@Aria999 when you make a google search, google will not offer links to content that has an intellectual property, therefor the prestigious medical journals (science, nature, cell, ...) who have a paywall on their medical papers will not come up. However, if you go on the medical library called pubmed pubmed.ncbi.nlm.nih.gov you will find them there.
There is also the effect called echo chamber , in which content that relates to your beliefs is offered by search algorithm . This has been clearly demonstrated during the antivax movement, Trump and so on. We are also more likely to dismiss whatever proof that disagrees with us. That's human and this is why trying to convince someone, an antivaxxer, a trumpist, or whatever ideology, religion, diet is pointless and a waste of time.
There is plenty of science that has tested the insulin model, and it was disproven again and again and again. An again.
Of course, if you do a study of junk food vs low carb, low carb is better, but when you test low carb vs low fat, with equal calories and equal protein, there is nothing to be gained by controlling insulin. All the feeding tests in which you control the food given to participants failed.
Kevin Hall locks people up for a living. He puts a group of people in a clinic with no access to outside food, every single morsel is monitored , and he alternates groups between low carb and low fat with equal calories and equal proteins. And before you scream "conflict of interest", I have to tell you, there was a big conflict of interest because the main blow to the insulin theory was done in a study paid by the low carb, and despite that , despite paying millions and having enrolled one of the highly regarded nutrition researcher , despite all that, they failed the insulin model.
A review paid by the low carb www.nature.com/articles/ejcn2016260 this has a paywall, but I have access through work and here is the review:
START
REVIEW
A review of the carbohydrate–insulin model of obesity KD Hall
European Journal of Clinical Nutrition (2017) 71, 323–326
© 2017 Macmillan Publishers Limited, part of Springer Nature. All rights reserved 0954-3007/17
www.nature.com/ejcn
The carbohydrate–insulin model of obesity theorizes that diets high in carbohydrate are particularly fattening due to their propensity to elevate insulin secretion. Insulin directs the partitioning of energy toward storage as fat in adipose tissue and away from oxidation by metabolically active tissues and purportedly results in a perceived state of cellular internal starvation. In response, hunger and appetite increases and metabolism is suppressed, thereby promoting the positive energy balance associated with the development of obesity. Several logical consequences of this carbohydrate–insulin model of obesity were recently investigated in a pair of carefully controlled inpatient feeding studies whose results failed to support key model predictions. Therefore, important aspects of carbohydrate–insulin model have been experimentally falsified suggesting that the model is too simplistic. This review
describes the current state of the carbohydrate–insulin model and the implications of its recent experimental tests.
European Journal of Clinical Nutrition (2017) 71, 323–326; doi:10.1038/ejcn.2016.260; published online 11 January 2017
INTRODUCTION
Obesity is defined as an excess accumulation of body fat, and understanding obesity at the most basic level requires knowledge of how adipose tissue fat storage and mobilization are regulated. Insulin has a major role in modulating the activity of several enzymes whose net effect is to promote the uptake, retention and net storage of fat in adipose tissue.1 These basic facts of adipose tissue physiology, along with the observation that dietary carbohydrates are the primary driver of insulin secretion, have led to the hypothesis that high carbohydrate diets are particularly fattening.
In particular, the ‘carbohydrate–insulin model’ of obesity posits that diets with a high proportion of carbohydrate elevate insulin secretion and thereby suppress the release of fatty acids from adipose tissue into the circulation and direct circulating fat toward adipose storage and away from oxidation by metabolically active tissues such as heart, muscle and liver.2–5 This altered fuel availability is theorized to lead to a state of cellular ‘internal starvation’ leading to adaptive decreases in energy expenditure and increased hunger.2,5–7 Therefore, the positive energy balance associated with development of obesity is purported to be a consequence of the insulin-driven shift in fat partitioning toward storage in adipocytes, which decreases energy expenditure and increases food intake in an attempt to remediate the cellular internal starvation of metabolically active tissues. Rather than being a passive accumulator of fat as a result of overeating, the carbohydrate–insulin model suggests that endocrine dysregula- tion of adipose tissue is the primary driver of positive energy balance.
The carbohydrate–insulin model provides a plausible explana- tion of why insulin therapy tends to cause weight gain in people with diabetes8 and why outpatient diet trials comparing low carbohydrate diets to others tend to show greater short-term weight loss despite low carbohydrate diets being unrestricted in calories.9–11 Several popular books have promoted the carbohy- drate–insulin model to the public as the reason why they have
gained excess weight in the past and why they should follow a low carbohydrate, high fat diet for weight loss.12–14 However, despite the apparent explanatory power of the carbohydrate– insulin model, its scientific basis is questionable and recent studies have challenged key predictions of the model.
SCIENTIFIC MODELS AND THE PRINCIPLE OF EXPERIMENTAL FALSIFICATION
Scientific models seek to integrate a variety of data and explain a set of observations about a system within an overarching theoretical and mechanistic framework. Experimental confirma- tion of a model’s predictions provides support for the validity of the model and repeated confirmations may eventually lead to widespread acceptance of the model as the scientific standard. However, scientific models cannot be proven to be true. Rather, models represent provisional representations of our understand- ing, and countering evidence may require substantial model corrections or possibly outright rejection of the model. Impor- tantly, scientific models go beyond providing putative explana- tions and make experimentally testable predictions that are capable of falsifying the models.15
As model falsification is relatively rare in the field of nutrition, I will use a well-known example from physics to illustrate the process.16 In the late nineteenth century, physicists postulated that light propagated as a wave through a medium called the ‘luminiferous ether’. Like the carbohydrate–insulin model, the ether model seemed highly plausible as the wave-like nature of light was well-known and all other waves propagated through a medium. It was difficult to conceive how a wave could propagate through a vacuum without a medium and scientists readily accumulated evidence in favor of the ether model. (For example, comet tails were thought to be caused by ‘ether drag’ as they moved through the medium.) The ether model explained a lot and it made sense. Unfortunately, it was also wrong.
As with all scientific models that attempt to explain certain phenomena, the ether model made predictions that were experimentally testable. More specifically, experiments can be designed that are capable of falsifying the model meaning that failure of any necessary model prediction requires that the model be abandoned as either too simple or simply incorrect. It does not matter how many model predictions are successfully confirmed by the experiment, failure of any single prediction means that the model is falsified.
For the ether model of light propagation, falsification came with the classic Michelson–Morley experiment in 1887 that failed to detect a significant difference in the speed of light moving in different directions through the hypothesized ether. Since then, several more definitive experiments were conducted that confirmed these results. The experimental falsifications of the ether model did not imply that light does not have wave-like properties, but the simple ether model of light propagation was untenable.
EXPERIMENTAL FALSIFICATION OF THE CARBOHYDRATE–
INSULIN MODEL
Whereas some models of obesity are so complex that it is difficult to know where to begin when assessing their validity,17 the carbohydrate–insulin model provides clear experimentally testa- ble predictions. For example, the carbohydrate–insulin model predicts that diets with decreased proportion of carbohydrate to fat, but identical protein and calories, will reduce insulin secretion, increase fat mobilization from adipose tissue and elevate fat oxidation. The altered metabolic and hormonal milieu associated with reduced dietary carbohydrate will therefore relieve the state of cellular internal starvation resulting in decreased hunger, increased body fat loss and increased energy expenditure compared with an isocaloric diet with higher carbohydrates and higher insulin secretion.2 If any of these predictions fail, then the carbohydrate–insulin model is falsified and a more commensurate model must be sought.
Testing the model predictions requires inpatient feeding studies as diet adherence cannot be guaranteed in outpatient studies.18 Recently, two metabolic ward studies directly tested the logical consequences of the carbohydrate–insulin model in humans.19,20 Both studies were conducted while subjects were continuously residing in metabolic wards where they consumed carefully controlled diets. Both studies found the expected rapid and sustained decrease in insulin secretion when dietary carbohy- drates were restricted. Therefore, the experimental conditions required to test the predictions of the carbohydrate–insulin model were fully satisfied.
In concordance with the model predictions, carbohydrate restriction led to increased fat oxidation reaching a maximum within a few days and remaining constant thereafter. However, neither study found the predicted augmentation of body fat loss with carbohydrate restriction. Rather, despite the reduction in insulin secretion, both studies found slightly less body fat loss during the carbohydrate restricted diets compared with isocaloric higher carbohydrate diets with identical protein.13,14
In one study, the reduced carbohydrate diet led to a significant decrease in energy expenditure, both during sleep and through- out the day, a result counter to the carbohydrate-insulin model.19 In the other study, a very low carbohydrate ketogenic diet led to increased daily energy expenditure of only 57 kcal/day, and the effect waned over time.20 Although this small energy expenditure increase during the ketogenic diet was in the direction predicted by the carbohydrate–insulin model, it was quantitatively much less than what was expected. Specifically, the effect size of the pre-specified primary energy expenditure outcome was substan- tially smaller than the 150kcal/day threshold determined in advance to be the smallest change that would be considered physiologically important. Furthermore, the observed energy expenditure effect was several-fold lower than the 400–600 kcal day effect previously estimated to be the ‘sizable metabolic advantage’ of a very low carbohydrate diet21 and incompatible with the popular claim of Dr Robert Atkins that such diets increase energy expenditure to an extent that they offer a ‘high calorie way to stay thin forever’.12
CONCORDANCE WITH PREVIOUS INPATIENT FEEDING STUDIES
Despite achieving the desired differences in insulin secretion via isocaloric manipulation of dietary carbohydrate and fat, the recent studies19,20 clearly demonstrated that the energy expenditure and body fat predictions of the carbohydrate–insulin model failed experimental interrogation. These results are in accord with previous inpatient controlled feeding studies that have either found small decreases in energy expenditure with lower carbohydrate diets22–25 or reported no statistically significant differences26–35 when comparing diets with equal calories and protein, but varying carbohydrates from 20 to 75% of total calories. Furthermore, the small effects on body fat loss were similar to those of previous inpatient feeding studies finding no significant differences in body fat resulting from isocaloric variations in carbohydrate and fat.30,36–39
There has never been an inpatient controlled feeding study testing the effects of isocaloric diets with equal protein that has reported significantly increased energy expenditure or greater loss of body fat with lower carbohydrate diets.
THE END
www.nature.com/articles/s41591-020-01209-1
Christopher Gardner is another university professor and he made the famous DIETFIT study which followed hundreds of people doing either low fat or low carb ,and at the end, people lost weight on both studies and people gained weight on both studies. Again millions spent on several studies and there is no superiority to the LCHF. Again, that study was paid by a low carb foundation and nope, low carb is not superior.
Taubes' foundation that was going to prove to the world how bad carbs and insulin were , Nutrition Science Initiative , lost credibility and funds, and you can read a bit about the rise and fall here. www.wired.com/story/how-a-dollar40-million-nutrition-science-crusade-fell-apart/. The theory couldn't pass the test.
The science has been there for years. Done, dusted, move on. Once a fact is scientifically established, science moves to other topics
People can lose weight in many ways. You need to find the way that suits you and fits with your life. It is low carb, go for it, but don't preach a superiority or patronise people on something you have watched on YouTube or because of the influencer-du-jour, an osteopath (for some reason, osteopaths love low carb), a journalist, a MNetter, a podcast, and the list goes on and on .
Have a look around pubmed @Aria999 if there is a paper you want to read that has a paywall, send me a PM, and I will see if I have access and send you a PM with the unlocked paper.