tag:blogger.com,1999:blog-36840063.post4351786613347683581..comments2024-03-18T22:09:37.509+00:00Comments on Hyperlipid: Adipotide and the Bad FatPeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger97125tag:blogger.com,1999:blog-36840063.post-26386904452815925952012-12-31T09:40:42.729+00:002012-12-31T09:40:42.729+00:00Hi, I'm very naive, so I apologize ahead of ti...Hi, I'm very naive, so I apologize ahead of time.<br /><br />1) I could be wrong here, but I thought visceral fat didn't really secrete, or at least contribute that much to circulating leptin. At least not compared to subcutaneous adipose. <br /><br />2) If studies show different gene expression in different locations of adipocytes(subcutaneously) then can one infer it will do the same with visceral fat? That is to say that not all visceral fat is the equal?<br /><br />This could help explain certain psychological functionHumble To Learnhttps://www.blogger.com/profile/12120024336301795185noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-82153727416562449662011-12-27T19:07:41.983+00:002011-12-27T19:07:41.983+00:00This is a pretty advanced discussion about adipot...This is a pretty advanced discussion about <a href="http://adipotide.com" rel="nofollow">adipotide</a> and fat loss. Does anybody know if the kidney damage from adipotide was the result of higher than normal dosing or just normal dosing. I realize that the kidneys in the study returned to normal after being taken off the drug, but kidney damage is one hell of a side effect!Adminhttps://www.blogger.com/profile/02880350361936257240noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-35619222434732614172011-12-22T21:43:15.203+00:002011-12-22T21:43:15.203+00:00@Wooo:
Despite what everyone says (even Taubes an...@Wooo:<br /><br />Despite what everyone says (even Taubes and Lustig who are sworn enemies of HFCS), it seems that HFCS is not equivalent to sucrose after all, and we are not just talking about the small 5% difference in fructose content:<br /><br />http://www.princeton.edu/main/news/archive/S26/91/22K07/<br /><br />or<br /><br />http://www.fasebj.org/cgi/content/meeting_abstract/24/1_MeetingAbstracts/562.1<br /><br />Also, I've heard Ray Peat say that HFCS contains residues left over from the original corn starch, so consuming HFCS is a bit like consuming a bunch of sweetened flour.<br /><br /><br />@Mary:<br /><br />Another thing with meat is the high phosphorous to calcium ratio.<br /><br />Milk on the other hand has a more ideal phosphorous to calcium ratio so consuming both milk (and/or cheese) and meat could help balance things out. I don't know about the respective copper-zinc ratios though.<br /><br /><br />Regards,<br />Mikemontmorencyhttps://www.blogger.com/profile/12879422255762834319noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-45170516199202185892011-12-22T21:21:41.261+00:002011-12-22T21:21:41.261+00:00@Blogblog:
British Navy "dinner":
Inte...@Blogblog:<br /><br />British Navy "dinner":<br /><br />Interesting, but as a Brit, there is an interesting class/region thing about meal names.<br /><br />Working class people and people generally in the north of England (where most of the heavy industry used to be), called the mid-day meal "dinner" and the evening meal (usually quite early evening) "tea" (even if it was still a hot meal).<br /><br />Middle class people and southerners tended to call the mid-day meal "lunch" and the evening meal (usually a bit later) "dinner".<br /><br />I think the point is that the main meal was referred to as "dinner", and working class people had this in the middle of their working day to fuel themselves up. "Tea" would be smaller, and probably starchy, e.g. beans on toast. "Supper" was a little snack at bedtime, e.g. cocoa and a chocolate biscuit. (Middle-class people sometimes referred to "supper" when they meant their main evening meal, to confuse the issue).<br /><br /><br />Interestingly, at school (even in middle class areas) the mid-day meal was always "dinner", and I think is still referred to that way. You had to take your "dinner money" in every week.<br /><br />Working patterns have now changed, heavy industry has largely disappeared, and class distinctions are more blurred, but the regional meal-name differences are still there, I am fairly sure.montmorencyhttps://www.blogger.com/profile/12879422255762834319noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-22786473215621900382011-12-22T21:08:51.625+00:002011-12-22T21:08:51.625+00:00@Wooo:
I respect a lot of what you write, but no ...@Wooo:<br /><br />I respect a lot of what you write, but no low-carbers or low-carb spokespeople that I know of say stuff your face regardless of hunger.<br /><br />Most people in my experience say only eat when you are hungry. Eat until you stop feeling hungry. When you stop feeling hungry, stop eating.<br /><br />The point is that on low-carb people tend to be easily sated on their low-carb fare, and know when to stop eating, and then don't feel hungry again for quite some time afterwards, usually around their next normal meal time. (This very simple point is one that the "Food Reward" crowd seem to have great difficulty getting their heads around; that or they simply don't want to understand it).montmorencyhttps://www.blogger.com/profile/12879422255762834319noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-72082333962112791682011-12-22T20:31:56.635+00:002011-12-22T20:31:56.635+00:00@Mnature (and detractors):
On what is an ideal we...@Mnature (and detractors):<br /><br />On what is an ideal weight:<br /><br />My Pa-in-law lived to 90 and was very overweight (but still active) all the time I knew him, although he slowed down in his last few years).<br /><br />My Ma-in-law lived to nearly 88, and was very overweight all the time I knew her, but was in fine health, although a bit frail in her last few years.<br /><br />My mother is 88, looks after herself, walks to town, shops, cooks for herself (and others quite often), rarely ill. She lived through the depression (her family knew unemployment and poverty, but living in the country, kept chickens and grew vegetables and ate real food, albeit not much of it), worked 12-hour-shifts in an aircraft factory in the war, worked hard all her life (retiring at 70). She has been dieting since I was a kid, and is still significantly overweight.<br /><br />My Dad went through similar experiences, worked hard all his life (retired well into his 70s). He gradually put on weight from middle age onwards, and certainly would have had visceral fat, but was hardly ever ill. Died at 84.<br /><br /><br />So that's 4 out of 4 people with visceral fat, who all lived active lives till at least 80, and longer.<br /><br /><br />Can't give you an exact quote, but in Barry Groves' "Natural Health and Weight Loss", he also casts doubt on the obsession with body weight, and shows studies where higher weight than average was associated with longevity, not lower weight than average.<br /><br /><br />And of course it's a similar story with cholesterol. As perhaps most of us here know, longevity has been shown to peak on average around 270-280 mg/dl.<br />(If it goes much higher, then maybe something is definitely wrong, e.g. thyroid, but artificially lowering it with statins or other drugs is definitely not the answer. The answer is to find why it's going up and it is almost certainly the body's (healthy) response to some kind of stress or inflammation).<br /><br />Regards,<br />Mikemontmorencyhttps://www.blogger.com/profile/12879422255762834319noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-38545288624821469732011-12-19T17:42:07.575+00:002011-12-19T17:42:07.575+00:00+1 for next post+1 for next postKRAM Labshttps://www.blogger.com/profile/18205338103602853389noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-91884356311534175632011-12-16T11:56:29.769+00:002011-12-16T11:56:29.769+00:00Hi Gladina,
'..I'm just a bit confused o...Hi Gladina, <br /><br />'..I'm just a bit confused on what you think is the primary cause of this iron overload.'<br /><br />Sorry, I haven't explained myself very well. The primary cause appears to be a diet high in muscle meat and refined carbs. The evidence suggests that the crucial thing is the ratio between iron and manganese, which in beef muscle is about 100. <br /><br />Iron and manganese share an uptake system in the gut, so if you eat a lot of iron you will absorb less manganese. <br /><br />White flour has had most of its manganese removed and replaced with iron. This is insane, of course. The grain has manganese because it's needed for processing the carbohydrate during germination, and we need it for the same reason.<br /><br />You can see how the combination of beef muscle and white flour (McDonalds) will have an iron-manganese ratio somewhere in the stratosphere.Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-91796454268460756252011-12-16T04:01:52.102+00:002011-12-16T04:01:52.102+00:00@ Jane
There is no mechanism for iron excretion. ...@ Jane<br /><br />There is no mechanism for iron excretion. <br /><br />Iron overload may be the primary cause of carbohydrate intolerance.<br /><br />How does this overload become manifested in the first place? Is this an interaction between iron and carbohydrates? I'm just a bit confused on what you think is the primary cause of this iron overload.<br /><br />Yes, iron overload is of course toxic, and the mechanism you explained how it leads to oxidative stress, which leads to improper clearence of unfolded proteins makes sense. I just want to know where you stand on the cause (other than the manganese/copper deficiency standpoint). What causes these deficiencies. I will not tell for you on any carbohydrate/insulin hypothesis, since you might have a different hypothesis to explain this overload (and deficiency). <br /><br />Thanks.Zorica Vuletichttps://www.blogger.com/profile/05793548904884383364noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-15403495070578630192011-12-13T22:40:33.882+00:002011-12-13T22:40:33.882+00:00ding-ding-ding: evil fructose gets along just fine...ding-ding-ding: evil fructose gets along just fine with evil SFA over here... btw, cant wait for dat next post peter ;)D1Shttps://www.blogger.com/profile/08750123947536499341noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-88140315492707217022011-12-12T22:12:15.187+00:002011-12-12T22:12:15.187+00:00"Indeed, both palmitoleic acid and SCD-1 inde..."Indeed, both palmitoleic acid and SCD-1 index increase in response to SFA intake180, results also supported by animal data suggesting that dietary SFA induce SCD-1 activity and hence increase endogenous fatty acid synthesis of MUFA181. Moreover, in the Western societies, especially in elderly populations and decades ago, oleic acid is mainly provided by animal derived fat, and not from olive oil, which is the major source for MUFA in for example the Mediterranean countries. Thus, MUFA in cholesterol esters reflects dietary saturated fat intake rather than dietary MUFA intake14, suggesting that the present correlation between MUFA, SCD-1 index and CRP probably reflects high meat and dairy fat intake. SCD-1 index can also be influenced by a high carbohydrate intake (especially from sugars) via de novo lipogenesis182-184. This endogenous synthesis of fat is however believed to be small in Western populations due to the relatively high fat intake3,4,184,185. Whereas SCD-1 index shows a strong positive relation to insulin resistance in Amerindians living under Western conditions, this association is absent in Amerindians with traditional hunter/gatherer lifestyle despite a higher SCD-1 index. Thus, if the diet is very low in fat and high in non-refined carbohydrate the plasma SCD-1 index might reflect enzyme activity in adipose tissue rather than in the liver, whereas activity in the latter probably is the case in Western diets with a higher fat content186. SFA was not related to inflammation, perhaps because inflammation is promoted by a metabolic disordered state associated with elevated SCD-1 activity rather than the SFA intake per se."<br /><br />Hi YME,<br /><br />The above quote, from pages 47-8, seems to sum up the PhD. It's very clear that HGs have a high SCD-1 index and this has no association with insulin resistance. In acculturated Amerindians there is an association between SCD-1 and insulin resistance. The thesis then speculates that HGs eat a diet very low in fat and very high in non refined carbohydrate (WTF, this reminds me of the joke I saw on facebook which goes along the lines of: What is the HG term for a failed hunter? A vegetarian) and that under these conditions SCD-1 is active in adipocytes rather than hepatocytes. Which is apparently Good. Or alternatively I could, with a high probability of being correct, speculate that acculturated people are using SCD-1 on fructose induced DNL-derived saturated fat and the fructose is the cause of the insulin resistance in these acculturated folks... Genuine HGs can eat saturated fat and use SCD-1 with impunity whenever needed to (like myself) because they eat no HFCS. Basing your PhD on looking at fat without thinking about fructose is going to be depressing and will certainly make you go far in obesity research! Like Bengt Vessby and Nils-Georg Asp.<br /><br />More comments when I get the chance.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-51824700926634338832011-12-12T16:39:39.352+00:002011-12-12T16:39:39.352+00:00OT: Peter, have you had a look at this doctoral th...OT: Peter, have you had a look at this doctoral thesis: http://uu.diva-portal.org/smash/get/diva2:432322/FULLTEXT01<br /><br />Conclusions: High proportions of MUFA in serum cholesterol esters and a high SCD-1 index are related to increased CRP concentrations, independently of obesity, lifestyle factors and insulin resistance. In these Swedish popula<br />tions, these associations may partly be a reflection of a long-term high SFA intake. It may also be a reflection of a link between lipogenic activity and inflammation. <br />A low proportion of linoleic acid (18:2 n-6, the major dietary n-6 PUFA) in serum cholesterol esters, indicating a low vegetable fat intake, is associated with higher CRP levels. <br />Supplementation with a low dose of n-3 PUFA for 12 weeks did not <br />affect systemic inflammation and lipid peroxidation in individuals with the metabolic syndrome. <br />Neither the macronutrient proportions (i.e. fat versus carbohydrates) nor a diet high in MUFA from e.g. olive oil or a diet high in SFA did influence markers of inflammation or oxidative stress. <br />A high intake of dietary n-6 PUFA (linoleic acid) during 10 weeks does not increase systemic inflammation and lipid peroxidation. Instead it may reduce plasma levels of some inflammatory markers compared with <br />a diet rich in SFA. <br />Taken together, this thesis suggests that systemic low grade-<br />inflammation is to some extent associated with certain dietary fatty acids. In addition, indices of endogenous fatty acid desaturation (i.e. increased SCD-1 activity index) were also shown to be associated with higher systemic inflammation.YMEhttps://www.blogger.com/profile/01051729786474202102noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-11796807231181198342011-12-07T11:46:18.136+00:002011-12-07T11:46:18.136+00:00This is quite a new drug, isn't it? I'm no...This is quite a new drug, isn't it? I'm nowhere near as versed in body biology, so I probably should be keeping my mouth shut, but all the same a drug that kills off your fat cells sounds scary and potentially harmful...who knows what long-term effects it could cause? Just my emotional response..Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-42709911456374928542011-12-06T11:42:47.692+00:002011-12-06T11:42:47.692+00:00Travis Culp,
Have you come across a link between ...Travis Culp,<br /><br />Have you come across a link between fructose and copper deficiency? <br /><br />'Dietary copper deficiency is associated with a variety of manifestations of the metabolic syndrome, including hyperlipidemia and fatty liver. Fructose feeding has been reported to exacerbate complications of copper deficiency. ...Our data suggest that high fructose-induced nonalcoholic fatty liver disease (NAFLD) may be due, in part, to inadequate dietary copper. Impaired duodenum Ctr-1 [copper transporter] expression seen in fructose feeding may lead to decreased copper absorption, and subsequent copper deficiency.'<br /><br />http://www.ncbi.nlm.nih.gov/pubmed/21781943<br /><br />BTW, I just read the comment you wrote yesterday on WHS. Great stuff.Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-83756652841634472512011-12-05T19:08:19.222+00:002011-12-05T19:08:19.222+00:00A Cross-Sectional Characterization of Insulin Resi...A Cross-Sectional Characterization of Insulin Resistance by Phenotype and Insulin Clamp in East Asian Americans with Type 1 and Type 2 Diabetes<br /><br /><br />http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0028311<br /><br />Peter, please delete if not interested.john1https://www.blogger.com/profile/13122738730155221839noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-20884695658566517162011-11-28T23:24:01.542+00:002011-11-28T23:24:01.542+00:00gallier: I agree that the glycosidic bond between ...gallier: I agree that the glycosidic bond between fructose and glucose in sucrose makes metabolism hugely different. The odds of a particular fructose bolus reaching the blood stream and glycating proteins or ending up far down in the GI tract and causing digestive issues is much higher. To be fair, the mixed fructose and glucose does occur with honey, but we 1) didn't evolve to eat it every day and 2) studies have shown that metabolism is different, for whatever reason.<br /><br />There's so much talk about the Kitavans and carb tolerance in general, but I would wager that those fellows aren't sedentary, and that makes a massive difference. There are piles of studies that show a difference in glucose tolerance between the trained and untrained. It ain't the beta cells that proliferate when you lift weights....Travis Culphttps://www.blogger.com/profile/02611059005476928227noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-38321109566296490272011-11-28T16:28:07.464+00:002011-11-28T16:28:07.464+00:00Arby, I'm with you on that. The question of wh...Arby, I'm with you on that. The question of whether HGs or pre-industrial Americans ate breakfast or not is interesting. But I guess I'll let personal experience answer it for me. <br /><br />My experience right now is that, while not easy to maintain on a daily basis, one plus I do note from increasing a.m. protein is an increase in dream recall.bopeshttps://www.blogger.com/profile/04363650834196106133noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-76172533152448248922011-11-28T15:56:12.106+00:002011-11-28T15:56:12.106+00:00@David, Blogblog,
According to Marie Antoinette, ...@David, Blogblog,<br /><br />According to Marie Antoinette, french peasants in the 18th century ate a lot of cake. <br /><br />I don't think I follow the end conclusion/inference here. Is it worth all this debate over the facts?Arbyhttps://www.blogger.com/profile/14410677491085665147noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-87413833189400257752011-11-28T12:46:12.494+00:002011-11-28T12:46:12.494+00:00@blogblog
No, humans cannot 'store or excrete...@blogblog<br /><br />No, humans cannot 'store or excrete minerals as needed' in one important case: iron. There is no mechanism for iron excretion. <br /><br />Iron overload may be the primary cause of carbohydrate intolerance. <br /><br />It works like this: iron causes oxidative stress by converting excess superoxide into the very toxic hydroxyl radical. Excess superoxide comes from deficiencies of copper and manganese, which activate superoxide dismutases. <br /><br />Beta cells are very sensitive to oxidative stress, like all cells that make large amounts of proteins for export, because the proteins cannot fold properly.<br /><br />Unfolded/misfolded proteins are normally cleared by the UPR (unfolded protein response), and if they aren't, inflammation follows. This is what causes your inflammatory bowel disease.<br /><br />Carbohydrate intolerance involves exactly the same process, happening in beta cells and many other tissues including the hypothalamus and the midbrain. Endocrine and brain cells are especially susceptible.Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-65081662543061769532011-11-28T03:00:40.850+00:002011-11-28T03:00:40.850+00:00@blogblog:
Excuse me, but your statement was &quo...@blogblog:<br /><br />Excuse me, but your statement was "Before the 1870s most Americans skipped breakfast."<br /><br />You then go on to argue<br /><br />"Only a 1/4 of Americans lived on farms by the 1870s." <br /><br />The data I find most readily says that the population in 1870 was 38.6 million; the farm population was 18.4 million. Half the labor force was still working in agriculture (The latter figure is from the 1870 census. It's available from the US Census Bureau, although the pdf is 154 MB.)<br /><br />Note also that "agricultural laborers" were almost as large a percentage of the population as "farmers," so the percentage of people "living on farms" <br />I am sure that you read somewhere that only 25% of Americans lived on "farms," but that must be a very resticted definition of farm, which excludes things like, say, ranches.<br /><br />Im any case, you were talking about BEFORE 1870, when the farm population was a much larger share of the total. For instance, when I talk about what was eaten at Monticello, that was well before 1870.<br /><br />Prior to refrigeration and highly mechanized transport, I seriously doubt that farm families in America always sold all of their eggs and never ate them. <br /><br />When de Tocqueville toured America in 1831, he wrote back home, "At first we found the absence of wine from meals a serious deprivation, and we are still baffled by the sheer quantity of food that people somehow stuff down their gullets. Besides breakfast, dinner, and tea*, with which Americans eat ham, they have very copious suppers and often a snack." (*"tea" referring to the meal rather than the substance.")<br /><br />Most of the visitors to America prior to the Civil War remark on how well-fed all the people except the urabn poor are.<br /><br />The height of American soldiers in the Civil War was certainly lower than it is today, but it was higher than in Europe. It is also not clear how fine a proxy this is for anything, as slaves in the plantation south were much taller than any other group (which has led some authorities to claim that slaves were treated especially well).<br /><br />In GCBC, Taubes makes a pretty convincing case that we really don't have good statistics on what people ate until quite recently; and that the numbers we do have probably greatly underestimated the past consumption of eggs, meat, milk, and fresh vegetables, since these were the products most likely to be consumed locally without ever being recorded. <br /><br />I also am unable to find evidence that "most" Hunter-Gatherers never eat before mid-afternoon. It certainly isn't true of the Inuit, who eat whenever they are hungry, and are also likely to snack throughout the day. <br /><br />And I know people who have spent time with the Bushmen; whether they eat in the morning has to do mostly with whether they have food on hand in the morning.<br /><br />Can you point me to a source that has done any kind of systematic evaluation of the meal frequency of hunter-gatherer peoples?David Isaakhttps://www.blogger.com/profile/04928598446742324391noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-72861681235370627522011-11-27T15:13:41.438+00:002011-11-27T15:13:41.438+00:00@Wooo, Gallier2 -
At roughly the same time as th...@Wooo, Gallier2 - <br /><br />At roughly the same time as the rapid increase in HFCS, we see the major shift to industrial seed oils accelerate under the "guidance" of the US government health campaign (and I believe that was slavishly followed by other governments). We may be seeing a synergistic effect of the two unnatural "foods" in vivo.annleehttps://www.blogger.com/profile/17666381399321975755noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-67418984781020322382011-11-27T10:36:56.737+00:002011-11-27T10:36:56.737+00:00@Itsthewoo
I disagree that HFCS and sucrose are m...@Itsthewoo<br /><br />I disagree that HFCS and sucrose are metabolized in the same way. HFCS is a racemic mix (http://en.wikipedia.org/wiki/Racemic_mixture) of fructose and glucose <b>mono-</b>saccharides, while sucrose is a <b>di-</b>saccharide which needs an enzymatic cleavage before the chiral fructose and the chiral glucose can be absorbed. <br />These 2 differences (chirality and mono/di form) suggest that there might be also a metabolic difference. I have searched for more info on that subject but haven't found a lot, more because it hasn't be studied at all than the effect of not being existent.<br /><br />Your other point about putting that stuff everywhere because of cheapness and practicality is still valid.gallier2https://www.blogger.com/profile/04285836062429366578noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-39154005846875635502011-11-27T08:48:42.862+00:002011-11-27T08:48:42.862+00:00@Arby
I agree. Our bodies have no natural mechanis...@Arby<br />I agree. Our bodies have no natural mechanism for large scale apoptosis. This is why obesity is a permanent disorder. There is no way to remain at a reduced weight and to magically become naturally thin, without medical intervention to remove superflucous adipocytes (either drugs or surgery).<br /><br />We never evolved to become obese, this is purely a modern disease. We have no counterregulation against it. Our bodies evolved without knowing that chronic hyperinsulinism for years and years is even possible. Obesity itself suggests that humans prone to it do not have counterregulation against hyperinsulinemia-induced fat storage.<br />The only defense is artful control of insulin levels, after inducing adipocyte hypotrophy by being in energy deficit for a few months.<br /><br /><br />I understand you would like to succeed, I can understand that... but, it's just a suggestion, you might find that trying to eat a bit less can help. Is it more important to be a posterchild for a perfect paleo low carb diet, whatever that means, or is it more important to be in control of obesity and your glucose/insulin levels?<br /><br />When I was very young starting LC, I often heard the propaganda that on LC you need to "force yourself to eat". I heard the propaganda that you would gain weight if you "stopped eating". I was so young and new I believed them and began frying up steaks and forcing myself to eat them, EVEN THOUGH my body was like "well I really don't want food, why are you eating now?"<br /><br />This lasted a very short while until common sense kicked in . Sitting there feeling very full and nauseated , listening to my body, lead me to conclude that it is patently irrational to assume that eating food will produce weight loss. My body generates tehse signals for a reason - nausea and fullness is telling me my body does not at this moment need food.ItsTheWooohttps://www.blogger.com/profile/12057537399918684119noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-85068650558456463912011-11-26T22:08:52.355+00:002011-11-26T22:08:52.355+00:00@blogblog
Interesting historical info. I do not k...@blogblog <br />Interesting historical info. I do not know if it is true or not, but I trust you, and suddenly the "excellent health" of people in past centuries makes a slight bit more sense.<br /><br />Though your writing seagues into the idea that all carbs cause disease, the fact is that most people were slim until about the 1970s/80s. I know, because I was a baby in the 80s, and I distinctly remember wearing adults clothing and being the only fat kid in my classes. Today, any class of very small children has tons and tons of quite fat children, obesity is now relatively normal for children. This was not at all the case when I was a small child; it was usually myself, and maybe 1 or 2 other children who were distinctly fat.<br /><br /><br />It seems that severity/rates of obesity have risen substantially circa 1970. This suggests more than carbohydrate is involved as americans were eating lots of carbs prior to 1970.<br /><br />The piece that is causing this is not carbs in general, but the invention of HFCS. HFCS is metabolically equal to sucrose, the reason it is bad is that it incentives manufactureres to bloat portions sizes and to put sugar in everything. If HFCS was never invented, the obesity epidemic could not have occurred, that is my belief. It would have been economically infeasible to create monster slushies and tons of cheap baked goods which are nothing but transfat (remember that crap? lol) and sugar.ItsTheWooohttps://www.blogger.com/profile/12057537399918684119noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-40085365661470261922011-11-26T17:09:22.683+00:002011-11-26T17:09:22.683+00:00Large scale adipoptosis (is that a word yet?) prob...Large scale adipoptosis (is that a word yet?) probably doesn't make sense under the paleo paradigm. If humans only cycled between a winter weight and a summer weight, then the adipocyte set shouldn't need to be reduced under historicle circumstances. Evolution would not need to provide for adipocyte apoptosis of as much as 1/2 of all adipocytes.<br /><br />On the other hand, people do succeed after stalls in weight loss on low carb when the shouldn't be able to due to adipocyte hyperplasia. <br /><br />@wooo, I want to see this thing through. Many of my friends are counting on me as an example.Arbyhttps://www.blogger.com/profile/14410677491085665147noreply@blogger.com