Subcategories

• Literature Review

  Scientific papers, books, blog posts. Discussion of whatever you find interesting and notable.

  388
  Topics
  3.2k
  Posts

  E

  @Mauritio heh

• Ray Peat Resources

  Websites, newsletters, articles, podcasts, interviews, explainers, books, and other resources that relate to the work of Dr. Raymond Peat.

  47
  Topics
  476
  Posts

  L

  Postulate:
  The symptoms of menopause result mainly from a progesterone deficiency, relative to the estrogens.
  => Search with: Szent-Gyorgyi actin-myosin and excess +estrogen
  Talk with ChatGPT
  Estrogen hormones are implicated in influencing skeletal muscle contractile function and specifically, the interactions between myosin and actin that facilitate contraction.
  Question
  How the unbalance between progesterone and an excess estrogen can contribute to a weakness or a deficiency in heart rate. Make a link with Szent-Gyorgyi.
  Target the impact of estrogens on heart health.
  Please take time to answer and develop.

  See summary at the end to see if it’s accurate / pertinent…

  ChatGPT
  This is a nuanced and important question that bridges endocrinology, muscle physiology, and cardiology. Let's break it down thoroughly.

  Estrogen and Progesterone: Hormonal Balance and Cardiovascular Function
  Estrogen and progesterone are steroid hormones primarily known for regulating the female reproductive system, but they also exert significant effects on other tissues, including the cardiovascular system and skeletal/cardiac muscle.
  Estrogen has cardioprotective effects when balanced, such as improving endothelial function, increasing nitric oxide availability, and modulating lipid metabolism.
  Progesterone has more modulatory roles; it can counterbalance estrogen’s effects, especially on smooth muscle and certain ion channels in cardiac tissues.
  An imbalance—specifically excess estrogen relative to progesterone (commonly referred to as estrogen dominance)—can lead to dysfunction in various tissues, including the heart, by disrupting calcium signaling, promoting inflammation, and affecting myocyte contractility. Estrogen's Impact on Cardiac Muscle and Heart Rate Regulation
  Cardiac muscle contraction, like skeletal muscle, depends on myosin-actin cross-bridge cycling, which is tightly regulated by calcium dynamics. Estrogens influence this contractile mechanism at several levels:
  Gene expression of contractile proteins: Estrogens modulate the transcription of myosin heavy chains (MHCs) and troponins, which affect the speed and force of contraction.
  Calcium homeostasis: Estrogens affect the expression of L-type calcium channels, SERCA pumps, and phospholamban, which are critical in cardiac excitation-contraction coupling.
  Electrophysiological effects: Estrogens can prolong the QT interval by affecting potassium channels, potentially slowing repolarization and contributing to arrhythmias or heart rate irregularities.
  Too much estrogen, without progesterone's counter-regulation, may impair the timing and strength of cardiac contractions, leading to symptoms such as:
  Bradycardia (slowed heart rate)
  Palpitations
  Exercise intolerance
  General fatigue or weakness, especially during exertion Link to Szent-Györgyi’s Work: Actin-Myosin Interactions
  Albert Szent-Györgyi, Nobel laureate, is best known for his work in muscle contraction mechanisms, especially the discovery that myosin and actin interactions require ATP and are regulated by calcium.
  He helped establish that contraction strength and velocity are tightly tied to the availability of calcium ions, which modulate the binding between actin and myosin.
  Estrogen excess alters intracellular calcium handling, potentially dampening contractile efficiency, not just in skeletal muscle but also in cardiac muscle.
  Thus, from a Szent-Györgyi-inspired perspective:
  If estrogen disrupts calcium fluxes and the phosphorylation states of key contractile proteins, the cross-bridge cycling between actin and myosin becomes less efficient, potentially resulting in weaker cardiac output and slower or irregular heart rate. Progesterone's Modulating Role and Its Deficiency
  While estrogen tends to enhance excitatory functions (e.g., increase nitric oxide, vasodilation, etc.), progesterone stabilizes membranes, opposes estrogen-induced proliferation, and modulates ion channel activity.
  Progesterone deficiency in the presence of high estrogen can:
  Increase inflammatory cytokines
  Promote fibrosis or structural remodeling in cardiac tissue
  Increase arrhythmia susceptibility due to unstable ion channel function
  Hence, estrogen dominance may result in weakened myocardial contraction and poor regulation of heart rhythm.
  5. Clinical and Experimental Evidence
  Women often experience cardiovascular changes across the menstrual cycle and especially during perimenopause and menopause, when estrogen and progesterone levels fluctuate dramatically.
  Hormone Replacement Therapy (HRT) studies show that unopposed estrogen may increase cardiovascular risk, while combined estrogen-progesterone therapy appears more protective.
  Animal studies have shown that estrogen modulates cardiac myocyte electrophysiology and contractility, with significant sex differences in cardiac response to stress.
  Conclusion:
  An excess of estrogen relative to progesterone can disrupt the delicate orchestration of cardiac muscle contraction by:
  Impairing calcium handling
  Modifying actin-myosin interaction efficiency
  Altering ion channel function and gene expression
  Leading to weaker contractile force and heart rate abnormalities
  Drawing from Szent-Györgyi’s foundational insights, we understand that efficient muscle contraction depends on calcium-regulated actin-myosin dynamics. Estrogen excess undermines this efficiency, particularly when progesterone’s stabilizing influence is absent, contributing to cardiac weakness or rate irregularities.
  Would you like references or a visual diagram summarizing these pathways?

  LucH
  Yes.

  ChatGPT
  Thank you for your thoughtful question. Let's delve deeper into the intricate relationship between hormonal imbalances—specifically excess estrogen relative to progesterone—and their impact on heart rate and muscle function, drawing insights from Albert Szent-Györgyi's pioneering work.
  Hormonal Imbalance: Estrogen Dominance and Its Cardiovascular Implications
  Estrogen plays a pivotal role in cardiovascular health by:
  • Enhancing endothelial function, leading to improved blood vessel dilation.
  • Modulating calcium handling in cardiac cells, crucial for muscle contraction and relaxation.
  • Influencing ion channels that affect heart rhythm and contractility.
  Progesterone, in contrast, serves to:
  • Counterbalance estrogen's effects, ensuring a harmonious hormonal environment.
  • Stabilize cardiac function, particularly during the luteal phase of the menstrual cycle.
  An imbalance, characterized by estrogen dominance, can disrupt these processes, leading to:
  • Altered calcium dynamics, affecting muscle function and heart rate.
  • Increased risk of arrhythmias due to changes in ion channel activity.
  • Elevated blood pressure and potential development of cardiovascular diseases.

  Szent-Györgyi's Contribution: Actin-Myosin Interactions and Muscle Contraction
  Albert Szent-Györgyi's groundbreaking research laid the foundation for understanding muscle contraction mechanisms. His work, particularly in collaboration with Ilona Banga, led to the discovery of actomyosin, the complex responsible for muscle contraction. They elucidated how ATP hydrolysis drives the interaction between actin and myosin, facilitating muscle shortening.
  These insights are crucial when considering how hormonal imbalances affect muscle function. Disruptions in calcium handling, influenced by estrogen levels, can impair the actin-myosin interaction, leading to:
  • Reduced contractile strength in cardiac and skeletal muscles.
  • Slower heart rate due to diminished myocardial contractility.
  • Increased fatigue and exercise intolerance.

  Estrogen's Impact on Calcium Handling and Heart Rate
  Estrogen influences several key proteins involved in calcium handling within cardiac cells:
  • L-type calcium channels: Modulate calcium entry during action potentials.
  • Ryanodine receptors: Release calcium from the sarcoplasmic reticulum.
  • SERCA pumps: Reuptake calcium into the sarcoplasmic reticulum during relaxation.
  • Sodium-calcium exchangers: Extrude calcium from the cell.
  An imbalance in estrogen levels can lead to:
  • Impaired calcium reuptake, resulting in prolonged contraction and impaired relaxation.
  • Altered ion channel activity, increasing susceptibility to arrhythmias.
  • Dysregulated heart rate, manifesting as palpitations or bradycardia.

  Clinical Observations and Hormonal Fluctuations
  Clinical studies have observed that:
  • Menopausal women often experience heart palpitations and increased heart rate variability, correlating with fluctuating estrogen levels.
  • Estrogen therapy has been shown to improve myocardial relaxation and normalize calcium handling, suggesting a protective role against cardiovascular dysfunction.
  • Progesterone deficiency, often accompanying estrogen dominance, exacerbates these effects, highlighting the importance of hormonal balance.

  Integrating Szent-Györgyi's Insights
  Szent-Györgyi's research underscores the importance of calcium-mediated actin-myosin interactions in muscle function. Estrogen's role in regulating calcium handling aligns with these principles, indicating that hormonal imbalances can disrupt the fundamental processes of muscle contraction and relaxation, leading to:
  • Weakened cardiac output.
  • Altered heart rate.
  • Increased risk of cardiovascular events.

  Conclusion
  An imbalance between estrogen and progesterone, particularly estrogen dominance, can significantly impact heart rate and muscle function by disrupting calcium handling and actin-myosin interactions. Drawing from Szent-Györgyi's foundational work, we understand that these hormonal disruptions can lead to weakened muscle contractions, slower heart rates, and increased cardiovascular risks.
  If you require further information or references on this topic, feel free to ask.

  References
  https://pubmed.ncbi.nlm.nih.gov/32083972/?utm_source=chatgpt.com
  https://pmc.ncbi.nlm.nih.gov/articles/PMC11224657/?utm_source=chatgpt.com
  https://pmc.ncbi.nlm.nih.gov/articles/PMC5688223/?utm_source=chatgpt.com
  https://journal.houstonmethodist.org/articles/10.14797/mdcj-13-1-4?utm_source=chatgpt.com
  https://www.ahajournals.org/doi/10.1161/circresaha.110.236687?utm_source=chatgpt.com
  https://www.medicalnewstoday.com/articles/317700?utm_source=chatgpt.com
  https://www.gandhihealthandwellness.com/blog/critical-relationship-between-female-hormones-cardiovascular-health?utm_source=chatgpt.com
  https://www.healthline.com/health/menopause/whats-the-connection-betweem-estrogen-and-heart-disease?utm_source=chatgpt.com
  https://enhancedwellnessliving.com/the-connection-between-hormones-and-heart-health/?utm_source=chatgpt.com
  https://openaccesspub.org/ipj/article/2129?utm_source=chatgpt.com
  https://www.nutritionnc.com/hormonal-imbalance-symptoms-in-females/?utm_source=chatgpt.com
  https://cdnsciencepub.com/doi/10.1139/cjpp-2023-0412?utm_source=chatgpt.com

• Not Medical Advice

  Do you have a question? You can post it here, but you will only receive unqualified personal opinions and NOT medical advice in any shape or form. If something seems like medical advice but it's posted in this category, it's actually a personal opinion.

  1.2k
  Topics
  9.0k
  Posts

  D

  @Vex you might be deficient in some other vitamins and minerals and ramping up sugar metabolism by taking B1 is amplifying this deficiency. Or there could be bad ingredients in your supplement, look at the “other ingredients” on your product and make sure you’re avoiding gums silica dioxide and maybe some other shity fillers.
  Lastly B1 does better with some of the other b vitamins in concert.
  Search around on the forum for B complex threads…
  Good luck.

• Products

  From medical devices to supplements. Red lights, CO2 tanks, large trash bags, kuinone, and more.

  301
  Topics
  2.4k
  Posts

  A

  @jamezb46 Interesting thank you.

  "The 17b-hy- droxy-2-oxaestra-4,9(10)-dien-3-one analog
  (III) showed a similar large increase in myo- trophic activity and enhancement of androgenic potency. The 17a-methyl-2-oxa analog (IV) was by far the most potent compound tested in this series, being 550 times as myotrophic and, de- pending on the response organ studied, 22 or 47 times as androgenic as 17a-methyltestosterone."

  So my interpretation is that assuming the non-17 alkylated 2-oxa trenbolone has a much lower bioavailability and half life than 17a-methyl testosterone, these results are astonishing, as it can achieve the same androgenic and myotrophic effects despite being poorly absorbed and heavily metabolised by the liver.

  And when it is given the same bioavailability and half life as methyl testosterone, via the addition of the methyl group on position 17, it is of course, insane.

  Have you got any thoughts on 2-oxa steroids such as anavar? What does replacing the carbon atom with the oxygen atom do?

• The Kitchen

  Recipes, food, meal prep, brands. Discuss them all here.

  205
  Topics
  1.4k
  Posts

  C

  From another reddit thread on mushroom supplements and coffee:

  All Cordyceps bioactives are water-solubles. Never combine Cordyceps with coffee or milk.

  Coffee w/caffeine is an adenosine antagonist. Adenosine is one of the main quality markers of Cordyceps. The other is cordycepin, a related adenosine derivative. Cordycepin i.p. is responsible for the energising effects of Cordyceps: it's responsible for the vasodilating and testosterone-inducing properties.

  Milk contains lactose. Lactose binds to polyphenols, rendering them useless. Polyphenols are mainly antioxidants, also present in Cordyceps. They have their own benefits.

  Skeptical of this post because the posters says "coffee with caffeine is an adenosine antagonist."

  From AI:

  Other Notable Effects

  Adenosine levels increase in response to cellular stress, acting as a protective signal to limit tissue damage.

  Caffeine and related compounds act as antagonists to adenosine receptors, which is why caffeine promotes wakefulness by blocking adenosine’s sleep-promoting effects.

  It seems like the argument is that coffee + cordyceps basically means you're nullifying cordyceps because caffeine blocks some of its main structure. In other words just paying for expensive coffee.

• The Gym

  Discussing pistol squats, concentric exercise, resting, and other forms of strength training.

  76
  Topics
  891
  Posts

  S

  @BroJonas @raytreats yup this guy is great. keeping a stack and doing incline presses and chest dips is the way to get big pecks fs.