Channel Title: Science Simplified Channel Description: My MCAT score was 99% Biochem/Biology and 97% Physics/Chem. This channel was made to provide free MCAT content that focuses on the most high-yield topics for the MCAT. <video> Induction vs Resonance (Rules of Organic Chemistry #4) Description: The Most Important Principle you must Understand to get an A+ in Organic Chemistry https://www.youtube.com/watch?v=7gIQySNjqPk Carbocation vs Carboanion Stability https://www.youtube.com/watch?v=jXCbXZNtuuM Acid Strength vs Base Strength https://www.youtube.com/watch?v=L6_m-y5Y3qM Leaving Group Stability https://www.youtube.com/watch?v=NiyuQ4QGiuI&t=783s Induction vs Resonance https://www.youtube.com/watch?v=-7klbNXGQyg&t=727s Analyzing Nucleophile vs Electrophiles Strength https://www.youtube.com/watch?v=EeO6hSGm6s0&t=262s Melting Point, Freezing Point and Boiling Point Trends https://www.youtube.com/watch?v=JASxAtNPxfE Introduction to Electron Orbital Hybridization (sp3, sp2, sp) https://www.youtube.com/watch?v=00O0j40mKV0 </video> <video> The Most Important Principle you need to Understand to get an A+ in Organic Chemistry!!! Description: The Most Important Principle you must Understand to get an A+ in Organic Chemistry https://www.youtube.com/watch?v=7gIQySNjqPk Carbocation vs Carboanion Stability https://www.youtube.com/watch?v=jXCbXZNtuuM Acid Strength vs Base Strength https://www.youtube.com/watch?v=L6_m-y5Y3qM Leaving Group Stability https://www.youtube.com/watch?v=NiyuQ4QGiuI&t=783s Induction vs Resonance https://www.youtube.com/watch?v=-7klbNXGQyg&t=727s Analyzing Nucleophile vs Electrophiles Strength https://www.youtube.com/watch?v=EeO6hSGm6s0&t=262s Melting Point, Freezing Point and Boiling Point Trends https://www.youtube.com/watch?v=JASxAtNPxfE Introduction to Electron Orbital Hybridization (sp3, sp2, sp) https://www.youtube.com/watch?v=00O0j40mKV0 </video> <video> Why Health Guidelines Recommend Majority Plant Based Diet (Brief Summary In Description) Description: The totality of longevity research suggests HIGH mTOR activity accelerates the rate of aging, and therefore the onset of virtually every age-related disease (including cancer). This is because mTOR is a large protein complex that regulates global changes in gene expression that regulate the rate of GROWTH (e.g. rate of aging through biological stages of life). However, some argue 1) exercise activates mTOR 2) exercise is good for health 3) therefore mTOR cannot be relevant in human disease. I disagree with this narrative. Exercise activates mTOR only in skeletal muscle (through a unique mechanism involving muscle contraction). However, skeletal muscle cells VIRTUALLY NEVER BECOME CANCEROUS because they’re non-dividing post-mitotic cells with negligible capacity for malignancy due to lacking cellular machinery for cell division, and therefore are NOT subject to the pathological effects of high mTOR activity. Ironically, exercise actually REDUCES mTOR activity in virtually every OTHER cell in the body (outside of skeletal muscle cells). This is because exercise increases muscle-mass, increasing insulin sensitivity, which reduces insulin production, and therefore reduces “insulin activation of mTOR” that occurs in virtually every tissue in the body comprised of mitotically dividing cells. This reduced mTOR activity will rate-limit cell division, thus slowing the rate of telomere attrition, onset of replicative cellular senescence, and burning through Stem Cell reserves. Therefore, stating that exercise disproves the health effects of mTOR is irrational. What is accepted unanimously among longevity researchers is that HIGH mTOR activity DECREASES lifespan. mTORs effect on longevity really isn't a debated topic in research. However, protein is a hot topic for debate. This is because Insulin & IGF-1 partially activate mTOR, however you need Protein (e.g. BCAA, Methionine) for full complete activation of mTOR. Therefore high-protein diets should theoretically accelerate aging rate and onset of all age-related disease. To support this, Human Epidemiology is screaming that all data consistently points in this direction (opposed to what would be expected from data filled with random noise), many animal studies show HIGH protein will DECREASE lifespan, and the biochemistry mechanisms have been well established. So why the controversy? (outside of virtually every medical association guidelines) This is because high-protein increases muscle-mass, and increased muscle-mass is associated with improved health outcomes. I think this is misunderstood. First of all, muscle-mass has a "U-shaped” mortality curve, meaning low muscle-mass AND high muscle-mass are associated with shortened lifespan. So the notion "more muscle = better health" may simply be false. Second of all, I believe muscle-mass is associated with improved health outcomes because muscle-mass is a proxy for EXERCISE, and its the exercise that improves health outcomes, NOT protein (which totality of evidence suggests high-protein is associated with age-related disease). Essentially protein is stealing the credit of exercise, and having an optimal range of muscle-mass is beneficial because it’s a proxy for exercise, which is beneficial (VO2 Max is a clear marker of longevity). Excess amino acids get deaminated to enter central metabolism(basically function as carbs) & will NOT increase muscle mass because Muscle Protein Synthesis becomes REFRACTORY to amino acids after ~20-30 grams. Facts many high-protein advocates have trouble reconciling: 1)The #1 gold-standard for increasing lifespan in virtually every animal model (this is not debated) is Rapamycin which works by DECREASING mTOR, the exact opposite effect of Protein which INCREASES mTOR. Therefore, high-protein diets have the literal exact opposite biochemical effect of the #1 longevity intervention. Increased rate of protein turn-over is prone to forming mis-folded proteins. 2) In 2024, the current hottest topic in anti-aging research is Autophagy, the process where a low-protein diet triggers the SELECTIVE degradation of DYSFUNCTIONAL misfolded proteins in the cell to be used as a source of amino acids(think of activating a “spring cleaning” in old worn-out cells by breaking down ONLY the damaged proteins to be used as a source of amino acids). 3)Chronically HIGH mTOR blocks the activation of apoptosis in precancerous cells(due to tonic growth signal), thus enabling continued cell-division in precancerous cells, accumulation of additional mutations, and potentially increasing oncogenesis. Therefore, i’d be extremely hesitant to recommend a high-protein diet in healthy adults. My belief is the recommended dietary guidelines of a high plant-based diet, animal protein limited to 10%-35% of calories, 150 minutes of exercise per week, and avoiding obesity is optimal for longevity. These are the dietary guidelines, it’s not a conspiracy. (A growing child requires plenty of protein for optimal GROWTH) </video> <video> Beta Oxidation and Fatty Acid Metabolism (EVERYTHING YOU NEED TO KNOW FOR BIOCHEMISTRY MCAT) Description: Below is a video link that goes over every single major metabolic pathway you need to know for the MCAT!! https://www.youtube.com/watch?v=CCvAey4iwYM Ketogensis https://www.youtube.com/watch?v=oyNYa2Wj1to&t=36s </video> <video> The Advanced Pathophysiology of Insulin Resistance, Metabolic Syndrome, and Cardiovascular Disease Description: Hypertrophic adipose tissue — ectopic lipid -- lpl modification — higher residence time -- oxLDL LDLr -- liver lipid turnover — Gluconeogensis? Subcutaneous hypertrophy — macrophage THF-alpha & IL-6 & Lipolysis NEFA— DAG in liver — PKC epsilon in liver, PKC theta in muscle Iron -- Pancreas? </video> <video> Melting Point vs Boiling Point Polarity Trends (Rules of Organic Chemistry #5) Description: The Most Important Principle you must Understand to get an A+ in Organic Chemistry https://www.youtube.com/watch?v=7gIQySNjqPk Carbocation vs Carboanion Stability https://www.youtube.com/watch?v=jXCbXZNtuuM Acid Strength vs Base Strength https://www.youtube.com/watch?v=L6_m-y5Y3qM Leaving Group Stability https://www.youtube.com/watch?v=NiyuQ4QGiuI&t=783s Induction vs Resonance https://www.youtube.com/watch?v=-7klbNXGQyg&t=727s Analyzing Nucleophile vs Electrophiles Strength https://www.youtube.com/watch?v=EeO6hSGm6s0&t=262s Melting Point, Freezing Point and Boiling Point Trends https://www.youtube.com/watch?v=JASxAtNPxfE Introduction to Electron Orbital Hybridization (sp3, sp2, sp) https://www.youtube.com/watch?v=00O0j40mKV0 Below is a video link that goes into more detail on Formal vs Partial Charges https://www.youtube.com/watch?v=6r0k2RszhD8 </video> <video> Carbocation vs Carbanion Stability (Rules of Organic Chemistry #1) Description: The Most Important Principle you must Understand to get an A+ in Organic Chemistry https://www.youtube.com/watch?v=7gIQySNjqPk Carbocation vs Carboanion Stability https://www.youtube.com/watch?v=jXCbXZNtuuM Acid Strength vs Base Strength https://www.youtube.com/watch?v=L6_m-y5Y3qM Leaving Group Stability https://www.youtube.com/watch?v=NiyuQ4QGiuI&t=783s Induction vs Resonance https://www.youtube.com/watch?v=-7klbNXGQyg&t=727s Analyzing Nucleophile vs Electrophiles Strength https://www.youtube.com/watch?v=EeO6hSGm6s0&t=262s Melting Point, Freezing Point and Boiling Point Trends https://www.youtube.com/watch?v=JASxAtNPxfE Introduction to Electron Orbital Hybridization (sp3, sp2, sp) https://www.youtube.com/watch?v=00O0j40mKV0 </video> <video> Acid Strength vs Base Strength Principles (Rules of Organic Chemistry #2) Description: The Most Important Principle you must Understand to get an A+ in Organic Chemistry https://www.youtube.com/watch?v=7gIQySNjqPk Carbocation vs Carboanion Stability https://www.youtube.com/watch?v=jXCbXZNtuuM Acid Strength vs Base Strength https://www.youtube.com/watch?v=L6_m-y5Y3qM Leaving Group Stability https://www.youtube.com/watch?v=NiyuQ4QGiuI&t=783s Induction vs Resonance https://www.youtube.com/watch?v=-7klbNXGQyg&t=727s Analyzing Nucleophile vs Electrophiles Strength https://www.youtube.com/watch?v=EeO6hSGm6s0&t=262s Melting Point, Freezing Point and Boiling Point Trends https://www.youtube.com/watch?v=JASxAtNPxfE Introduction to Electron Orbital Hybridization (sp3, sp2, sp) https://www.youtube.com/watch?v=00O0j40mKV0 </video> <video> A Common Root Cause Of Chronic Diseases? (Why Many Longevity Meds Treat Diabetes) READ SUMMARY BELOW Description: We store calories from our diet in adipocytes. However, excessive calorie intake eventually overwhelms our adipocytes capacity to store energy, resulting in excess energy from our diet being stored in other tissues (called ectopic fat). One of the tissues that accumulate ectopic fat is Skeletal Muscle, which store the excess energy from our diet as IntraMyoCellular Lipids (The Liver also stores this excess energy, causing MAFLD). Normally, Insulin signals Skeletal Muscle to use blood glucose as a source of energy. However, when Skeletal Muscles accumulate IntraMyoCellular Lipids, they resist insulin's signal to uptake and use blood glucose as a source of energy(this is insulin resistance) because they already have IntraMyoCellular Lipid as a source of energy. When skeletal muscle becomes insulin-resistant, glucose remains elevated in the blood, triggering the pancreas to respond with compensatory hyperinsulinemia, which may accelerate the onset of age-related disease. Blood Insulin interacts with virtually every cell in our body by activating the mTOR pathway, which is at the center of regulating the rate of aging. The 3 interventions that most reproducibly extend longevity in virtually all animal models are Calorie Restriction, Rapamycin, IGF-Receptor Mutation. All these interventions extend longevity by INHIBITING mTOR, however hyperinsulinemia ACTIVATES mTOR, and may explain why hyperinsulinemia is one of the most predictive markers of all-cause mortality (accelerates rate of aging). Insulin also affects FOXO, the prototypical gene variant associated with longevity in population studies. This may explain why a large percentage of medications proven successful in the Nation Institute of Health "Intervention Testing Program" are Type-II Diabetes medications that reduce blood glucose, which ultimately reduces hyperinsulinemia and mTOR activity. However, insulin is still recommended for diabetics because hyperglycemia significantly affects quality of life (i.g. blindness, amputation), and Hyperglycemia results in advanced glycated end products which theoretically accelerate aging. Therefore, the ideal scenario is lifestyle management to address the root cause of hyperglycemia AND hyperinsulinemia. The link below goes into more details on mTORs role in aging. https://m.youtube.com/watch?v=wukZ6NUiyUw&feature=youtu.be Excessive insulin provides cells with pro-growth signals, enabling PRE-cancerous cells continued cell division and further accumulation of mutations. This is because insulin's “pro-growth” signals blunt the pro-apoptosis signals responding from DNA damage, allowing further cell proliferation and accumulation of DNA mutations in precancerous cells that SHOULD activate apoptosis due to excessive DNA mutation signals. Insulin activates mTOR, which up-regulates mitochondrial HK2, which functions to inhibit BAX, thus effectively preventing upstream DNA damage signals from inducing apoptosis through BAX, in precancerous cells. mTOR inhibits AMPK, which down-regulates HK2. Insulin increases free IGF-1, which interferes multiple control points of apoptosis. Also, mouse models genetically modified for the ability to induce high rates of DNA mutations show we’ve evolved remarkably efficient systems designed to prevent accumulation of DNA damage and precancerous cells, however carcinogen exposure coupled with attenuated repair systems (e.g. unregulated hyperinsulinemia blunting apoptosis) allow gradual accumulation of cells with DNA mutations that produce a malignancy that becomes unmanageable. Elephants have 4 quadrillion cells but lower cancer rates than humans, they also have x20 more copies of p53 than humans (most common mutation in human cancer), as reduced p53 activity permits oncogenesis. Insulin activated mTOR induces MDM2 translation which down-regulates p53, leading to chronic inhibition of natural cellular repair systems. I believe larons syndrome, metformin, and calorie restriction create time-intervals where PRE-cancerous cells are primed for apoptosis and removal, BUT CAN NOT TREAT MATURE MALIGNANCIES WHICH HAVE ALREADY DEVELOPED THE ONCOGENES THAT CAUSE UNREGULATED CELL PROLIFERATION, UNLESS TREATED WITH CYTOTOXIC INTERVENTIONS SUCH AS CHEMO, RADIATION, IMMUNOTHERAPY. Some argue that MAFLD (ectopic fat in liver) produces metabolites (acetyl-coa) that activate enzymes resulting in up-regulating gluconeogenesis, therefore contributing to hyperinsulinemia. I believe visceral fat is “associated” with Metabolic Syndrome because it’s a proxy for Ectopic fat in Skeletal Muscle and Liver. There are many factors not related to insulin that influence Coronary Artery Diseases, most importantly ApoB (proxy for LDL and atherogenic particle count). However, Obesity, IMCL, and Hyperinsulinemia affect lipoprotein dynamics and residence time. However, it’s important to emphasize there are many factors contributing to CAD, such as endothelial inflammation, oxLDL and Lp(a). </video> <video> Leaving Group Stability Trends (Rules of Organic Chemistry #3) Description: The Most Important Principle you must Understand to get an A+ in Organic Chemistry https://www.youtube.com/watch?v=7gIQySNjqPk Carbocation vs Carboanion Stability https://www.youtube.com/watch?v=jXCbXZNtuuM Acid Strength vs Base Strength https://www.youtube.com/watch?v=L6_m-y5Y3qM Leaving Group Stability https://www.youtube.com/watch?v=NiyuQ4QGiuI&t=783s Induction vs Resonance https://www.youtube.com/watch?v=-7klbNXGQyg&t=727s Analyzing Nucleophile vs Electrophiles Strength https://www.youtube.com/watch?v=EeO6hSGm6s0&t=262s Melting Point, Freezing Point and Boiling Point Trends https://www.youtube.com/watch?v=JASxAtNPxfE Introduction to Electron Orbital Hybridization (sp3, sp2, sp) https://www.youtube.com/watch?v=00O0j40mKV0 </video> <video> How Chronic Inhibition of Apoptosis Promotes Cancer Formation and Oncogenesis (READ SUMMARY BELOW) Description: Elephants have 4 quadrillion cells, meaning 4 quadrillion opportunities to develop just ONE cancerous cell. Despite this, they have significantly lower cancer incidence than humans. They also have x20 more copies of p53, the most commonly mutated gene found in human cancer. SUMMARY OF THEORY -DNA damage provides signals that should initiate apoptosis in precancerous cells. However, chronic exposure to signals that prevent apoptosis (such as BCAA, Hyper-Insulinemia, IGF-1) block the activation of apoptosis, which enables precancerous cells continued cell division that may promote oncogenesis. However, sensitizing precancerous cells to sense DNA damage to initiate apoptosis may modestly reduce cancer incidence. DNA damage sensitizing/pro-Apoptosis -Hypoxic exercising, calorie-restriction, metformin, IGF receptor mutations provide signals that allow for robust cellular damage surveillance systems to initiate apoptosis upon exposure of cellular damage. Aspirin may prime cancerous cells for apoptosis by enhancing p53 mediated DNA repair. Anti-Apoptosis -BCAA, chronic hyperinsulinemia, growth hormones provide signals that integrate into downstream pathways that regulate apoptosis. For example, constitutive exposure to BCAA and hyperinsulinemia block the pro-apoptosis signals responding from DNA damage, thus enabling precancerous cells the opportunity for continued cell division and accumulation of DNA damage because the pro-apoptosis signals are obstructed by pro-growth signals from constitutive exposure to BCAA, hyperinsulinemia, IGF-1. This may modestly increase the rate that precancerous cells develop further mutations that result in malignancy. NOTES -Increased apoptosis results in increased cell turnover, which can be an energetically wasteful process and perhaps explains why evolution did not select for further robust tumor suppression. -There’s a lot of evidence showing we’ve evolved remarkably efficient systems designed to repair and prevent DNA damage. Therefore, although carcinogens absolutely play a role in developing cancer, we’ve evolved natural cancer prevention systems that are remarkably efficient at prevent mutagenesis and cancer development. However, this is only true if we have robust p53 and Apoptosis activation and my explain why the most common mutation in cancer cells is p53, because disrupted p53 and apoptosis provides a foundation for uncontrolled mutagenesis and accumulation of mutations. Stabilizing p53 and promoting robust apoptosis systems will not prevent all cancers, but may modestly reduce cancer incidence. Nicotine products are filled with carcinogens that are highly mutagenic, however nicotine also inhibit important tumor suppressors involved in mediating the DNA damage response and immunosurveillance. -It’s important to distinguish direct vs indirect increases in p53 activity. For example, cigarette smoke induces cellular stress, which indirectly result in up-regulated p53. This is dangerous due to collateral cellular damage. However, EGCG directly stabilizes p53, without any collateral cellular damage. p53 plays a central role in integrating cellular stress towards the regulation of apoptosis. The goal would be to directly stabilize tumor suppressor proteins without the normally prerequisite collateral damage signals needed to upregulate p53. (Aspirin, diallyl disulfide, sulphurophane, apigenin, melatonin?). -Insulin activates mTOR, which upregulate pro-survival/antiapoptosis signals that inhibit apoptosis. There are several mechanisms, such as insulins activation of mTOR, which upregulates mitochondrial hexokinase2 activity which potently inhibits Bax, which is the primary downstream activator of apoptosis through release of cytochrome C. Also, IGF has many potent pro growth/anti apoptosis signals that also attenuate apoptosis signaling. Consistent prolonged time-intervals where apoptosis is inhibited in cells, coupled with exposure to carcinogens is the perfect environment to promote gradual mutagenesis and eventual tumor formation. -Cellular Differentiation, Epigenetics play a mysterious role in cancer formation (along with the immune system!). The purpose of this video was to inspire students who are pursuing research </video> <video> Ka Association Constant vs Kd Dissociation Constant Biochemistry made simple! Description: </video> <video> Snells Law and Index of Refraction Physics Made Super Simple! Description: Introduction to Law of Reflection and Refraction https://www.youtube.com/watch?v=x0j3_SruD0k </video> <video> The Biology of Aging & Interventions That Increase Animal Lifespan (Summary in Description) Description: $1,000,000 cash prize was offered to the research lab that could create the longest lived mice. No rules or limitations, simply create the mice that live longest. The winning lab won by creating mice with an IGF receptor mutation. But what does the IGF pathway have to do with aging? Well, there are three interventions that consistently and reproducibly extend lifespan in a wide variety of organisms. These interventions include rapamycin, calorie restriction, and of course blunting the IGF pathway. Why do these interventions extend longevity, do they have anything in common? They all reduce mTOR activity. mTOR is a large protein complex found in virtually all cells and highly conserved throughout evolution. When mTOR is activated, it accelerates physiologic growth and progression through a genetically programmed aging process. If your life is a 1 hour movie, excessive activation of mTOR plays your movie in x2 speed. But why does mTOR accelerate growth through the aging process? (BELOW IS MY INTERPRETATION) When cells progress through the cell cycle, they replicate DNA to undergo cell division. However, every time the cell replicates chromosomes, it shortens the chromosomes telomeres, and after a genetically pre-determined number of cell divisions, the telomere shortening reaches a threshold length that triggers cells to stop dividing, enter a post-mitotic state called cellular senescence. Cellular senescent cells slowly accumulate cellular damage (DNA damage, protein misfolding, ER stress) and secrete a characteristic set of cytokines (SASP) which triggers inflammation and cellular stress. Accumulation of senescent cells is a hallmark of the aged organism, and contributes to cell deterioration, tissue dysfunction and aging of an organism. (BELOW IS MY INTERPRETATION) Inhibition of mTOR may rate limit the progression through these processes, thus slow the rate of aging. Excessive mTOR activation accelerates progression through cell cycle, cell division, telomere attrition, and replicative senescence, therefore accelerating the rate of physiologic aging. However, by preventing obesity, hyperinsulinemia, BCAA intake, one can minimize mTOR activity, thus slowing progression of “cell cycle telomere shortening induced cellular senescence”. This is akin to aging in slow motion, prolonging the time-period an organism maintains production of fresh somatic cells, and delay the accumulation of post-mitotic senescent cells which begin to accumulate cellular damage. Also, reducing mTOR slows progression through the phase of the cell cycle needed for DNA repair, theoretically reducing accumulation of DNA damage, which is another trigger for senescence. Reducing mTOR also sensitizes cells to induce apoptosis in response to DNA damage, thus removing DNA-damaged cells within a given tissue. Reducing mTOR also enhances the removal of misfolded proteins and damaged organelles through the process of autophagy. These mechanisms prevent the accumulation of cellular damage to promote the maintaince of optimally functioning tissues. Empirical evidence suggest reducing mTOR activity results in longer lived organisms with reduced morbidity. HOWEVER, it’s difficult to simplify the physiology of aging in a couple paragraphs, and more importantly there is still much we do not understand about aging. The critical role of the immune system, mitochondria, stem cell exhaustion, and epigenetics are still poorly understood. We do not have the high-quality HUMAN data needed to confidently infer which interventions optimize HUMAN longevity. The intention of this video was to provide a basic science foundation for those interested in further understanding the biology of aging. </video> <video> Lipid Biochemistry (EVERYTHING YOU NEED TO KNOW MCAT) glycerol, phospholipid, sphingosine, ceramide Description: </video>

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My MCAT score was 99% Biochem/Biology and 97% Physics/Chem.

This channel was made to provide free MCAT content that focuses on the most high-yield topics for the MCAT.

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