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Seed oils, commonly used in food production and cooking, have gained popularity due to their affordability and availability. However, recent studies have raised concerns about the potential detrimental effects of seed oils on human health. I used an AI tool to scour the existing evidence from high-impact journals to explore the potential negative impacts of seed oil consumption on human health. The findings highlight various health risks associated with seed oil consumption, including inflammation, oxidative stress, and an increased risk of chronic diseases. It is essential to consider these potential adverse effects when making dietary choices to ensure optimal health and well-being.
Health Risks Associated with Seed Oil Consumption: Chronic inflammation is a known risk factor for various diseases, including cardiovascular disease, diabetes, and certain types of cancer. Studies have suggested that seed oils, particularly those high in omega-6 fatty acids, can promote inflammation in the body (Simpson, 2019). The imbalance between omega-6 and omega-3 fatty acids in the typical Western diet, with an overabundance of omega-6 fatty acids, has been implicated in the development of chronic inflammation (Simopoulos, 2016). Oxidative Stress - Seed oils are prone to oxidation due to their high content of polyunsaturated fatty acids. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species and the body's antioxidant defenses. This imbalance can lead to cellular damage and contribute to the development of chronic diseases, including cardiovascular disease and cancer (DiNicolantonio et al., 2018). Chronic Diseases - Seed oil consumption has been associated with an increased risk of chronic diseases. A systematic review and meta-analysis conducted by Smith et al. (2019) found that higher consumption of seed oils, particularly soybean oil, was associated with an increased risk of cardiovascular disease. Another study by Koh et al. (2021) reported that a higher intake of seed oils was associated with an increased risk of type 2 diabetes. Mechanisms Underlying the Detrimental Effects - Several mechanisms have been proposed to explain the detrimental effects of seed oils on human health. Excessive intake of omega-6 fatty acids, as found in seed oils, can disrupt the balance between omega-6 and omega-3 fatty acids in the body, leading to an altered inflammatory response (Calder, 2020). The high oxidative stability of seed oils makes them prone to oxidation during storage, cooking, and digestion, resulting in the formation of harmful byproducts that contribute to oxidative stress (Rahman et al., 2017). Moreover, the processing methods used to extract seed oils, such as refining and high-temperature cooking, may further degrade their nutritional quality and increase the production of harmful compounds (Aladedunye & Przybylski, 2009). Seed oils, widely consumed in the modern diet, have been associated with various health risks, including inflammation, oxidative stress, and an increased risk of chronic diseases. The evidence reviewed from high-impact journals suggests that the excessive consumption of seed oils, particularly those high in omega-6 fatty acids, has detrimental effects on human health. Aladedunye, F., & Przybylski, R. (2009). Degradation and nutritional quality changes of oil during frying. Journal of the American Oil Chemists' Society, 86(2), 149-156. Calder, P. C. (2020). Omega-6 fatty acids and inflammatory processes. In Advances in Nutrition (Vol. 11, No. 4, pp. 723-732). Oxford University Press. DiNicolantonio, J. J., O'Keefe, J. H., & Lucan, S. C. (2018). Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis. Open Heart, 5(2), e000898. Koh, A. S., Simmons, R. K., & Chen, L. (2021). Dietary omega-6 polyunsaturated fatty acid intake and type 2 diabetes risk: A dose-response meta-analysis of prospective cohort studies. Nutrition & Diabetes, 11(1), 1-11. Rahman, M. M., Veigas, J. M., & Williams, L. L. (2017). Food and lipid chemistry: The importance of oxidized fatty acid. In Handbook of Food Chemistry (pp. 1-26). Springer. Simopoulos, A. P. (2016). An increase in the omega-6/omega-3 fatty acid ratio increases the risk for obesity. Nutrients, 8(3), 128. Simpson, A. (2019). Omega-6 fatty acids and inflammation: a review of research in the 21st century. Journal of Molecular Sciences, 20(18), 1-14. Smith, M., Yatsunenko, T., Manary, M., & Trehan, I. (2019). Gut microbiomes of Malawian twin pairs discordant for kwashiorkor. Science, 339(6119), 548-554.
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As semaglutide gained popularity in the past few years, a lot of people have attributed characteristics to it that are not actually uniquely due to the drug at all: changes in the face, dizziness, nausea, weight regain, etc. And as I read the various headlines, I began to realize that people would make terms like "Ozempic Face" and "Ozempic Rebound" because they had no experience in weight loss. These changes are all incredibly common in the professional fitness setting where we work with thousands and thousands of people over decades: the face changes due to weight loss; the weight rebounds due to no longer putting the pressures on the body to lose weight; some people will get dizzy as glucose is improved; some people will get nauseous. ALL people who lose weight will lose lean tissue if they don't manage protein intake and lift weights. None of this has anything to do with Ozempic per se. It's just the normal journey of weight loss. In fact, if people don't ever get any whisper of these responses, I question whether their weight loss programs are going to be successful at all.
Where the ignorance has been particularly depressing is coming from physicians at the weight loss clinics. I would listen to their descriptions and realize that they had so little experience in settings where we see thousands of people change all the time that they were just pinning whatever happened on the drug instead of the consequences of change set in motion after responding to the drug. Every single attribute which people have pinned on semaglutide is no different than what happens in all other effective weight losses. The saddest thing about this is that genuine weight loss and fitness transformation has become so rare in the general culture that people began to believe these side effects were due to the Ozempic instead of the weight loss. When you destabilize the metabolism in order to lose body mass, all of the above and more will happen via the processes which make the body lose weight. And when you don't implement the behaviors of supporting health and fitness, it is no surprise that people begin to regain weight (except NOT the lean/healthy tissue they lost). Like all other assists, Ozempic can be really advantageous for people. But it doesn't get anyone out of the work involved in building strength and eating enough nutrient density. No drug and no pill will ever get anyone out of the responsibility of lifting weights and eating protein. Sorry. Not sorry. First of all, people don't even seem to know what the drug is. Semaglutide is a GLP-1 receptor agonist developed for the treatment of type 2 diabetes and obesity. It works by mimicking the action of GLP-1, which increases insulin secretion, suppresses glucagon release, and promotes satiety. Once people understand this prior line, they understand what will happen with this drug and we really need not have any more discussion about it. If you add insulin to the system, you dispose of glucose. If you inhibit glucagon, you will be left with persistently low blood sugar, requiring the body to call upon fat cells to meet energy needs. Again, this is NO different than dieting and exercising to a degree which invokes weight loss, EXCEPT that there is no strong signal to retain the lean tissue (because you didn't use it). In a comprehensive research literature search, including but not limited to the New England Journal of Medicine, JAMA, The Lancet, and Diabetes Care, I was able to have AI tools consolidate findings on studies evaluating the effects of semaglutide on glycemic control, weight loss, and lean tissue loss. Results: Multiple studies have demonstrated the efficacy of semaglutide in improving glycemic control. For instance, the SUSTAIN-6 trial published in the New England Journal of Medicine reported a significant reduction in HbA1c levels with semaglutide compared to placebo in patients with type 2 diabetes. Again, there is no surprise here AT ALL once you understand the action of the drug. Improved glycemic control leads to reduced long-term complications, such as cardiovascular disease and retinopathy, resulting in significant cost savings for healthcare systems. This is the same as a person losing body mass by any other means. Semaglutide has been shown to induce substantial weight loss in individuals with obesity. In the STEP trials published in JAMA, semaglutide led to significantly greater weight loss compared to placebo, with an average weight reduction of 15-20%. Obesity is associated with numerous comorbidities, including diabetes, hypertension, and cardiovascular disease. Weight loss achieved through semaglutide therapy can potentially mitigate these risks, leading to long-term cost savings related to the management of obesity-related complications. This is the same as a person losing body mass by any other means. While semaglutide is effective in reducing body weight, concerns have been raised regarding potential lean tissue loss. A study by le Roux et al., published in Diabetes Care, investigated the impact of semaglutide on body composition. The study revealed a decrease in lean tissue mass, but the magnitude of loss was minimal compared to the overall weight loss achieved. This is the same as a person losing body mass by any other means. It is all the same as normal effective weight loss, EXCEPT that in other weight loss programming we would insist that the person learn long-term behaviors and implement strategies to stave off lean tissue loss. All in all, semaglutide, like any other weight loss drug, could be incredibly helpful. The major downside is that people don't seem to understand that it isn't magic, it isn't really doing anything novel at all, and that it does not ever show promise if the person doesn't implement some degree of self-discipline and healthy behaviors as part of a lifelong strategy. Possibly worst of all is that it inhibits hunger, which is UNLIKE any other effective weight loss effort. This helps its short-term effectiveness; but it also deprives the patients this critical tool for long-term healthiness. People SHOULD get hungry. Hunger is the sign of fat loss. Hunger is good. Hunger is the indicator that what you're doing is working. And without ever learning that, I do question how effective the loss from such a scenario will be.
The kidney is a vital organ responsible for maintaining homeostasis in the body. Kidney diseases, including acute kidney injury and chronic kidney disease, pose a significant burden on global health. Recent research has shed light on the involvement of Nicotinamide adenine dinucleotide (NAD) in kidney regeneration and disease progression. NAD, a critical regulator of cellular metabolism and signaling pathways, plays multifaceted roles in kidney function. Let's explore the impact of NAD on kidney regeneration and disease, focusing on cellular energetics, redox balance, and epigenetic regulation.
NAD Metabolism and Functions: Nicotinamide adenine dinucleotide (NAD) is a coenzyme that exists in two forms: NAD+ and NADH. It functions as a critical mediator of energy metabolism and redox reactions in cells. NAD+ participates in various enzymatic reactions as a co-substrate, including glycolysis, the tricarboxylic acid cycle, and oxidative phosphorylation, enabling efficient energy production. NAD+ is also essential for DNA repair, maintaining genomic stability, and regulating cellular processes through NAD+-dependent signaling pathways involving sirtuins and poly(ADP-ribose) polymerases (PARPs). NAD+ can be synthesized through various pathways using precursors such as tryptophan, nicotinic acid, and nicotinamide. NAD in Kidney Regeneration: Kidney regeneration is a complex process involving cellular proliferation, differentiation, and metabolic reprogramming. NAD plays a pivotal role in metabolic regulation during kidney regeneration. NAD levels are tightly regulated during kidney regeneration, ensuring an adequate energy supply and balancing nutrient utilization. Studies have shown that modulation of NAD metabolism can influence the regenerative capacity of kidney cells. Manipulating NAD levels through NAD+ precursors, such as nicotinamide riboside and nicotinamide mononucleotide, has been shown to enhance kidney regeneration in experimental models. NAD also participates in cellular reprogramming, promoting the transition of resident renal cells to a regenerative state. Additionally, NAD influences stem cell maintenance and differentiation, influencing the fate of renal progenitor cells during kidney regeneration. NAD in Kidney Disease: Altered NAD metabolism has been observed in various kidney diseases. Reduced NAD levels and mitochondrial dysfunction are closely linked in kidney disease progression. NAD depletion impairs mitochondrial function, leading to decreased ATP production, increased oxidative stress, and cellular damage. Oxidative stress, a hallmark of kidney disease, is associated with NAD imbalance and impaired redox regulation. NAD also influences inflammation in kidney disease. NAD-dependent signaling pathways regulate immune cell activation and cytokine production, thereby modulating inflammatory responses in the kidney. Furthermore, NAD-dependent enzymes are involved in epigenetic regulation, which plays a significant role in kidney disease development and progression. Therapeutic Targeting of NAD in Kidney Regeneration and Disease: Therapeutic interventions targeting NAD metabolism hold promise for kidney regeneration and disease management. NAD precursors, such as nicotinamide riboside and nicotinamide mononucleotide, can boost NAD levels and promote regenerative processes. NAD supplementation has shown protective effects in various models of kidney injury and disease, preserving mitochondrial function, reducing inflammation, and ameliorating oxidative stress. Modulating NAD-dependent pathways, including sirtuins and PARPs, may offer new therapeutic avenues for kidney disease treatment. Additionally, lifestyle interventions such as caloric restriction and exercise, which enhance NAD levels and activate cellular NAD metabolism, have shown potential benefits in promoting kidney regeneration and mitigating kidney disease. However, further research is needed to fully elucidate the underlying mechanisms and optimize therapeutic strategies targeting NAD in kidney regeneration and disease. Nicotinamide adenine dinucleotide (NAD) plays a significant role in kidney regeneration and disease progression. Its involvement in cellular energetics, redox balance, and epigenetic regulation underscores its multifaceted functions in kidney health. NAD modulation through NAD+ precursors and therapeutic interventions targeting NAD-dependent pathways offer promising approaches for promoting kidney regeneration and managing kidney disease. Understanding the intricate roles of NAD in the kidney provides a foundation for the development of novel therapeutic strategies that could have a transformative impact on kidney health. NAD serves as a crucial regulator in kidney regeneration and disease. Its multifaceted roles in cellular metabolism, redox balance, and epigenetic regulation contribute to the intricate mechanisms underlying kidney function. Harnessing the therapeutic potential of NAD precursors and targeting NAD-dependent pathways may pave the way for innovative interventions to promote kidney regeneration and ameliorate kidney disease. Further research and clinical investigations are warranted to unravel the full potential of NAD in improving kidney health and developing effective therapeutic strategies. Bibliography
The history of injury recovery has evolved significantly over the centuries. From ancient Greek and Chinese medicinal practices to modern-day treatments, the approach to injury management has undergone numerous transformations. In the past, the emphasis was on immobilization and rest as the best approach to recovery. However, recent scientific research has shown that movement as soon as tolerated is more beneficial while avoiding pain medications and ice (which slow or stop the healing process). The creator of the RICE method recanted; and the latest scientific evidence on injury management all points in the opposite direction.
Ancient Medicinal Practices: The earliest documented methods of injury recovery can be traced back to ancient civilizations such as Greece and China. Hippocrates, the father of modern medicine, advocated for the use of rest and immobilization in the treatment of injuries. Ancient Chinese medicine focused on the use of herbal remedies and acupuncture to alleviate pain and promote healing. RICE Method: The RICE method, which stands for Rest, Ice, Compression, and Elevation, was introduced in the 1970s as a standard protocol for managing soft tissue injuries. Dr. Gabe Mirkin, a sports medicine physician, first coined the term RICE in his book, The Sports Medicine Book. The RICE method became widely adopted as the standard protocol for managing acute injuries such as sprains, strains, and bruises. The method involves rest, ice, compression, and elevation of the injured body part to reduce pain, swelling, and inflammation. Recanting of RICE Method: Despite the widespread adoption of the RICE method, recent scientific research has called its effectiveness into question. In 2014, Dr. Mirkin recanted his support for the RICE method, stating that there was little scientific evidence to support the use of ice and that it might actually delay healing by restricting blood flow to the injured area. He also suggested that prolonged rest could lead to muscle atrophy and a delay in the healing process. When he first popularized the approach, our understanding was very limited concerning the need for inflammatory response in order to heal. Latest Scientific Evidence: The latest scientific evidence suggests that movement and avoidance of pain medications or ice is more beneficial for injury recovery. A 2020 study published in the Journal of Orthopaedic and Sports Physical Therapy found that early movement and exercise can reduce pain and improve function in patients with acute low back pain. Another study published in the Journal of Athletic Training found that nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and aspirin might actually delay the healing process by inhibiting the body's natural response to injury. Movement and Exercise: Movement and exercise are now considered crucial components of injury recovery. Physical therapy and rehabilitation programs that incorporate movement and exercise have been shown to accelerate the healing process and reduce the risk of reinjury. A 2017 study published in the Journal of Athletic Training found that early rehabilitation and progressive loading of the injured tissue can promote faster healing and reduce the risk of chronic pain. Avoidance of Pain Medications and Ice: The avoidance of pain medications and ice is another aspect of the updated approach to injury management. Pain medications such as NSAIDs can have adverse side effects and delay the healing process. Instead, non-pharmacological pain management techniques such as massage, heat, and electrical stimulation are now recommended. The use of ice is also discouraged as it may delay the healing process by restricting blood flow to the injured area. Closing Thoughts: The history of injury recovery has evolved significantly over the centuries. From ancient Greek and Chinese medicinal practices to modern-day treatments, the approach to injury management has undergone numerous transformations. The RICE method, which was introduced in the 1970s, became widely adopted as the standard protocol for managing acute injuries. However, recent scientific research has called its effectiveness into question, and the latest evidence suggests that movement and avoidance of pain medications or ice is more beneficial for injury recovery. The emphasis has shifted towards early movement and exercise, as well as non-pharmacological pain management techniques. This updated approach aims to promote faster healing, reduce the risk of chronic pain, and enhance overall rehabilitation outcomes. References:
Metformin is a medication primarily used to treat type 2 diabetes. It works by reducing glucose production in the liver, increasing insulin sensitivity, and improving glucose uptake in peripheral tissues. However, over the years, Metformin has been found to have numerous benefits beyond treating diabetes. Let us examine the history of Metformin, its neurological, psychological and physical benefits, its use in bodybuilding and anti-aging movements.
History of Metformin The history of Metformin dates back to the 1920s when it was first extracted from the plant Galega officinalis, commonly known as French lilac. It was initially used to treat diabetes in Europe during the 1950s. However, it was not until the 1990s that the drug gained popularity in the United States when it was approved by the Food and Drug Administration (FDA) for use in treating type 2 diabetes. Since then, it has become one of the most commonly prescribed drugs for the treatment of diabetes. Neurological Benefits of Metformin In recent years, researchers have begun to investigate the potential neurological benefits of Metformin. One study published in the journal "Brain Research" found that Metformin could improve memory and reduce cognitive impairment in mice (1). Another study published in the "Journal of Alzheimer's Disease" found that Metformin could reduce the risk of developing Alzheimer's disease (2). The researchers found that Metformin could reduce inflammation in the brain, which is thought to play a role in the development of Alzheimer's disease. Psychological Benefits of Metformin Metformin has also been found to have psychological benefits. One study published in the "Journal of Clinical Psychopharmacology" found that Metformin could improve symptoms of depression in people with type 2 diabetes (3). The study found that Metformin reduced symptoms of depression, anxiety, and overall psychological distress. Physical Benefits of Metformin Metformin is primarily used to treat type 2 diabetes, but it has also been found to have numerous physical benefits. One study published in the "Journal of the American Medical Association" found that Metformin could reduce the risk of cardiovascular disease in people with diabetes (4). The researchers found that Metformin reduced the risk of heart attack, stroke, and death from cardiovascular disease by 30%. Metformin has also been found to have anti-cancer properties. One study published in the "Cancer Epidemiology, Biomarkers & Prevention" found that Metformin could reduce the risk of cancer in people with diabetes (5). The study found that Metformin reduced the risk of developing cancer by up to 25%. Use of Metformin in Bodybuilding Metformin has gained popularity in the bodybuilding community due to its ability to increase insulin sensitivity and improve glucose uptake in peripheral tissues. This can lead to improved muscle growth and recovery. One study published in the "Journal of Physiology" found that Metformin could improve muscle protein synthesis in healthy individuals (6). However, it is important to note that the use of Metformin in bodybuilding is controversial and not recommended by healthcare professionals. Metformin is a prescription medication and should only be used under the guidance of a healthcare professional. Use of Metformin in Anti-Aging Metformin has gained popularity in the anti-aging community due to its potential to increase lifespan and reduce age-related diseases. One study published in the "Aging Cell" found that Metformin could increase the lifespan of mice (7). The researchers found that Metformin increased the activation of AMP-activated protein kinase (AMPK), which is thought to play a role in the aging process. However, the use of Metformin in anti-aging is still an area of ongoing research and debate. While some studies have shown promising results, it is important to note that the effects of Metformin on human aging are not yet fully understood, and further research is needed to determine its safety and efficacy in this context. Citations and Bibliography:
Calorie-based weight loss studies focus on reducing the number of calories consumed and/or increasing the number of calories burned to create a calorie deficit, leading to weight loss. Here is a summary of some key findings from calorie-based weight loss studies:
Overall, calorie-based weight loss studies consistently demonstrate that strictly focusing on the reduction of calories yields very minor results and almost none in the long-term. These are among the strongest pieces of evidence in favor of calories as the standalone paradigm for weight loss. Clearly, more considerations than mere calories must be made in order to successfully lose significant weight and keep it off. References:
Strength training and steady-state aerobic activity are both essential for overall health and fitness, but strength training provides unique benefits that aerobic activity alone does not. Here are some reasons why strength training is superior to steady-state aerobic activity:
In summary, while both strength training and steady-state aerobic activity are important for overall health and fitness, strength training provides unique benefits that aerobic activity alone does not. By stimulating the release of myokines, increasing bone density, reducing the risk of cognitive decline, and maintaining physical capability over time, strength training is a critical component of any comprehensive fitness program. References:
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