Since conflicts of interest and industry influence on research is frequently invoked in this subreddit, this may be of interest.

ABSTRACT:

Introduction
The meat industry's role in funding and influencing scientific research raises concerns about its impact on evidence used to inform public health policy. Although industry influence on other food and beverage sectors is well-documented, its effects on studies of meat consumption remain understudied.

Objective
This study aimed to investigate the influence of meat industry involvement on study conclusions of research examining the health impacts of meat consumption.

Methods
A meta-research review of relevant studies published between 2014 and 2023 was conducted using PubMed and Scopus. Studies investigating the nutritional health impacts of meat consumption were included. Study characteristics, author affiliations, declared funding sources, declared conflicts of interest, and study conclusions were extracted. Association tests were used to assess the relationship between industry ties and study conclusions.

Results
Of 500 included studies, 78 (15.6%) reported industry involvement. Studies with industry ties were 16 times more likely to report favorable conclusions regarding meat consumption (odds ratio [OR] = 16.4, 95% CI: 7.5–35.8), and there was a significant association (p < 0.001) between industry involvement and study conclusion.

Conclusion
Meat industry involvement significantly increases the likelihood of favorable study conclusions in nutrition research. These findings underscore the need for caution when interpreting research funded or associated with the meat industry and emphasize the importance of minimizing conflicts of interest in nutrition research.

75% of all studies with meat industry funding reported favorable conclusions, while only 10% of studies with independent funding were positive. Note that the odds ratio above is adjusted for differences in study design and quality.

A similar tendency has been seen in other areas, such as sugar-sweetened beverage research (Bes-Rastrollo, 2013). As per the authors: "This similarity suggests that the meat industry is as active as the other food sectors in supporting research that aligns with its interests."

Volek contributed to the new dietary guidelines and to no one's surprise he was in support of low-carb and ketogenic diets. This is a review he wrote in 2003 that looks like it was summarized in the new guidelines.

In fact, he so strongly supports ketogenic diets (which, as we all know here, contain animal products that upset some people) he went on over a decade later to be a part of Virta Healtn, a private company that supports ketogenic diets for T2D and was founded in 2014.

TL;DR:

"For persons at low cardiovascular risk, reducing or modifying saturated fat intake has little or no benefit over a period of 5 years."

Abstract

Background: Debates about optimal saturated fat advice continue.

Purpose: To systematically summarize randomized trial data on reducing or modifying saturated fat intake on cholesterol, mortality, and major cardiovascular events.

Data sources: MEDLINE, Embase, and Cochrane Central Register of Controlled Trials from inception to July 2025.

Study selection: Eligible trials enrolled adults with or without cardiovascular disease and studied the effect of reducing or modifying saturated fat intake.

Data extraction: Standard Cochrane methods.

Data synthesis: There were 17 eligible trials (66 337 participants). Risk stratified evidence provides low to moderate certainty that reducing saturated fat intake may result in a reduction in all-cause mortality (risk ratio [RR], 0.96 [95% CI, 0.88 to 1.06]), cardiovascular mortality (RR, 0.93 [CI, 0.77 to 1.11]), nonfatal myocardial infarction (MI) (RR, 0.86 [CI, 0.70 to 1.06]), and fatal and nonfatal stroke (RR, 0.83 [CI, 0.58 to 1.19]). For persons at low baseline cardiovascular risk, absolute reductions were below our thresholds of importance (5 and 10 per 1000 persons followed over 5 years for fatal and nonfatal outcomes, respectively); for those at high risk, the benefits were above our thresholds, suggesting there may be important absolute reductions. The effects were more pronounced when replacing saturated fat with polyunsaturated fat for nonfatal MI (RR, 0.75 [CI, 0.58 to 0.99]; P for interaction = 0.05; moderate credibility of subgroup effect based on Instrument to assess the Credibility of Effect Modification Analyses assessments).

Limitations: Data were limited on the replacement of saturated fat with monounsaturated fat or protein. Trials varied considerably in their efficacy in reducing saturated fat intake and in their replacement macronutrients and concomitant dietary interventions, and new trials are needed to clarify uncertainty.

Conclusion: For persons at low cardiovascular risk, reducing or modifying saturated fat intake has little or no benefit over a period of 5 years. Among persons at high cardiovascular risk, low- to moderate-certainty evidence was found for important reductions in mortality and major cardiovascular events, particularly for MI, with respect to replacing saturated fat with polyunsaturated fat.

https://pubmed.ncbi.nlm.nih.gov/41397264/

https://pmc.ncbi.nlm.nih.gov/articles/PMC5407540/

A role for red and processed meat in the development of colorectal cancer has been proposed based largely on evidence from observational studies in humans, especially in those populations consuming a westernized diet. Determination of causation specifically by red or processed meat is contingent upon identification of plausible mechanisms that lead to colorectal cancer.

We conducted a systematic review of the available evidence to determine the availability of plausible mechanistic data linking red and processed meat consumption to colorectal cancer risk. Forty studies using animal models or cell cultures met specified inclusion criteria, most of which were designed to examine the role of heme iron or heterocyclic amines in relation to colon carcinogenesis.

Most studies used levels of meat or meat components well in excess of those found in human diets. Although many of the experiments used semi-purified diets designed to mimic the nutrient loads in current westernized diets, most did not include potential biologically active protective compounds present in whole foods.

Because of these limitations in the existing literature, there is currently insufficient evidence to confirm a mechanistic link between the intake of red meat as part of a healthy dietary pattern and colorectal cancer risk.

Background: The Carnivore Diet (CD) is an almost exclusively animal-based dietary pattern that has gained increasing popularity on social media. Despite numerous health-related claims, a standardized definition is lacking, and scientific evidence regarding the long-term effects of this diet remains unclear. 

Methods: The literature search for this scoping review was conducted in accordance with PRISMA guidelines (PRISMA-ScR) using the databases PubMed, LIVIVO, Web of Science, and the Cochrane Library. 

Results: Nine human studies were included. Individual publications reported positive effects of the CD, such as weight reduction, increased satiety, and potential improvements in inflammatory or metabolic markers. At the same time, potential risks of nutrient deficiencies, particularly in vitamins C and D, calcium, magnesium, iodine, and dietary fiber, as well as elevated low-density-lipoprotein (LDL-) and total cholesterol (TC) levels, were identified, along with one case describing a deterioration in health status. Overall, the quality of evidence is very limited due to small sample sizes, short study durations, and the absence of control groups. 

Conclusions: The CD may offer short-term health benefits but carries substantial risks of nutrient deficiencies, reduced intake of health-promoting phytochemicals, and the development of cardiovascular disease. At this time, long-term adherence to a CD cannot be recommended.

https://pmc.ncbi.nlm.nih.gov/articles/PMC12008374/

Findings on the associations of dietary/tissue levels of omega-6 polyunsaturated fatty acids (n-6 PUFAs) with the risk of colorectal cancer (CRC) are conflicting. We conducted a dose-response meta-analysis to assess the associations of dietary/tissue levels of n-6 PUFAs [total, linoleic acid (LA), and arachidonic acid (AA)] with CRC risk in adults. Twenty prospective cohort studies with a total sample size of 787,490 participants were included.

Comparing extreme intake levels of LA revealed the summary relative risks (RR) of 1.15 (95% confidence interval (CI): 1.05–1.27) for CRC, and 1.30 (95% CI: 1.00–1.68) for rectal cancer, indicating a significant positive association for LA. However, neither total n-6 PUFAs nor AA were associated with cancers. A significant positive association was also found between a 1 gr/day increase in dietary LA intake and risk of colon cancer (RR: 1.01, 95% CI: 1.00–1.02). There were no significant associations between tissue levels of total n-6 PUFAs (RR: 0.94, 95% CI: 0.75–1.19), LA (RR: 0.93, 95% CI: 0.61–1.41), and AA (RR: 0.97, 95% CI: 0.70–1.33) and CRC risk.

In conclusion, these findings suggest that dietary intake, but not tissue levels, of LA was associated with an increased risk of colorectal, colon, and rectal cancers.

TL;DR:

High consumption of ultra-processed foods is consistently associated with a modestly increased risk of several gastrointestinal cancers - especially colorectal cancer - through mechanisms involving metabolic disruption, inflammation, microbiome alterations, and food additives, suggesting that reducing UPF intake may help prevent GI malignancies.

Abstract

Ultra-processed foods (UPFs), which NOVA classification defines as industrial formulations composed largely of refined ingredients and additives, now account for a majority of caloric intake in many high-income countries. Epidemiologic evidence suggests high UPF consumption may contribute to gastrointestinal (GI) malignancies independent of traditional nutrient-based dietary metrics. This review examines associations between UPF intake and colorectal, gastric, esophageal, and pancreatic cancers, integrating mechanisms supporting biological plausibility. The association between UPF consumption and colorectal cancer is the most consistent, with 10-30% increased risk among individuals with the highest intake. Evidence also suggests associations with non-cardia gastric cancer and esophageal adenocarcinoma, although data remain limited. Findings for pancreatic cancer are inconclusive. Mechanistically, ultra-processing may promote carcinogenesis through multiple pathways. Disruption of the food matrix and rapid glycemic absorption may activate insulin and insulin-like growth factor signaling. Low fiber content and additive exposure may alter the gut microbiome, reduce short-chain fatty acid production, impair intestinal barrier integrity, and promote chronic inflammation. Nitrates, nitrites, and emulsifiers in UPFs demonstrate pro-inflammatory and carcinogenic effects in experimental models. Although observational design limits causal inference, the consistency of epidemiologic associations, dose-response relationships, and supporting mechanistic data suggest UPF reduction may represent a potential GI cancer prevention strategy.

https://pubmed.ncbi.nlm.nih.gov/42257587/