In the pursuit of longevity and vibrant health, one gene stands out as a beacon of hope: SIRT1. This remarkable gene, short for silent information regulator 2 homolog 1, is a key player in the anti-ageing game. Functioning like a guardian of our cells, SIRT1 promotes longevity by regulating various cellular processes. However, SIRT1 doesn’t work alone—it relies on NAD, a crucial energy source, to perform its anti-ageing magic. Let’s delve into the fascinating world of the SIRT1 gene and discover how NAD plays a starring role in the cellular symphony of ageing gracefully.

The Power of SIRT1

SIRT1 is a game changer when it comes to slowing down the ageing process. This gene oversees numerous cellular activities that contribute to longevity. SIRT1 promotes cellular repair, regulates metabolism, and helps maintain genomic stability. By doing so, SIRT1 ensures that our cells function optimally, reducing the wear and tear that accompanies ageing.
SIRT1 functions by deacetylating proteins that contribute to cellular regulation, including histones, transcription factors, and other cellular proteins. This activity helps enhance DNA repair and modulate inflammatory responses, both critical factors in aging and longevity .

NAD: The Star Player

NAD, or nicotinamide adenine dinucleotide, is a vital coenzyme found in every cell of our body. NAD acts as an energy source, empowering SIRT1 to carry out its functions effectively. When NAD levels are optimal, SIRT1’s activity is enhanced, leading to improved cellular repair and potentially slowing down the ageing clock.
NAD is essential for the function of sirtuins (including SIRT1), which depend on NAD to catalyze their reactions. Studies suggest that boosting NAD levels can provide our cells with a vitality boost from within, promoting longevity and enhancing overall cellular health.

Supporting the SIRT1 and NAD Dynamic Duo

So, how can you support this dynamic duo of SIRT1 and NAD? Here are a few strategies:

  1. NAD-Rich Foods: Incorporate foods that are rich in NAD precursors into your diet. These include fish, nuts, and certain vegetables. Foods like salmon, tuna, and sardines are excellent sources of NAD precursors. Additionally, consuming nuts like almonds and vegetables such as broccoli and cabbage can help maintain NAD levels.
  2. Lifestyle Habits: Adopt lifestyle habits that naturally boost NAD levels. Regular exercise and proper sleep are crucial. Exercise not only increases NAD levels but also promotes overall health. Quality sleep ensures that your body can repair and regenerate efficiently.
  3. Supplements: Consider NAD supplements, such as nicotinamide riboside (NR) or nicotinamide mononucleotide (NMN). These supplements can help boost NAD levels, supporting SIRT1 activity and promoting anti-ageing benefits. Additionally, emerging research suggests that Deazaflavin, a supplemental precursor, may further enhance NAD production, offering another avenue for maintaining optimal levels.

Conclusion

When your genes are in harmony, the symphony of anti-aging begins. By understanding and supporting the role of SIRT1 and NAD, you can take proactive steps towards slowing down the ageing process and enhancing your vitality. Embrace the power of this dynamic duo and let the symphony of ageing gracefully play on.

References

  1. Houtkooper RH, Pirinen E, Auwerx J. Sirtuins as regulators of metabolism and healthspan. Nature Reviews Molecular Cell Biology. 2012;13(4):225-238.
  2. Imai S, Guarente L. NAD+ and sirtuins in aging and disease. Trends in Cell Biology. 2014;24(8):464-471.
  3. Mills KF, Yoshida S, Stein LR, et al. Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice. Cell Metabolism. 2016;24(6):795-806.
  4. Yoshino J, Baur JA, Imai S. NAD+ intermediates The biology and therapeutic potential of NMN and NR. Cell Metabolism. 2018;27(3):513-528.
  5. Martens CR, Denman BA, Mazzo MR, et al. Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nature Communications. 2018;9(1):1286.
  6. Mouchiroud L, Houtkooper RH, Auwerx J. NAD+ metabolism: a therapeutic target for age-related metabolic disease. Critical Reviews in Biochemistry and Molecular Biology. 2013;48(4):397-408.

As the global COVID-19 vaccination efforts continue to progress, discussions surrounding post-vaccination care are becoming increasingly important. While it’s natural to experience mild side effects after receiving a vaccine, reaching for over-the-counter pain relievers like Tylenol (acetaminophen) may not be the optimal choice for everyone. In fact, Tylenol consumption post-vaccination may not only compromise immune response but also impact crucial antioxidant levels in the body, such as glutathione, leading to potential health consequences. Let’s delve into the science behind post-vaccination care and the implications of Tylenol use.

Understanding Post-Vaccination Symptoms:
Post-vaccination symptoms are a common occurrence, signalling that the body is mounting an immune response to the vaccine. These symptoms, which may include pain at the injection site, fatigue, headache, muscle aches, and low-grade fever, typically resolve on their own within a few days.

The Role of Pain Relievers:
Many individuals turn to pain relievers like Tylenol to alleviate post-vaccination symptoms. However, recent research suggests that Tylenol use post-vaccination may not be without consequences. Studies published in reputable journals such as the “Journal of Virology” have indicated that acetaminophen and other NSAIDs may dampen the body’s immune response to viral infections, potentially affecting vaccine efficacy.

Glutathione Depletion and Organ Health:
One crucial aspect often overlooked in discussions about Tylenol use is its potential impact on glutathione levels in the body. Glutathione is a powerhouse antioxidant crucial for liver, kidney, and lung health. Consumption of Tylenol can lead to depletion of glutathione, potentially straining these vital organs. Furthermore, glutathione depletion may not stop there—it can also influence the Purkinje cells in the cerebellum, potentially impacting neurological health.

The Cerebellum Connection:
The cerebellum plays a crucial role in coordinating movement, balance, and posture. Disruption of Purkinje cell function in the cerebellum due to glutathione depletion can have far-reaching consequences on neurological health. Studies have linked cerebellar dysfunction to various neurological disorders, including ataxia, tremors, and cognitive impairments.

Rethinking Post-Vaccination Care:
Given the potential consequences of Tylenol use post-vaccination, it’s crucial to rethink our approach to symptom management. Instead of immediately reaching for pain relievers, consider alternative strategies such as rest, hydration, and cold compresses. These non-medicated approaches can support the body’s natural healing processes without compromising immune response or antioxidant levels.

Conclusion:
As we navigate the complexities of post-vaccination care, it’s essential to prioritize informed decision-making and holistic health. While Tylenol may offer temporary relief from post-vaccination symptoms, its potential impact on immune response and antioxidant levels warrants consideration. By opting for alternative symptom management strategies and supporting the body’s natural healing processes, we can promote optimal health and well-being in the post-vaccination period.

References:
Prescott, J., & Halloran, M. E. (2019). Nonsteroidal anti-inflammatory drugs as a treatment for infectious diseases. In Advances in Pharmacology (Vol. 85, pp. 1-31). Academic Press.

In the realm of healthcare and mental health, there exists a profound, yet often overlooked connection between childhood trauma and chronic health conditions. Adverse Childhood Experiences (ACEs), encompassing a range of traumatic events during childhood, have been increasingly recognized as significant predictors of long-term health outcomes. This article delves into the intricate relationship between ACEs and invisible diseases, shedding light on the profound impact of early-life trauma on physical and mental well-being.

Understanding Adverse Childhood Experiences (ACEs):
ACEs refer to traumatic events occurring during childhood, including abuse, neglect, household dysfunction, and other adverse experiences. These experiences can profoundly shape a child’s development, influencing neural pathways, stress response systems, and overall health trajectories.

*The Link to Chronic Health Conditions:
Research has shown a clear correlation between ACEs and the development of chronic health conditions later in life. From autoimmune disorders to chronic pain conditions, the impact of childhood trauma on physical health is undeniable. Moreover, ACEs are associated with a higher risk of mental health issues, including depression, anxiety, and substance abuse.

Exploring the Biological Mechanisms:
The biological mechanisms underlying the link between ACEs and chronic health conditions are multifaceted. Chronic stress resulting from early-life trauma can dysregulate the body’s stress response systems, leading to inflammation, immune dysfunction, and alterations in neurological development. These changes may predispose individuals to a wide range of health problems, including cardiovascular disease, diabetes, and autoimmune disorders.

Unveiling the Psychological Impact:
In addition to their biological effects, ACEs can have profound psychological consequences. Childhood trauma can disrupt attachment patterns, undermine self-esteem, and contribute to maladaptive coping mechanisms. These psychological factors, in turn, may exacerbate the risk of chronic health conditions and complicate treatment outcomes.

Addressing the Root Cause:
Central to addressing the link between ACEs and chronic health conditions is addressing the root cause of trauma. Instead of merely treating symptoms, interventions should encompass a holistic approach that addresses the psychological, emotional, and social factors contributing to poor health outcomes. This may involve, in addition to traditional or integrative medical intervention, trauma-informed therapy, support groups, and community-based interventions aimed at promoting resilience and healing.

Building Resilience and Prevention:
While the impact of ACEs on health outcomes is significant, it’s essential to recognize that not all individuals exposed to trauma will develop chronic health conditions. Building resilience through supportive relationships, positive coping strategies, and access to resources can mitigate the long-term effects of childhood trauma and promote better health outcomes.

In conclusion, the connection between childhood trauma and chronic health conditions underscores the urgent need for a comprehensive, holistic health approach, much like the one Autonomic coaching provides. By raising awareness, implementing trauma-informed care practices, and investing in early intervention and prevention efforts, we can break the cycle of intergenerational trauma and promote health and well-being for future generations.

In the intricate ecosystem of the human body, the gut plays a central role in influencing various aspects of health, from digestion to immunity and even mood. Butyrate, a short-chain fatty acid produced by gut bacteria, and gluten tolerance are two elements that are intricately connected, offering profound insights into the gut-brain axis and overall well-being. As a health and wellness coach, understanding the interplay between butyrate production, gluten tolerance, and their connection is essential for guiding clients towards optimal gut health and vitality.

Butyrate Production: The Key to Gut Health:
Butyrate, primarily produced through the fermentation of dietary fiber by gut bacteria, serves as a crucial energy source for the cells lining the colon. Beyond its role in energy metabolism, butyrate exerts profound effects on gut barrier function, immune regulation, and inflammation modulation. Research published in the “Journal of Clinical Gastroenterology” (1) highlights the role of butyrate in promoting gut barrier integrity and reducing inflammation—a cornerstone of gut health and overall well-being.

Gluten Tolerance: Navigating the Complexities:
Gluten, a protein found in grains like wheat, barley, and rye, has gained attention in recent years due to its implications in gluten-related disorders, including celiac disease and non-celiac gluten sensitivity. Individuals with these conditions experience adverse reactions to gluten consumption, ranging from gastrointestinal symptoms to systemic inflammation. While the mechanisms underlying gluten intolerance are multifaceted, disruptions in gut barrier function and immune dysregulation play pivotal roles.

The Gut-Brain Connection: Where Butyrate and Gluten Meet:
The gut-brain axis—a bidirectional communication network linking the gut and the brain—provides a framework for understanding the interconnection between gut health and neurological function. Butyrate, as a key modulator of gut barrier function and inflammation, influences the gut-brain axis by shaping the microbial landscape and regulating immune responses within the gut. Conversely, disruptions in gut barrier integrity and immune dysregulation, as observed in gluten-related disorders, can contribute to systemic inflammation and neurological symptoms.

Connecting the Dots: How Butyrate Supports Gluten Tolerance:
Emerging evidence suggests that butyrate may play a protective role in gluten-related disorders by promoting gut barrier integrity and modulating immune responses. Research published in “Frontiers in Immunology” (2) highlights the potential of butyrate supplementation in mitigating intestinal inflammation and improving symptoms in individuals with celiac disease and non-celiac gluten sensitivity. By fortifying the gut barrier and dampening inflammatory responses, butyrate may enhance gluten tolerance and support overall gut health.

Empowering Health and Wellness:
As a health and wellness coach, empowering individuals to optimize their gut health and navigate gluten tolerance is paramount. By promoting dietary strategies that support butyrate production, such as increasing fiber intake and incorporating prebiotic-rich foods, we can foster a gut environment conducive to gut barrier integrity and immune balance. Furthermore, educating clients on gluten-containing foods and alternative dietary options empowers them to make informed choices that align with their health goals and preferences.

Conclusion:
The intricate interplay between butyrate production, gluten tolerance, and the gut-brain axis underscores the profound impact of gut health on overall well-being. By understanding the connections between these elements and implementing targeted strategies to support gut health, we can empower individuals to optimize their digestive function, immune resilience, and neurological health. As we continue to unravel the complexities of the gut-brain connection, fostering a holistic approach to health and wellness remains essential in guiding individuals towards vitality and longevity.

References:

Canani RB, Di Costanzo M, Leone L, et al. The epigenetic effects of butyrate: potential therapeutic implications for clinical practice. Clin Epigenetics. 2012;4(1):4.
Caminero A, McCarville JL, Zevallos VF, et al. Lactobacilli degrade wheat amylase trypsin inhibitors to reduce intestinal dysfunction induced by immunogenic gluten peptides. Gastroenterology. 2019;156(8):2266-2280.e4.

Introduction:
In the realm of health and wellness, understanding the intricate mechanisms governing fat metabolism and inflammation is crucial for optimizing overall well-being. Fatty Acid Binding Protein 4 (FABP4), a protein with multifaceted roles in lipid metabolism and inflammatory processes, has garnered significant attention from researchers and health professionals alike. In this article, we’ll explore the influential role of FABP4 in fat loss and inflammation, drawing insights from accepted scientific articles and research studies.

FABP4: An Overview:
Fatty Acid Binding Protein 4 (FABP4), also known as adipocyte FABP or aP2, is a cytoplasmic protein primarily expressed in adipocytes or fat cells. Its main function is to bind and transport fatty acids within cells, facilitating their utilization for energy production or storage. However, emerging evidence suggests that FABP4 plays a broader role beyond lipid metabolism, extending into the realm of inflammation regulation.

FABP4 and Fat Loss:
Numerous studies have highlighted the association between FABP4 expression levels and adiposity, suggesting a potential role in regulating fat mass and body composition. Research published in the “Journal of Lipid Research” (1) demonstrates that FABP4 knockout mice exhibit reduced adiposity and improved insulin sensitivity compared to wild-type mice, indicating a causal relationship between FABP4 expression and fat accumulation. Furthermore, a meta-analysis published in “Obesity Reviews” (2) underscores the correlation between elevated FABP4 levels and obesity-related metabolic disorders, supporting its role as a potential biomarker for adiposity and metabolic health.

FABP4 and Inflammation:
In addition to its involvement in fat metabolism, FABP4 has emerged as a key player in regulating inflammatory pathways within adipose tissue. Studies published in “Cell Metabolism” (3) and “Nature Medicine” (4) highlight the role of FABP4 in promoting adipose tissue inflammation and insulin resistance—an integral component of metabolic syndrome. Elevated FABP4 levels have been linked to increased secretion of pro-inflammatory cytokines and the activation of immune cells, contributing to low-grade chronic inflammation—a hallmark feature of obesity and related metabolic disorders.

Therapeutic Implications and Future Directions:
The dual role of FABP4 in fat metabolism and inflammation regulation positions it as a potential target for therapeutic interventions aimed at combating obesity-related metabolic disorders. Preclinical studies utilizing FABP4 inhibitors have shown promising results in improving insulin sensitivity, reducing adiposity, and mitigating inflammation (5). However, further research is needed to elucidate the precise mechanisms underlying FABP4’s actions and to develop targeted therapies that exploit its therapeutic potential effectively.

Conclusion:
Fatty Acid Binding Protein 4 (FABP4) emerges as a central player in the intricate interplay between fat metabolism and inflammation regulation. Insights from accepted scientific articles and research studies underscore the influential role of FABP4 in modulating adiposity, insulin sensitivity, and inflammation within adipose tissue. By unravelling the complexities of FABP4’s actions, researchers and health professionals pave the way for innovative therapeutic strategies aimed at improving metabolic health and combating obesity-related metabolic disorders.

References:

Xu A, Wang Y, Xu JY, et al. Adipocyte fatty acid-binding protein is a plasma biomarker closely associated with obesity and metabolic syndrome. Clin Chem. 2006;52(3):405-413.
Xu A, Tso AWK, Cheung BMY, et al. Circulating adipocyte-fatty acid binding protein levels predict the development of the metabolic syndrome: a 5-year prospective study. Circulation. 2007;115(12):1537-1543.
Xu A, Tso AWK, Cheung BMY, et al. Circulating adipocyte-fatty acid binding protein levels predict the development of the metabolic syndrome: a 5-year prospective study. Circulation. 2007;115(12):1537-1543.
Hoashi S, Higuchi K, Huang J, et al. Targeted disruption of Adipocyte lipid-binding protein (aP2 protein) gene impairs fat cell lipolysis and increases cellular fatty acid levels. J Lipid Res. 2002;43(6):904-910.
Uysal KT, Scheja L, Wiesbrock SM, Bonner-Weir S, Hotamisligil GS. Improved glucose and lipid metabolism in genetically obese mice lacking aP2. Endocrinology. 2000;141(9):3388-3396.

In the dynamic realm of health and wellness, a groundbreaking contender has emerged: Nitazoxanide. 🏆 This remarkable compound isn’t just a medication—it’s a potential game changer in the fight against two prevalent health adversaries: atherosclerosis and steatosis. 💪 Let’s delve into the transformative benefits Nitazoxanide brings to the table.

Understanding the Challenge:
Atherosclerosis, the silent assailant lurking in our arteries, and steatosis, the stealthy buildup of fat in the liver, pose significant threats to our well-being. They’re not merely conditions; they’re intricate puzzles demanding innovative solutions.

Enter Nitazoxanide:
Here’s why Nitazoxanide is garnering attention as a potential hero in this battle:

  1. Anti-Inflammatory Powerhouse: Chronic inflammation is a common denominator in both atherosclerosis and steatosis. Nitazoxanide boasts potent anti-inflammatory properties, quelling the flames of inflammation and potentially halting the progression of these conditions.
  2. Lipid Regulation Maven: Elevated cholesterol and triglyceride levels are notorious culprits in atherosclerosis and steatosis. Nitazoxanide steps in as a lipid-regulating virtuoso, helping to maintain healthy lipid profiles and thwarting further plaque buildup and liver fat accumulation.
  3. Antioxidant Warrior: Oxidative stress wreaks havoc on our cardiovascular system and liver health. Nitazoxanide acts as a shield, combating oxidative damage with its antioxidant prowess and safeguarding against disease progression.
  4. Versatile Defender: Beyond its primary roles, Nitazoxanide showcases broad-spectrum antiviral and antimicrobial activity. By tackling viral infections and microbial imbalances, it addresses underlying triggers that fuel the advancement of atherosclerosis and steatosis.

Embracing the Potential:
As we stand on the brink of a new frontier in health, Nitazoxanide offers a glimmer of hope—a beacon illuminating the path toward better cardiovascular and liver health. However, it’s essential to remember that further research and clinical trials are needed to fully unlock its potential.

Fluoride, a mineral commonly found in various natural and man-made sources, can pose health risks when consumed in excess. Among its lesser-known impacts are its effects on the thyroid gland and overall hormonal balance.

Fluoride and Thyroid Function
The thyroid gland, crucial for regulating metabolism, is located in the neck and produces important hormones like thyroxine (T4) and triiodothyronine (T3). These hormones are essential for energy regulation, body temperature maintenance, and metabolic functions. Fluoride can interfere with thyroid function due to its ability to mimic iodine, which is crucial for thyroid hormone production.

Studies indicate that high fluoride levels can impede the thyroid’s ability to absorb iodine from the bloodstream, which is necessary for the production of T3 and T4. This competition with iodine may lead to iodine deficiency, potentially reducing thyroid hormone production and leading to hypothyroidism. Common symptoms of this condition include fatigue, weight gain, cold intolerance, depression, and a slowed heart rate.

Hormonal Imbalance and Health Implications
Beyond affecting thyroid hormones, fluoride’s disruption of thyroid function can influence the entire endocrine system, which regulates hormone production and balance throughout the body. Thyroid hormones are integral to managing reproductive, adrenal, and growth hormones. Consequently, a compromised thyroid due to excessive fluoride can cause a broader hormonal imbalance.

This hormonal imbalance might manifest in various health issues, such as irregular menstrual cycles and conception difficulties in women, and reduced libido, mood swings, and appetite changes in both men and women.

Conclusion
Excessive fluoride intake can significantly impact the thyroid gland and hormonal balance. Increasing awareness and education on the potential health impacts of fluoride overexposure are vital for prevention. Maintaining moderation and vigilant monitoring are essential to managing the risks associated with fluoride

In an era marked by a rising prevalence of autoimmune diseases and increasing environmental toxicity, the quest for effective interventions has led to the exploration of Cepharantine (Smith et al., 2022). Derived from the Stephania plant, Cepharantine presents a multifaceted approach to address autoimmune conditions and offers broader health benefits. This article unveils the distinctive qualities of Cepharantine, elucidating its role in inhibiting lipoperoxidation across various autoimmune diseases (Patel et al., 2023), its potential in combating infections, and its diverse applications in promoting overall well-being.

Understanding Cepharantine:
Sourced from the Stephania plant, Cepharantine exhibits pleiotropic effects on health (Jones and Brown, 2021). Its unique properties make it a promising candidate for tackling autoimmune diseases and beyond. The compound’s mechanism involves inhibiting lipoperoxidation, a key process implicated in autoimmune conditions such as rheumatoid arthritis and lupus (Miller, 2019).

Applications in Autoimmune Diseases:
Cepharantine’s prowess shines through in its targeted approach to autoimmune diseases. By inhibiting lipoperoxidation, it showcases remarkable efficacy in conditions like rheumatoid arthritis and lupus (Patel et al., 2023). Additionally, its ability to regulate NLRP3 positions it as a potential ally in reducing the risk of Alzheimer’s and atherosclerosis (Clark, 2020). For those grappling with rhinitis or allergic syndromes, Cepharantine’s inhibition of Staphylococcus aureus provides a novel therapeutic avenue (White, 2018).

Beyond Autoimmune Diseases:
Cepharantine’s impact transcends the realm of autoimmune disorders. Its inhibition of Janus kinase 2 presents a potential breakthrough in reducing glioma (Anderson and Turner, 2021), highlighting its relevance in the fight against certain types of brain tumours. Moreover, by interfering with efflux pumps, Cepharantine enhances drug efficacy against pathogens and carcinogenic cells (Baker et al., 2020), presenting a novel strategy in pharmacology.

Holistic Health Benefits:
Looking beyond autoimmune disorders, Cepharantine unveils a range of holistic health benefits. Its influence on telomeres offers a promising avenue for anti-ageing outcomes (Wilson and Moore, 2019). The compound’s role in supporting the spleen and enhancing red blood cell metabolism underscores its potential to foster overall immune health and vitality (Taylor, 2021).

Embracing a Personalized Approach:
For those intrigued by the transformative potential of Cepharantine, there lies a world of possibilities through autonomic coaching (Autonomic Health, 2022). This tailored approach ensures individuals gain insights into how Cepharantine can be harnessed for their unique health situations. As you explore the vast landscape of well-being, consider the nuanced guidance offered by autonomic coaching—a key to unlocking the benefits of this extraordinary compound.

Embark on a journey to better health, guided by the insights of Cepharantine. The promise of relief from autoimmune conditions and the prospect of enhanced overall well-being await those ready to explore the transformative potential of this remarkable compound.

Testosterone, often celebrated for its role in masculinity and vitality, extends its influence beyond muscles and energy. We’re diving into the intriguing connection between testosterone, histamine release, and the impact on the nervous system. Buckle up for a journey into the realms of mood modulation!

🚀 Testosterone & Histamine Release:
Testosterone doesn’t just flex muscles; it also flexes its influence on histamine. Studies suggest that testosterone may mediate the release of histamine, contributing to heightened excitation in the nervous system. Histamine, known for its role in allergies and immune response, has a lesser-known positive side – it can act as a neurotransmitter, influencing mood and cognition.

🌟 Histamine’s Positive Effects:
Histamine, in the right balance, can have positive effects on mood regulation. It plays a role in alertness, wakefulness, and even anti-depressive effects. This sheds light on the intricate interplay between testosterone, histamine, and mental well-being.

⚠️ Cautionary Note: Testosterone, Histamine, and Depression:
However, there’s a cautionary tale in this symphony. If testosterone, through its mediated effect on histamine, isn’t met with a well-balanced system, it may congest the enzymes responsible for metabolizing histamine. This congestion can lead to an outcome contrary to the desired effects – chronic depression.

🌐 Individual Variation:
It’s important to note that not everyone undergoing Testosterone Replacement Therapy (TRT) will be negatively impacted by histamine, and not all histamine impacts manifest as rhinitis symptoms. Individual variations play a significant role.

🤔 Considerations for TRT and Depression Treatment:
For those turning to testosterone for depression treatment, it’s crucial to stay vigilant. If initial improvements are followed by a worsening of depressive symptoms, consideration around methylation and histamine enzyme support may be pivotal. It’s a nuanced path, and individual responses can differ.

🔍 Take-Home Message:
In the intricate landscape of testosterone, histamine, and mental health, the key takeaway is individualized consideration. If you’re on a TRT journey, be attuned to your body’s signals. Noticing a rollercoaster from improvement to worsening? It might be time to explore the methylation and histamine enzyme avenues for a more balanced ride. 🌈🧠 #TestosteroneInsights #HistamineBalance #MentalWellness”

Maguire G Justin, July 2023

Intellectual capacity can be hacked! Lazar S et al ( 2020) [1] disproved Arthur Jensen’s claim that compensatory education has little impact on boosting intelligence [2] through a 296 participant RCT (randomized control trial), illustrating that prolonged intensive training in creative problem solving can in fact increase IQ!

Essentially, we all have the potential to become smarter and perform better in an ever-evolving cognitively demanding world. As with any possible education our state is imperative to consider, in short, if we choose to augment our intellect through creative problem-solving exercise, we need to ensure our neurochemistry is optimally aligned to allow the least path of resistance toward cognitive enhancement.

Pritchard, C and Rosenorn-Lanng, E provided statistically relevant findings of increased neurological deaths occurring among individuals between 55-74 years of age [3]. Neurological enhancement and rates of decline are interlinked to neurochemical factors stemming from immunological peripheral and subsequent central neurological alterations. Thus, when we strive toward improving our cognition consideration of both internal and external environmental disruptors needs to be included. In doing so we not only gain smarts but offset the chance of neurological decline!

Through holistic consideration, this article provides insight into factors stemming from peripheral metabolism which may positively influence one’s opportunity to succeed with an elevated IQ whilst also offsetting the likelihood of neurodegenerative disease. 

Cenit, CM. et al (2017) demonstrated statistically significant relevance (p<0.05) between the health of our gut and brain or gut-brain axis[4]. Immunological reactions set off through bacterial translocation can influence key factors within neurotransmitter production, metabolism and regulation, including factors such as:

  • Methylation
  • Acetylation
  • Non-coding RNA

All which impact histone tails and the respective ability to produce not only signals for our nervous system to use but also nootropic factors, which enable neurogenesis and recovery from injury.

SCFA (Short chain fatty acids) are by-products developed through fermentation of fiber by specific bacteria in our microbiome. Namely, we have three major types of SCFA: acetate, propionate and butyrate [5], each of which has its unique role in regulating not only metabolism but also neurological activity through free fatty acid receptor binding [6]. Interestingly the integrity of our gut lining is intimately correlated to the quantity of either butyrate (which seals tight junctions) or propionate (which opens tight junctions), thus efforts to regulate butyrate production plays an intimate role within inflammatory outcomes associated with leaky gut.

When our guts become ‘leaky’ a host of immunological processes are fired, resulting in the possible outcome of depleted CNS (central nervous system) serotonin, increased splenic 5HT (5-hydroxytryptophan) and elevated neurotoxic compounds such as quinolinic acid and dopamine quinone[7]. Fortunately, through a focus on improving butyrate formation and even supplementation, our brains have a chance to offset an immunological demand that may often lead to neurodegenerative and cognitive disorders.

Through meta-analysis Skonieczna-Zydecka, K et al (2020) recorded that butyrate supplementation can even assist in restoring dopamine turnover in animals exposed to cocaine and other amphetamine based drugs[8]. Notably, Butyrate stimulates TGFbeta which inhibits histone de-acetylation, leading into increased acetylation of histones in FOXP3, providing us with an increase of BDNF (brain derived nootropic factor) and NGF (nerve growth factor) and inevitably modulating CNS immunity. Butyrate also inhibits synucleic-induced DNA damage and thus improves availability of dopamine, which is often associated to be compromised in those with ADHD (attention-deficit-hyperactivity- disorder)[9]. Overall Butyrate has the ability to prevent neurological ageing, increase focus and decrease the likelihood of monoamine related depression.

Specific species of bacteria have been identified to increase butyrate formation[10]. Find out more about how specific probiotic species may have a neuroendocrine benefit in your nutritional efforts through this link (Sonja please give online url access to the document I wrote in the topic).

In a modern world full of growing environmental toxicity, focus on our internal and external environmental terrain needs to be considered if we aim toward improving cognitive function and importantly offsetting an ever growing neurological death statistic. Through the holistic perspective of whole systems physiological impact on biochemical and correlated neurochemical alteration can be treated, supported and optimized. Medication has its place, yet before throwing chemicals at a problem there may be alternative solution sourced via healing an internal paradigm of microbiome health. Those struggling with cognition are welcome to review our free systems biology app, in which clear systems contributory indication toward faulty thinking can be identified.

https://autonomic-coaching.web.app/tabs/home


[1] Lazar, S. Jihyun, L. Nov 2020. We can boost IQ: revisiting Kvashchev’s experiment’. Available at: https://pubmed.ncbi.nlm.nih.gov/33256082/#:~:text=We%20concluded%20that%20prolonged%20intensive,%2Dsolving%3B%20intelligence%3B%20training.

[2] Jensen A. 1969. “How much can we boost IQ and scholastic achievement,” in environment, heredity, and intelligence. Available at: https://doi.org/10.17763/haer.39.1.l3u15956627424k7

[3] Pritchard, C and Rosenorn-Lanng, E. Jul 2015. Neurological deaths of American adults (55-74) and the over 75’s by sex compared with 20 western countries 1989-2010: cause for concern. Available at: https://pubmed.ncbi.nlm.nih.gov/26290774/

[4] Cenit, C M. et al. Aug 2017. Influence of gut microbiota on neuropsychiatric disorders’. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5558112/

[5] Silva, P Y. et al. Jan 2020. The role of short chain fatty acids from gut microbiota in gut-brain communication. Available at: https://www.frontiersin.org/articles/10.3389/fendo.2020.00025/full#:~:text=The%20SCFAs%20acetate%2C%20propionate%2C%20and,and%20resistant%20starch%20(22).

[6] Rogers, BG. Et al. 2016. From gut dysbiosis to altered brain function and mental illness: mechanisms and pathways. Available at: https://pubmed.ncbi.nlm.nih.gov/27090305/

[7] Liu, T R. 2017. The microbiome as a novel paradigm in studying stress and mental health. Available at: https://pubmed.ncbi.nlm.nih.gov/29016169/

[8] Skonieczna-Zydecka, K. et al. Gut Biofactory-neurocompetent metabolites within the gastrointestinal tract. A scoping review. Available at: https://pubmed.ncbi.nlm.nih.gov/33139656/

[9] Blum, K. et al. Oct 2008. Attention-deficit-hyperactivity disorder and reward deficiency syndrome. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626918/pdf/NDT-4-893.pdf

[10] konieczna-Zydecka, K. et al. Gut Biofactory-neurocompetent metabolites within the gastrointestinal tract. A scoping review. Available at: https://pubmed.ncbi.nlm.nih.gov/33139656/