Eating Pattern Comparison Table

Lmao, and OPs chart says high levels of saturated fat is a good thing. This is borderline dangerous misinformation.

If you want to eat fibre you can, nobody is stopping you.

If you find observational epidemiology compelling, great! But the science minded people here don't - https://www.diagnosisdiet.com/full-article/epidemiological-studies

You can't use epidemiology to establish cause and effect; You can't made causal statements that eating more beans reduces heart attacks, it has to be contextualized to the study conditions and populations that are observed post-hoc using FFQ and that don't isolate other variables.

I’m not sure if you see the bias. They all already share the conclusion.

I absolutely see the bias, but that is why i read the original papers when i can. I read extensively, and I hope broadly, but of course you and I both have our biases.

This one in particular is interesting as it regards Gary Taubes, who you seem to favor, and the organization he create and which rebutted his conclusions.

I don't feel the need to defend Taubes, he is more then capable of defending himself. If you want to talk about a specific paper saying fibre is a essential nutrient I'll read it

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https://doi.org/10.3945/ajcn.116.133561 - Energy expenditure and body composition changes after an isocaloric ketogenic diet in overweight and obese men

If we look at the study it was only a 4 week intervention - It takes about 12 weeks to get fully fat adapted, ketones were not measured, but you don't have to take my word for it!

https://doi.org/10.3945/ajcn.116.142182 - Raising the bar on the low-carbohydrate diet - In a direct response to Hall's paper

According to the clinical trials registry, this study was designated a pilot, presumably with the aim of acquiring preliminary data for a future study. By definition, pilot studies are not powered to make precise estimates of effect sizes or rigorously test a hypothesis. Thus, it is surprising that the authors dismissed the importance of the primary outcome: an increase in energy expenditure on the KD on the basis of 2 independent state-of-the-art methods. A fairer interpretation would be to reject the null hypothesis (i.e., all calories are alike from a metabolic perspective)—a remarkable finding for a pilot.

the pilot study likely underestimated the true effect of the KD because of several fundamental methodologic limitations, most importantly the nonrandomized (technically observational) design. Because the baseline diet was given first to all participants, any factor that changes with time could confound outcomes.

In addition, the protocol failed to measure energy losses from ketones and fat in the breath, urine, and stool, which would have been greater when consuming the KD.

metabolic chamber respirometry was shown to be inferior to doubly labeled water in the detection of adaptive thermogenesis, according to a comparative study involving several coauthors of the present investigation (6). Therefore, the doubly labeled water measurements collected during the final 2 wk of the assessment period flatly contradict the authors’ inferences about time course.

the authors overinterpret the initial reduced rate of change in fat mass after initiation of the KD. For individuals who habitually consume a high-carbohydrate diet, it may take several weeks for fat oxidation to reach steady state after they increase fat intake (9, 10). Although disregarded, their data actually support this possibility, with an apparent acceleration in fat-mass loss in the final 2 wk of the KD (as visually demonstrated in Figure 2B of the study).

The conventional “calories in, calories out” approach to obesity has been largely unsuccessful in practice throughout the last 40 y, as evidenced by the continuing high prevalence rates and the difficulty of most individuals in maintaining weight loss over the long term. The carbohydrate-insulin model proposes an alternative approach to obesity treatment that is based on considerable theoretical and clinical data. Properly controlled and adequately powered randomized controlled trials are urgently needed to test this model.

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https://doi.org/10.1038/s41591-020-01209-1 - Effect of a plant-based, low-fat diet versus an animal-based, ketogenic diet on ad libitum energy intake

This paper isn't open access, so I can't read it directly - would you mind sharing it with me so I can actually respond in detail?

I can see from the abstract the crossover design without adequate adaptation/washout window - Rapid diet switching can produce carryover effects; metabolic and hormonal adaptations require time. Short periods bias results against low-carb/keto when no keto-adaptation phase is allowed. (same issue as with the above paper on cico)

Since the Hall paper isn't open access, but Soto's response is, let's dive into the identified issue with Halls second CICO paper: https://doi.org/10.1016/j.tjnut.2023.12.017 - Physiologic Adaptation to Macronutrient Change Distorts Findings from Short Dietary Trials: Reanalysis of a Metabolic Ward Study

We found that energy intake on the LCD was much lower when this diet was consumed first compared with second (a difference of −1164 kcal/d, P = 3.6 × 10-13); the opposite pattern was observed for the LFD (924 kcal/d, P = 2.0 × 10-16). This carry-over effect was significant (P interaction = 0.0004) whereas the net dietary effect was not (P = 0.4). Likewise, the between-arm difference (LCD - LFD) was −320 kcal/d in the first period and +1771 kcal/d in the second. Body fat decreased with consumption of the LCD first and increased with consumption of this diet second (−0.69 ± 0.33 compared with 0.57 ± 0.32 kg, P = 0.007). LCD-first participants had higher β-hydroxybutyrate levels while consuming the LCD and lower respiratory quotients while consuming LFD when compared with LFD-first participants on their respective diets. Change in insulin secretion as assessed by C-peptide in the first diet period predicted higher energy intake and less fat loss in the second period. These findings, which tend to support rather than oppose the CIM, suggest that differential (unequal) carry-over effects and short duration, with no washout period, preclude causal inferences regarding chronic macronutrient effects from this trial.

Two papers from Hall in a row, I think Hall has a bias too!

What I think is demonstrated here is that CICO has not been proven by Hall, and the Carbohydrate Insulin Model still stands viable. Clean studies will be most welcome here. I can point you at interesting hypercaloric feeding case series where we see a strong signal of the CIM!

Update - I saw that WALTER WILLET, the man himself, called this study "worse then useless because its misleading"...... If Walter Willet the king of weak epidemiology is against you..... man.... you got problems. https://youtu.be/tIPX_TnUAWQ - I'd really love to read this full paper!

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I'm a little confused first you discussed fibre, and the main thrust of your last post was about CICO. Could we limit each thread to a single topic so our goal posts don't get moved around too much.

I’m entirely in favor of deep dives into topics. I appreciate that you have done some extensive reading if it is fairly narrow. Keep at it and keep learning!

Fantastic, me too, I'm wrong about many things. Please don't be arrogant and diminish my reading of the literature through negative framing such as "extensive reading if it is fairly narrow". I actually read quite a lot of papers for and against my positions. If you only know one side of a argument, you don't know much. No need for sniping here, we can all be friendly. I could use the same to describe your positions, but I don't - I entertain the possibility I'm wrong - I hope you can offer me the same grace going forward.

Keep at it and keep learning

You too buddy, you too.

why-the-carbohydrate-insulin-model-of-obesity-is-probably-wrong-a-supplementary-reply-to-ebbeling-and-ludwigs-jama-article/

First things first: this article is from 2018. We have a better understanding of the field of metabolic health now, and all the advancements point towards the fact that the insulin model is a better model for dietary outcomes than the caloric model.

I invite you to look up various resources to see that what I am saying is not just an vacuous assertion. Perhaps you could start with the Low Carb Down Under conference, and in particular if you're curious about insulin I would recommend Prof. Bikman's material.

Having prefaced my position with that, let me put down some of my thoughts with regards to the points that Guyenet makes:

1. Dietary fat can be fattening

This is not irreconcilable with the insulin model as Guyenet asserts. When consuming a mixed diet of all three macronutrients (fat, carbohydrates, and protein), the Randle Cycle is activated. There is a cross-inhibition of the metabolism of glucose and fat.

This results in mitochondrial dysfunction since both glucose and fatty acids flood the system, resulting in production of reactive oxygen species, glycation, and lipid metabolites. This reduces the effectiveness of insulin signalling in the body, and is in part the cause of metabolic syndrome.

See: https://pmc.ncbi.nlm.nih.gov/articles/PMC2739696/ for details.

Guyenet appears to be entirely unaware of the existence of the Randle Cycle.

1. Kitavans

The Kitavan diet of just starchy root vegetables avoids Randle cycle activation. The very same observation is made by Dr. Chris Knobbes in his talk about seed oils, about the Tukisenta who eat more than 90% of their diet in sweet potatoes.

However, the Tukisenta have poor dental conditions and commonly suffer from arthritis. Dr. Knobbes attributes this to poor availability fat soluble vitamins, in particular A and K2.

1. Japan

In the postwar period the Japanese had no access to meat, and were eating a low fat high carbohydrate diet, once again avoiding Randle Cycle activation. Modern Japan, eating a mixed standard diet, suffers from the same metabolically associated chronic diseases as all western nations. There is little difference in the amount of dietary carbohydrates consumed in the modern Japanese diet from the west, although the Japanese do eat less ultra-processed food than the Americans, which would explain their reduced incidence of chronic disease.

Guyenet often confuses correlation with causation.

1. Mouse studies

We aren't mice!

But even in mice, FIRKO mice actually support the insulin model. When insulin is unable to act on fat cells, fat accumulation is prevented. This is strong evidence that insulin signalling in adipose tissue is required for fat accumulation.

Guyenet's assertion that the brain drives obesity does not exclude nor refute the downstream mechanism of insulin.

1. Acipimox

Acipimox isn't insulin!

As a result, we do not know if it fully replicates insulin's effects, and cannot claim that it does. This invalidates Guyenet's assertion. Additionally, it is only one study, and hence cannot be extrapolated to the population in general.

I am unable to access the rest of the study, but would also consider the following factors if I could: the term of the study, the follow-up period, the sample size, and confounding factors such as compensatory metabolic mechanisms in the body.

I could go on and address things like the false dichotomies Guyenet makes against the insulin model or his overemphasis on calories (a calorie isn't a calorie, see the other posts in this community) but I'm sure you've noticed that already since you also critically read papers that support your position :)

I hope that you continue to engage in good faith and not presume that we are ignoring bias. I think I speak on behalf of everyone on Lemmy when I say that condescension detracts from all our communities.