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you need to avoid seed oils (PUFA's)
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<blockquote data-quote="Phil Goodman" data-source="post: 279409" data-attributes="member: 42777"><p>This.</p><p></p><p></p><p>Its well established that there are lots of negative impacts from consumption.</p><p></p><p></p><p>[URL unfurl="true"]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/[/URL]</p><p></p><p></p><p>While the evidence is still conflicting in some instances, the mechanisms underlying excessive LA intake are reflected in a wide variety of chronic diseases. A recent study [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B99-nutrients-15-03129" target="_blank">99</a>] found that high-fat diets increased the formation of vitamin A degradation products, known as bisretinoids, in ocular tissues. These degradation products are known to cause damage to the retina directly, but they also participate in the formation of lipofuscin in the retina. Lipofuscin is a byproduct of PUFA peroxidation. The study found the PUFA linoleic acid to be a causal factor of eye damage.</p><p></p><p>Soy oil is by far the most widely produced and consumed seed oil in the US. Using mice, researchers in 2020 found that a high soybean oil diet not only led to obesity and diabetes, but could also affect neurological conditions such as autism, Alzheimer’s disease, anxiety, and depression [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B100-nutrients-15-03129" target="_blank">100</a>]. The same research team found in 2015 [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B101-nutrients-15-03129" target="_blank">101</a>] that soy oil induced obesity, diabetes, insulin resistance, and fatty liver in mice. Then, in a 2017 study [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B102-nutrients-15-03129" target="_blank">102</a>], the same group learned that if soy oil was engineered to be low in LA, it induced less obesity and insulin resistance.</p><p></p><p>Type I diabetes is an autoimmune condition. The beta-cells of the pancreas are attacked by antibodies from the immune system, over time leading to their destruction and the inability to produce insulin. One study [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B103-nutrients-15-03129" target="_blank">103</a>] found that the reason for antibody production was the overexpression of the enzyme 12/15-lipoxygenase, which is an enzyme involved not only in synthesizing inflammatory leukotrienes, but also metastatic cancer.</p><p></p><p>Leukotrienes are PUFA metabolites and are responsible for the development of type I diabetes. This suggests that a 12/15-LOX inhibitor would be therapeutic. This study administered a leukotriene inhibitor and found it effective in preventing the development of beta-cell autoimmunity. A more fundamental approach would be to avoid or replace the source of leukotrienes, which would be dietary PUFAs.</p><p></p><h3>7.1. Obesity and LA</h3><p>In the US, nearly 43% of adults 20 years of age and older are obese [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B104-nutrients-15-03129" target="_blank">104</a>], while approximately 74% of all adults are overweight or obese [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B105-nutrients-15-03129" target="_blank">105</a>]. Although these statistics are alarming, the American Obesity Association suggests that by 2025, 50% of Americans may be obese. Predictions also indicate that the percentage is likely to rise to 60% by 2030 [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B106-nutrients-15-03129" target="_blank">106</a>]. There is a growing body of evidence based on animal studies suggesting that polyunsaturated fatty acids (PUFAs), such as those found in vegetable oils, contribute to the obesity epidemic [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B107-nutrients-15-03129" target="_blank">107</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B108-nutrients-15-03129" target="_blank">108</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B109-nutrients-15-03129" target="_blank">109</a>,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B110-nutrients-15-03129" target="_blank">110</a>].</p><p>It is also important to note that the US has both the highest obesity rate in the developed world [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B111-nutrients-15-03129" target="_blank">111</a>] and the highest consumption of seed oils per person than any other nation [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B112-nutrients-15-03129" target="_blank">112</a>]. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/figure/nutrients-15-03129-f003/" target="_blank">Figure 3</a>illustrates the ongoing shift in vegetable oil consumption that began in the early 20th century, as industrially processed vegetable and seed oils entered the food supply and gradually displaced natural animal fats.</p><p></p><p>While there appears to be a coincident rise in both the consumption of LA-containing seed oils and obesity, it should be noted that this does not imply causality. There are a number of other dietary (e.g., refined sugars, ultraprocessed foods, etc.) and nondietary (e.g., physical inactivity, environmental toxicants, poor sleep, etc.) risk factors that have also increased during this time. Nonetheless, LA is one such risk factor worthy of consideration.</p><p></p><p></p><p>The dramatic increase in LA intake in the standard American diet appears to contribute to the simultaneous rise in a wide variety of chronic diseases. While modest amounts of LA support human health, deleterious mechanisms of excessive LA intake include the formation of oxidized linoleic acid metabolites (OXLAMs) and a suboptimal cardiolipin composition. These disruptions to optimal physiology cause impairments in mitochondrial function, compromised metabolic function, and excessive inflammation, all of which contribute to obesity, cardiovascular disease, cancer, and many other chronic conditions that plague our healthcare system.</p><p></p><p>While other dietary factors, such as refined sugars and ultraprocessed foods, more generally, contribute to the rise in chronic diseases, the long half-life of LA and its integration into cardiolipin with excessive intake is particularly pernicious. Future prospective studies of low-LA diets in humans appear warranted and should consider the relatively long timeframe for the reduction in the harms of an excessive LA intake. Furthermore, while the standard American diet has become more pervasive worldwide, including in China [57.89] and India, the hypothesis that excessive LA intake may be contributing to chronic disease explored in this review should be evaluated more closely in populations outside of the United States.</p></blockquote><p></p>
[QUOTE="Phil Goodman, post: 279409, member: 42777"] This. Its well established that there are lots of negative impacts from consumption. [URL unfurl="true"]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/[/URL] While the evidence is still conflicting in some instances, the mechanisms underlying excessive LA intake are reflected in a wide variety of chronic diseases. A recent study [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B99-nutrients-15-03129']99[/URL]] found that high-fat diets increased the formation of vitamin A degradation products, known as bisretinoids, in ocular tissues. These degradation products are known to cause damage to the retina directly, but they also participate in the formation of lipofuscin in the retina. Lipofuscin is a byproduct of PUFA peroxidation. The study found the PUFA linoleic acid to be a causal factor of eye damage. Soy oil is by far the most widely produced and consumed seed oil in the US. Using mice, researchers in 2020 found that a high soybean oil diet not only led to obesity and diabetes, but could also affect neurological conditions such as autism, Alzheimer’s disease, anxiety, and depression [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B100-nutrients-15-03129']100[/URL]]. The same research team found in 2015 [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B101-nutrients-15-03129']101[/URL]] that soy oil induced obesity, diabetes, insulin resistance, and fatty liver in mice. Then, in a 2017 study [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B102-nutrients-15-03129']102[/URL]], the same group learned that if soy oil was engineered to be low in LA, it induced less obesity and insulin resistance. Type I diabetes is an autoimmune condition. The beta-cells of the pancreas are attacked by antibodies from the immune system, over time leading to their destruction and the inability to produce insulin. One study [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B103-nutrients-15-03129']103[/URL]] found that the reason for antibody production was the overexpression of the enzyme 12/15-lipoxygenase, which is an enzyme involved not only in synthesizing inflammatory leukotrienes, but also metastatic cancer. Leukotrienes are PUFA metabolites and are responsible for the development of type I diabetes. This suggests that a 12/15-LOX inhibitor would be therapeutic. This study administered a leukotriene inhibitor and found it effective in preventing the development of beta-cell autoimmunity. A more fundamental approach would be to avoid or replace the source of leukotrienes, which would be dietary PUFAs. [HEADING=2]7.1. Obesity and LA[/HEADING] In the US, nearly 43% of adults 20 years of age and older are obese [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B104-nutrients-15-03129']104[/URL]], while approximately 74% of all adults are overweight or obese [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B105-nutrients-15-03129']105[/URL]]. Although these statistics are alarming, the American Obesity Association suggests that by 2025, 50% of Americans may be obese. Predictions also indicate that the percentage is likely to rise to 60% by 2030 [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B106-nutrients-15-03129']106[/URL]]. There is a growing body of evidence based on animal studies suggesting that polyunsaturated fatty acids (PUFAs), such as those found in vegetable oils, contribute to the obesity epidemic [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B107-nutrients-15-03129']107[/URL],[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B108-nutrients-15-03129']108[/URL],[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B109-nutrients-15-03129']109[/URL],[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B110-nutrients-15-03129']110[/URL]]. It is also important to note that the US has both the highest obesity rate in the developed world [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B111-nutrients-15-03129']111[/URL]] and the highest consumption of seed oils per person than any other nation [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/#B112-nutrients-15-03129']112[/URL]]. [URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10386285/figure/nutrients-15-03129-f003/']Figure 3[/URL]illustrates the ongoing shift in vegetable oil consumption that began in the early 20th century, as industrially processed vegetable and seed oils entered the food supply and gradually displaced natural animal fats. While there appears to be a coincident rise in both the consumption of LA-containing seed oils and obesity, it should be noted that this does not imply causality. There are a number of other dietary (e.g., refined sugars, ultraprocessed foods, etc.) and nondietary (e.g., physical inactivity, environmental toxicants, poor sleep, etc.) risk factors that have also increased during this time. Nonetheless, LA is one such risk factor worthy of consideration. The dramatic increase in LA intake in the standard American diet appears to contribute to the simultaneous rise in a wide variety of chronic diseases. While modest amounts of LA support human health, deleterious mechanisms of excessive LA intake include the formation of oxidized linoleic acid metabolites (OXLAMs) and a suboptimal cardiolipin composition. These disruptions to optimal physiology cause impairments in mitochondrial function, compromised metabolic function, and excessive inflammation, all of which contribute to obesity, cardiovascular disease, cancer, and many other chronic conditions that plague our healthcare system. While other dietary factors, such as refined sugars and ultraprocessed foods, more generally, contribute to the rise in chronic diseases, the long half-life of LA and its integration into cardiolipin with excessive intake is particularly pernicious. Future prospective studies of low-LA diets in humans appear warranted and should consider the relatively long timeframe for the reduction in the harms of an excessive LA intake. Furthermore, while the standard American diet has become more pervasive worldwide, including in China [57.89] and India, the hypothesis that excessive LA intake may be contributing to chronic disease explored in this review should be evaluated more closely in populations outside of the United States. [/QUOTE]
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you need to avoid seed oils (PUFA's)
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