studies in order to better understand what role metabolism plays in mental illness. Dr. Palmer has been pioneering the use of the ketogenic diet and its applications in psychiatry. He has published case studies, pilot clinical trials, and is actively conducting research in this area. He is also working with researchers from around the world to further explore this treatment in clinical populations as well as pursuing more basic science research.
Changes in eating habits can have a beneficial effect on the condition of our body, but also on the development and course of many diseases. This review provides evidence that the ketogenic diet may provide therapeutic benefits in patients with neurological problems associated with increased oxidative stress and neuro-inflammation or disruption in brain energy metabolism. The review of the scientific literature shows that KD could affect not only the progression of neurological disorders but also the course and outcome of their treatment. The effectiveness of KD has been proven in epilepsy and in other neurological diseases, such as depression, migraine, or neurodegenerative diseases e.g., AD and PD. KD should be also considered as an adjuvant therapeutic option in other neurological diseases.
Schizophrenia is a complex mental disorder characterized by disruptions in thought processes, perceptions, emotions, and behaviour, with genetic, environmental, and neurobiological factors believed to be involved. Metabolic factors, such as insulin resistance and metabolic syndrome, relate to schizophrenia in several ways:
Neurological Manifestations: Schizophrenia affects brain function and neurotransmitter systems like dopamine and glutamate. Metabolic factors can influence neurotransmitter balance and synaptic transmission, potentially contributing to psychotic symptoms.
Inflammation and Oxidative Stress: Metabolic syndrome is linked to chronic inflammation and oxidative stress, implicated in schizophrenia's pathogenesis. Inflammatory cytokines and oxidative damage may disrupt neuronal function, contributing to neuroinflammation and neurodegeneration.
Hormonal Dysregulation: Hormonal abnormalities, including alterations in stress response systems, are observed in schizophrenia. Metabolic factors may exacerbate hormonal dysregulation, potentially worsening symptoms and cognitive impairment.
Treatment Considerations: Addressing metabolic abnormalities is crucial for optimizing schizophrenia treatment outcomes. Lifestyle changes and medications targeting metabolic syndrome may help improve metabolic health and reduce psychotic symptoms, although medication side effects should be monitored.
Understanding the interaction between schizophrenia and metabolic factors is essential for developing comprehensive treatment strategies, ultimately improving outcomes for affected individuals.
Purpose of review: The aim of this article is to review recent findings on the efficacy of ketogenic diet in preclinical models and in patients with schizophrenia. This review will also highlight emerging evidence for compromised glucose and energy metabolism in schizophrenia, which provides a strong rationale and a potential mechanism of action for ketogenic diet.
Recent findings: Recent transcriptomic, proteomic and metabolomic evidence from postmortem prefrontal cortical samples and in-vivo NMR spectroscopy results support the hypothesis that there is a bioenergetics dysfunction characterized by abnormal glucose handling and mitochondrial dysfunctions resulting in impaired synaptic communication in the brain of people with schizophrenia. Ketogenic diet, which provides alternative fuel to glucose for bioenergetic processes in the brain, normalizes schizophrenia-like behaviours in translationally relevant pharmacological and genetic mouse models. Furthermore, recent case studies demonstrate that ketogenic diet produces improvement in psychiatric symptoms as well as metabolic dysfunctions and body composition in patients with schizophrenia.
Summary: These results support that ketogenic diet may present a novel therapeutic approach through restoring brain energy metabolism in schizophrenia. Randomized controlled clinical trials are needed to further show the efficacy of ketogenic diet as a co-treatment to manage both clinical symptoms and metabolic abnormalities inherent to the disease and resulted by antipsychotic treatment.
Epidemiological research depicting the overall prevalence of mental health disorders in Malta is sparse. With a population of over 535,000 inhabitants, it is estimated that around 120,000 individuals have a mental disorder (1). The reported local percentage prevalence stands at 6.6% for depression; 7.8% for anxiety, and for schizophrenia, at 0.026% for the general population and 0.4% for asylum seekers (2, 3). Approximately 25.2% of individuals under the age of 14 are at risk of developing a mental disorder, which is higher than that estimated in Europe (3, 4)
2 https://pubmed.ncbi.nlm.nih.gov/27663818/
3 na
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