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<blockquote data-quote="Sean_Raymond" data-source="post: 2354082" data-attributes="member: 403497"><p>There can be limitations to the eating less approach and it hasn't been effective for many. I have worked with people that it has been very effective in also and used low Carb diets which were not tolerable. However I recognise a low carbohydrate diet is a great alternative option as many do find it just works better for them in achieving whatever particular goal they have. There are ways of manipulating a specifically calorie reduced diet to provide bulk, mitigate effects on satiety etc but it is a challenging area. Hunger is indeed a major barrier with the eat less/consume less calorie idea.</p><p></p><p>When we look at the diets of our ancestors, evidence typically favours diets that were higher in animal products than something like the 'eatwell' plate although tribes that come closest to hunter gatherers in the modern world do eat large amount sof plant foods (unprocessed).</p><p></p><p>Gary Taubes believes Insulin stimulates hunger driving over consumption of foods however the body of evidence indicates that insulin promotes satiety as a part of its role in energy homeostasis. Some may dismiss what research finds and prefer to be guided by their lived results, which I understand, but Gary is no different to me in offering a hypothesis and research to back it up. But I haven't seen research that definitively backs up the notion insulin makes you hungry (frank hypos which insulin has a role in can stimulate hunger).</p><p></p><p>The ease of access and availability to highly palatable high energy foods continues to increase and it makes sense that as a species which evolved seeking out high calorie foods to survive in an environment where food wasn't guaranteed we will be really attracted to them. Adding this to more sedentary behaviours is for me most likely the main factors driving the obesity epidemic rather than it being because of a particular macronutrient or hormone. We have not undergone a major genetic shift in just 50 years and I do not believe most people are inherently inflicted with greediness so maybe it is the unconscious aspects of the brain forged in a time of feast and famine that is what drives what are now unhealthy behaviours.</p><p></p><p>The topic of saturated fat as a cause of heart disease is a rabbit hole. I do not hold a firm opinion that it is as bad as some say or benign as others. Evidence exists linking it to heart disease and other evidence suggest there is not. People then argue over the strength of the studies on either side. My view is that whilst people do respond differently to fat, generally saturated fat does raise LDL cholesterol (if a person is losing weight on a high fat diet this potential rise may be offset by the cholesterol lowering effects of the weight loss). I've looked at many low CHO v High CHO studies and LDL does tend to go up more than down.</p><p></p><p>If we accept that saturated fat raises LDL cholesterol (as I do -many do not), it then follows that the next question should be, is this a risk for health? Again, we find studies that contradict each other over this. I cannot conclusively say either way. But even If we were to say it does a low CHO/high fat/sat fat diets also may cause an increase in HDL and decrease in TAG - so just because LDL went up have we increased our overall cardiovascular risk? Then we must consider that increasing LDL itself may not be as important as the number and size of LDL particles rather than the amount of cholesterol being carried. Large LDL particles may confer less atherogenic risk. When we look at MUFA/PUFA, in theory they do not raise LDL and so it is said that they are less likely to cause a furrying of the arteries. But, saturated fat in the arteries is unlikely to be oxidised because it is a saturated fat. This means the inflammation which sparks creation of plaque in arteries may not occur whilst MUFA/PUFA can be oxidised. So whilst unsaturated fats may be less likely to cause deposition of cholesterol in artery walls might be more readily oxidised if they do. Simply put - unsaturated fats may be more pro-inflammatory.</p><p></p><p>Again, this all needs to be considered in the context of energy balance, weight, other factors etc. So, I do not fear saturated fat however I am not sure MUFA/PUFA are the disaster some say. Saying that, I do try to avoid processed vegetable oils and get MUFA/PUFA from nuts, olive oil for example. So it may be not so much the type of fat per se but a shift towards consuming more unnatural oils in replace of natural SFA which may have had some unhealthy effects. So I can find some agreement with you on unsaturated fats but maybe not in quite the way. Sorry if I went on there.</p><p></p><p>The Randall cycle is interesting, it actually is closest to the topic I first raised about how dietary fat may exert an acute insulin resistant effect and consuming carbohydrate at the same time may mean the carbohydrate is less efficiently metabolised. This is in keeping with the Randall cycle principle but may not wholly be explained by it (this cycle looks at competition between fatty acids and glucose for fuel useage not acute insulin resistant effects of fat). If we look to our ancestors it is likely animal and plant foods were not generally consumed together (animal caught and eaten, berries forged and eaten). I think you do raise an interesting point here.</p><p></p><p>Unfortunately as we progress advice changes and advice once taught as healthy is shown not to be.</p></blockquote><p></p>
[QUOTE="Sean_Raymond, post: 2354082, member: 403497"] There can be limitations to the eating less approach and it hasn't been effective for many. I have worked with people that it has been very effective in also and used low Carb diets which were not tolerable. However I recognise a low carbohydrate diet is a great alternative option as many do find it just works better for them in achieving whatever particular goal they have. There are ways of manipulating a specifically calorie reduced diet to provide bulk, mitigate effects on satiety etc but it is a challenging area. Hunger is indeed a major barrier with the eat less/consume less calorie idea. When we look at the diets of our ancestors, evidence typically favours diets that were higher in animal products than something like the 'eatwell' plate although tribes that come closest to hunter gatherers in the modern world do eat large amount sof plant foods (unprocessed). Gary Taubes believes Insulin stimulates hunger driving over consumption of foods however the body of evidence indicates that insulin promotes satiety as a part of its role in energy homeostasis. Some may dismiss what research finds and prefer to be guided by their lived results, which I understand, but Gary is no different to me in offering a hypothesis and research to back it up. But I haven't seen research that definitively backs up the notion insulin makes you hungry (frank hypos which insulin has a role in can stimulate hunger). The ease of access and availability to highly palatable high energy foods continues to increase and it makes sense that as a species which evolved seeking out high calorie foods to survive in an environment where food wasn't guaranteed we will be really attracted to them. Adding this to more sedentary behaviours is for me most likely the main factors driving the obesity epidemic rather than it being because of a particular macronutrient or hormone. We have not undergone a major genetic shift in just 50 years and I do not believe most people are inherently inflicted with greediness so maybe it is the unconscious aspects of the brain forged in a time of feast and famine that is what drives what are now unhealthy behaviours. The topic of saturated fat as a cause of heart disease is a rabbit hole. I do not hold a firm opinion that it is as bad as some say or benign as others. Evidence exists linking it to heart disease and other evidence suggest there is not. People then argue over the strength of the studies on either side. My view is that whilst people do respond differently to fat, generally saturated fat does raise LDL cholesterol (if a person is losing weight on a high fat diet this potential rise may be offset by the cholesterol lowering effects of the weight loss). I've looked at many low CHO v High CHO studies and LDL does tend to go up more than down. If we accept that saturated fat raises LDL cholesterol (as I do -many do not), it then follows that the next question should be, is this a risk for health? Again, we find studies that contradict each other over this. I cannot conclusively say either way. But even If we were to say it does a low CHO/high fat/sat fat diets also may cause an increase in HDL and decrease in TAG - so just because LDL went up have we increased our overall cardiovascular risk? Then we must consider that increasing LDL itself may not be as important as the number and size of LDL particles rather than the amount of cholesterol being carried. Large LDL particles may confer less atherogenic risk. When we look at MUFA/PUFA, in theory they do not raise LDL and so it is said that they are less likely to cause a furrying of the arteries. But, saturated fat in the arteries is unlikely to be oxidised because it is a saturated fat. This means the inflammation which sparks creation of plaque in arteries may not occur whilst MUFA/PUFA can be oxidised. So whilst unsaturated fats may be less likely to cause deposition of cholesterol in artery walls might be more readily oxidised if they do. Simply put - unsaturated fats may be more pro-inflammatory. Again, this all needs to be considered in the context of energy balance, weight, other factors etc. So, I do not fear saturated fat however I am not sure MUFA/PUFA are the disaster some say. Saying that, I do try to avoid processed vegetable oils and get MUFA/PUFA from nuts, olive oil for example. So it may be not so much the type of fat per se but a shift towards consuming more unnatural oils in replace of natural SFA which may have had some unhealthy effects. So I can find some agreement with you on unsaturated fats but maybe not in quite the way. Sorry if I went on there. The Randall cycle is interesting, it actually is closest to the topic I first raised about how dietary fat may exert an acute insulin resistant effect and consuming carbohydrate at the same time may mean the carbohydrate is less efficiently metabolised. This is in keeping with the Randall cycle principle but may not wholly be explained by it (this cycle looks at competition between fatty acids and glucose for fuel useage not acute insulin resistant effects of fat). If we look to our ancestors it is likely animal and plant foods were not generally consumed together (animal caught and eaten, berries forged and eaten). I think you do raise an interesting point here. Unfortunately as we progress advice changes and advice once taught as healthy is shown not to be. [/QUOTE]
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