Saturated fatty acids cause/linoleic acid prevents lung adenocarcinoma

[ysdj]

Mendelian Randomization Reveals the Dietary Fat-Lung Adenocarcinoma Connection: Insights from GWAS Data​

Mendelian Randomization Reveals the Dietary Fat-Lung Adenocarcinoma Connection: Insights from GWAS Data

Background: Lung cancer has a high mortality rate and lung adenocarcinoma (LUAD) is one of the most common types of lung cancer. A high-fat diet had been reported to be connected with the development of the LUAD. Thus, this study aimed to investigate the causal relationship be...

www.researchsquare.com

Abstract​

Background: Lung cancer has a high mortality rate and lung adenocarcinoma (LUAD) is one of the most common types of lung cancer. A high-fat diet had been reported to be connected with the development of the LUAD. Thus, this study aimed to investigate the causal relationship between a high-fat diet and LUAD using Mendelian randomization (MR) analysis.
Methods: The study conducted MR analysis by using critically ill patients with the LUAD (n=18336, single nucleotide polymorphism (SNP)=8,881,354). Ratio of linoleic acid (LA) to total fatty acids (n=114,999, SNP=12,321,875), total cholesterol (n=115,078, SNP=12,321,875), and ratio of saturated fatty acids (SFA) to total fatty acids (n=114,999, SNP=12,321,875) summary statistics were obtained from the Open Genome Wide Association Study (GWAS) database. Exposure factor reading and instrumental variable (IVs) screening were performed by the TwoSampleMR function extract_instruments, and independent SNPs with p < 5×10-8 were selected as IVs. Notably, SNPs with linkage disequilibrium (LDA) were excluded by performing an aggregation procedure with r2=0.001 and kb=10,000 kb. The study combined different algorithms (Weighted median, Simple mode, Inverse variance weighted, MR Egger, Weighted mod) to perform MR analysis, and the results were mainly referred to Inverse variance weighted (IVW).
Results: Univariate MR analysis showed that both ratio of SFA to total fatty acids as well as total cholesterol were consequently connected with the development of LUAD and were risk factors (p<0.05, odd ratio (OR)>1). Ratio of LA to total fatty acids was consequently connected with the occurrence of LUAD and was a protection factor (p<0.05, OR<1). Moreover, multivariate MR analysis showed that total cholesterol was a significant risk factor (p<0.05). The ratio of SFA to total fatty acids was a risk factor and ratio of LA to total fatty acids was a safety factor.
Conclusion: Total cholesterol, ratio of saturated fatty acids to total fatty acids, and ratio of linoleic acid to total fatty acids were causally connected to the LUAD.

 

[ecstatichamster]

I can’t understand this at all.

If you want to see if there is a correlation between satfat and lung cancer then do a study on that with surveys or use existing study data. This is nonsense that seems to pretend genomics is the real deal wrt real life, which it is not.

This paper shows how difficult a real life study really is

Re: Saturated Fat Intake and Lung Cancer Risk Among Nonsmoking Women in Missouri

Several ( 1 – 8 ), but not all ( 9 – 12 ), epidemiologic studies indicate that consumption of fat-rich diets increases risk of lung cancer. In 1993, we reported

academic.oup.com

As Brown et al. ( 17 ) and others ( 18 ) noted, when estimating the effect of increasing intake from dietary fat while keeping total energy intake constant (substitution effect), the standard multivariate model exaggerates the true variation in fat intake when data are modeled as quantile-categorical variables. Because the variability of the nutrient residuals provides a better estimate of the true variation in the nutrient of interest when total energy intake is fixed, the quantiles of the residual distribution provide a more valid description of the actual ORs to be expected when changing dietary composition. The multivariate nutrient density approach has the added advantage of being readily interpretable, representing the effect of changing the percentage of fat (or saturated fat) in the diet while keeping total energy intake constant.

Despite years of discussion about energy adjustment methods, we noted that only two observational studies of dietary fat and lung cancer ( 12 , 13 ) used any method of energy adjustment. In part, this circumstance reflects the fact that both the rationale and the appropriate method of energy adjustment remain controversial ( 19 , 20 ). In summary, computer simulations ( 17 ) and two analytic studies of dietary fat and cancer risk ( 13 , 21 ) now provide evidence that risk estimates and subsequent conclusions can be profoundly influenced by the method of energy adjustment.


—-

In addition, people who consume lots of saturated fat eat a lot of meat. That means they may be eating a low calcium high phosphorus diet, which Dr. Peat stressed causes high parathyroid hormone and an inflammatory cascade including high calcium in the blood from lactate breaking down bone.

This could increase chance of this type of lung cancer.

 

[ecstatichamster]

In a real study satfat and PUFA is a mixed bag. High DHA is bad, and high omega 6 ratios are bad.

https://onlinelibrary.wiley.com/doi/full/10.1002/ijc.31608

Animal studies have shown that polyunsaturated fatty acids (PUFAs) have antineoplastic and anti-inflammatory properties. Results from epidemiologic studies on specific types of PUFAs for lung cancer risk, however, are inconclusive. We prospectively evaluated the association of specific types of dietary PUFA intakes and lung cancer risk in two population-based cohort studies, the Shanghai Women's Health Study (SWHS) and Shanghai Men's Health Study (SMHS) with a total of 121,970 study participants (i.e., 65,076 women and 56,894 men).

Dietary fatty acid intakes were derived from data collected at the baseline using validated food frequency questionnaires (FFQs). Cox proportional hazards model was performed to assess the association between PUFAs and lung cancer risk. Total, saturated and monounsaturated fatty acid intakes were not significantly associated with lung cancer risk.

Total PUFAs intake was inversely associated with lung cancer risk [HRs and respective 95% CIs for quintiles 2–5 vs quintile 1: 0.84 (0.71–0.98), 0.97 (0.83–1.13), 0.86 (0.74–1.01) and 0.85 (0.73–1.00), ptrend = 0.11]. However, DHA intake was positively associated with lung cancer risk [HRs and 95% CIs: 1.01 (0.86–1.19), 1.20 (1.03–1.41), 1.21 (1.03–1.42) and 1.24 (1.05–1.47), ptrend = 0.001]. The ratio of n-6 PUFAs to n-3 PUFAs (i.e., 7:1) was inversely associated with lung cancer risk, particularly among never-smokers and adenocarcinoma patients. Total PUFAs and the ratio between n-6 PUFAs and n-3 PUFAs were inversely associated with lung cancer risk. This study highlights an important public health impact of PUFA intakes toward intervention/prevention programs of lung cancer.

 

[lamassu]

Are Mendelian randomization studies actually reliable though?

 

[Diogo]

In a real study satfat and PUFA is a mixed bag. High DHA is bad, and high omega 6 ratios are bad.

https://onlinelibrary.wiley.com/doi/full/10.1002/ijc.31608

Animal studies have shown that polyunsaturated fatty acids (PUFAs) have antineoplastic and anti-inflammatory properties. Results from epidemiologic studies on specific types of PUFAs for lung cancer risk, however, are inconclusive. We prospectively evaluated the association of specific types of dietary PUFA intakes and lung cancer risk in two population-based cohort studies, the Shanghai Women's Health Study (SWHS) and Shanghai Men's Health Study (SMHS) with a total of 121,970 study participants (i.e., 65,076 women and 56,894 men).

Dietary fatty acid intakes were derived from data collected at the baseline using validated food frequency questionnaires (FFQs). Cox proportional hazards model was performed to assess the association between PUFAs and lung cancer risk. Total, saturated and monounsaturated fatty acid intakes were not significantly associated with lung cancer risk.

Total PUFAs intake was inversely associated with lung cancer risk [HRs and respective 95% CIs for quintiles 2–5 vs quintile 1: 0.84 (0.71–0.98), 0.97 (0.83–1.13), 0.86 (0.74–1.01) and 0.85 (0.73–1.00), ptrend = 0.11]. However, DHA intake was positively associated with lung cancer risk [HRs and 95% CIs: 1.01 (0.86–1.19), 1.20 (1.03–1.41), 1.21 (1.03–1.42) and 1.24 (1.05–1.47), ptrend = 0.001]. The ratio of n-6 PUFAs to n-3 PUFAs (i.e., 7:1) was inversely associated with lung cancer risk, particularly among never-smokers and adenocarcinoma patients. Total PUFAs and the ratio between n-6 PUFAs and n-3 PUFAs were inversely associated with lung cancer risk. This study highlights an important public health impact of PUFA intakes toward intervention/prevention programs of lung cancer.

Impact of cooking oil fume exposure and fume extractor use on lung cancer risk in non-smoking Han Chinese women - PubMed

Smoking tobacco is the major risk factor for developing lung cancer. However, most Han Chinese women with lung cancer are nonsmokers. Chinese cooking methods usually generate various carcinogens in fumes that may inevitably be inhaled by those who cook the food, most of whom are female. We...

pubmed.ncbi.nlm.nih.gov

It does not say which oil but on a quick research, Google says the most used cooking oils in China are: Soybean, Rapeseed, Palm and Peanutoil.

In terms of PUFA content per 100g, once again while on a quick research, it amounts for 58g, 4g, 37g and 46g respectively.

 

[haidut]

Mendelian Randomization Reveals the Dietary Fat-Lung Adenocarcinoma Connection: Insights from GWAS Data​

Mendelian Randomization Reveals the Dietary Fat-Lung Adenocarcinoma Connection: Insights from GWAS Data

Background: Lung cancer has a high mortality rate and lung adenocarcinoma (LUAD) is one of the most common types of lung cancer. A high-fat diet had been reported to be connected with the development of the LUAD. Thus, this study aimed to investigate the causal relationship be...

www.researchsquare.com

Abstract​

Background: Lung cancer has a high mortality rate and lung adenocarcinoma (LUAD) is one of the most common types of lung cancer. A high-fat diet had been reported to be connected with the development of the LUAD. Thus, this study aimed to investigate the causal relationship between a high-fat diet and LUAD using Mendelian randomization (MR) analysis.
Methods: The study conducted MR analysis by using critically ill patients with the LUAD (n=18336, single nucleotide polymorphism (SNP)=8,881,354). Ratio of linoleic acid (LA) to total fatty acids (n=114,999, SNP=12,321,875), total cholesterol (n=115,078, SNP=12,321,875), and ratio of saturated fatty acids (SFA) to total fatty acids (n=114,999, SNP=12,321,875) summary statistics were obtained from the Open Genome Wide Association Study (GWAS) database. Exposure factor reading and instrumental variable (IVs) screening were performed by the TwoSampleMR function extract_instruments, and independent SNPs with p < 5×10-8 were selected as IVs. Notably, SNPs with linkage disequilibrium (LDA) were excluded by performing an aggregation procedure with r2=0.001 and kb=10,000 kb. The study combined different algorithms (Weighted median, Simple mode, Inverse variance weighted, MR Egger, Weighted mod) to perform MR analysis, and the results were mainly referred to Inverse variance weighted (IVW).
Results: Univariate MR analysis showed that both ratio of SFA to total fatty acids as well as total cholesterol were consequently connected with the development of LUAD and were risk factors (p<0.05, odd ratio (OR)>1). Ratio of LA to total fatty acids was consequently connected with the occurrence of LUAD and was a protection factor (p<0.05, OR<1). Moreover, multivariate MR analysis showed that total cholesterol was a significant risk factor (p<0.05). The ratio of SFA to total fatty acids was a risk factor and ratio of LA to total fatty acids was a safety factor.
Conclusion: Total cholesterol, ratio of saturated fatty acids to total fatty acids, and ratio of linoleic acid to total fatty acids were causally connected to the LUAD.

Correlation "study", which means next to nothing. As far as real-world data, there is the Israeli Paradox, and they do have some of the highest rates of lung cancer on earth and perhaps the highest consumption of linoleic acid.

Diet and disease--the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet - PubMed

Israel has one of the highest dietary polyunsaturated/saturated fat ratios in the world; the consumption of omega-6 polyunsaturated fatty acids (PUFA) is about 8% higher than in the USA, and 10-12% higher than in most European countries. In fact, Israeli Jews may be regarded as a...

pubmed.ncbi.nlm.nih.gov

And in terms of intervention studies, here is one that shows saturated fats, and specifically heptadecanoic acid (C17:0, which is present in our new product LipOdd) may actually treat lung cancer.

Sheep tail fat inhibits the proliferation of non-small-cell lung cancer cells in vitro and in vivo - PubMed

Increasing evidence suggests that numerous edible oils may function as adjuvant dietary therapies to treat cancer. We previously reported that the odd-chain saturated fatty acid (OCSFA), heptadecanoic acid (C17:0), profoundly inhibits non-small-cell lung cancer (NSCLC) cell proliferation...

pubmed.ncbi.nlm.nih.gov

@ecstatichamster

 

[ecstatichamster]

Correlation "study", which means next to nothing. As far as real-world data, there is the Israeli Paradox, and they do have some of the highest rates of lung cancer on earth and perhaps the highest consumption of linoleic acid.

Diet and disease--the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet - PubMed

Israel has one of the highest dietary polyunsaturated/saturated fat ratios in the world; the consumption of omega-6 polyunsaturated fatty acids (PUFA) is about 8% higher than in the USA, and 10-12% higher than in most European countries. In fact, Israeli Jews may be regarded as a...

pubmed.ncbi.nlm.nih.gov

And in terms of intervention studies, here is one that shows saturated fats, and specifically heptadecanoic acid (C17:0, which is present in our new product LipOdd) may actually treat lung cancer.

Sheep tail fat inhibits the proliferation of non-small-cell lung cancer cells in vitro and in vivo - PubMed

Increasing evidence suggests that numerous edible oils may function as adjuvant dietary therapies to treat cancer. We previously reported that the odd-chain saturated fatty acid (OCSFA), heptadecanoic acid (C17:0), profoundly inhibits non-small-cell lung cancer (NSCLC) cell proliferation...

pubmed.ncbi.nlm.nih.gov

@ecstatichamster

Thank you for clarifying. I hate these “genomic” so-called studies that are the fad today.

 

[Birdie]

View: https://twitter.com/Babygravy9/status/1729888132034863291

 

[GreekDemiGod]

Are Mendelian randomization studies actually reliable though?

They are considered highest level of clinical evidence, if I’m not mistaken.

 

[lamassu]

They are considered highest level of clinical evidence, if I’m not mistaken.

I don't think they would be considered higher than an RCT or PCT or any type of controlled study (ie. with treatment and placebo groups)