This is so confusing, idk what to look at/what's it trying to say

I'm looking into recommendations on totally plant-based diets (no foods of animal origin). I can find many organizations endorsing them and a few advising against them, but only for special populations (children, pregnant women, ...). So is there any credible organization which doesn't consider them appropriate even for adults with no special nutritional requirements?

Doesn’t have to be a total anti stance, also fine with anyone cautioning or expressing skepticism.

"Continuous glucose monitoring (CGM) allows huge amounts of postprandial glycemic response (PPGR) data to be obtained. CGM has revolutionized the approach to improving glycemic control in people with diabetes [1]. In people without diabetes, an early study concluded that the relative ranking of PPGRs measured by CGM often differed from those predicted by the glycemic index (GI) [2]. In 2016, I argued that the unexpected rankings could be explained by day-to-day variation of PPGRs within-subjects [intraindividual variation (iiV)] [3]. However, the impact of iiV has not been recognized, and personalized nutrition using CGM to minimize PPGRs continues to be promoted [4,5]. The article by Hengist et al. [6], in today’s issue of AJCN, demonstrating large iiV of PPGRs measured by CGM casts doubt on the precision of “precision nutrition.” The iiV of PPGRs, expressed as coefficient of variation (CV = 100 × SD/mean) varies from 14% to 40% in different laboratories [7] and differs by diabetes status [8], the endpoint measured [9,10], and the method of glucose analysis [11]. The SD of GI values is strongly related to iiV [7] but between-individual variation of GI is virtually 0 [12]. Previous studies suggest the iiV of PPGRs measured by CGM is very high. The SD of GI values measured by CGM [13] were nearly twice those measured in capillary blood [14] despite 3 times as many tests per subject. One study found the iiV of incremental area-under-the-glucose-curve (ignoring area below fasting) measured by CGM to have a CV of 45% [15]. Hengist et al. [6] report an endpoint termed “iAUC” calculated as incremental area area-under-the-curve over 2 h (subtracting area below fasting) divided by 2 h; this represents the mean glucose increment over 2 h (MGinc). Because fasting-glucose is subtracted from all postprandial values, an X mg/dL error in fasting-glucose results in an X mg/dL error in MGinc. Hengist et al. [6] show an average MGinc of ∼15 mg/dL (Supplementary Figure 5) with the SD of the differences being ∼15 mg/dL (50% of the limits-of-agreement); this suggests that the CV of iiV was ∼100%. The CV of analytical precision is generally <2% for wet methods and >5% for glucometers. Analytical precision of CGMs is assessed from the mean and SD of the percent absolute difference (PAD) of simultaneous glucose readings from 2 CGMs worn by the same subject. The CGMs used by Hengist et al. [6] had an average mean ± SD PAD of 9.8 ± 10.9% [16]; thus, the 95% margin of error for a fasting-glucose of 90 mg/dL would be ∼28 mg/dL; with a mean MGinc of 15 mg/dL, this alone could account for a CV of ∼100%. The precision of “precision nutrition” depends on the magnitude of iiV which, in turn, determines the probability that the relative ranking of PPGRs is correct. I calculated mean MGinc (as per Hengist et al.) from PPGR data for 21 subjects without diabetes [12] (intraindividual CV = 28.6%); white bread (WB) elicited a ∼25% lower MGinc than instant-potato (IP), 1.28 compared with 1.70 mmol/L (P = 0.03). Assuming the 0.42 mmol/L difference is true, and that the CV of iiV = 100%, after a single test of WB and IP using CGM there would be a 42% chance of incorrect ranking (that is, WB > IP) (Figure 1). Likewise, for foods differing in MGinc by 33% and 50%, there would be a 39% and 32% chance of incorrect ranking. To be 95% confident of a correct ranking for differences of 25%, 33%, and 50%, each food test must be repeated 67, 35, and 13 times, respectively, and the means compared. Hengist et al.’s conclusion that personalized diet advice based on CGM measurements requires more reliable methods and repeated measurements is precisely right."

https://ajcn.nutrition.org/article/S0002-9165(24)00874-8/fulltext

Glycine

Glycine accelerates recovery from alcohol-induced liver injury

Glycine prevents hepatic damage caused by hypoxia-reoxygenation, diminishes mortality due to endotoxin and minimizes alcoholic liver injury by decreasing blood ethanol. Our purpose was to investigate the effect of dietary glycine during recovery from early alcohol-induced injury, using a model that mimics the clinical presentation and histopathology with alcoholics. Male Wistar rats were exposed to ethanol continuously for 6 wk via intragastric feeding that resulted in typical histology of alcoholic liver injury, including steatosis, inflammation, necrosis and increased serum levels of aspartate aminotransferase and alanine aminotransferase. After cessation of ethanol, one group of rats received a control diet, the other a glycine-containing diet for 2 wk. During this period, all parameters studied tended to return to baseline values. However, serum aspartate aminotransferase and alanine aminotransferase recovered about 30% more rapidly in rats fed glycine. Further, the hepatic pathology score was also significantly lower in the glycine group than in controls (0.5 vs. 2.6). After 1 wk, steatosis was reduced significantly more in the glycine group (5. 6%) than in controls (8.9%). Glycine also diminished numbers of infiltrating leukocytes and necrotic cells significantly more than in controls. This beneficial effect of glycine may be partly explained by the fact that glycine increased influx of chloride into Kupffer cells leading to diminished tumor necrosis factor-alpha production. These results indicate that a glycine containing diet expedites the process of recovery from ethanol-induced liver injury and may lead to its clinical application in alcoholic hepatitis.

https://pubmed.ncbi.nlm.nih.gov/9694963/

Glycine prevents alcohol-induced liver injury by decreasing alcohol in the rat stomach

Background & aims: Inactivation of Kupffer cells prevents alcohol-induced liver injury, and hypoxia subsequent to a hypermetabolic state caused by activated Kupffer cells probably is involved in the mechanism. Glycine is known to prevent hepatic reperfusion injury. The purpose of this study was to determine whether glycine prevents alcohol-induced liver injury in vivo.

Methods: Male Wistar rats were exposed to ethanol (10-12 g.kg-1.day-1) continuously for up to 4 weeks via an intragastric feeding protocol. The effect of glycine on the first-pass metabolism of ethanol was also examined in vivo, and the effect on alcohol metabolism was estimated specifically in perfused liver.

Results: Glycine decreased ethanol concentrations precipitously in urine, breath, peripheral blood, portal blood, feces, and stomach contents. Serum aspartate amino-transferase levels were elevated to 183 U/L after 4 weeks of ethanol-treatment. In contrast, values were significantly lower in rats given glycine along with ethanol. Hepatic steatosis and necrosis also were reduced significantly by glycine. Glycine dramatically increased the first-pass elimination of ethanol in vivo but had no effect on alcohol metabolism in the perfused liver.

Conclusions: Glycine minimizes alcohol-induced liver injury in vivo by preventing ethanol from reaching the liver by activating first-pass metabolism in the stomach.

https://pubmed.ncbi.nlm.nih.gov/8613061/

Taurine

Interactions between taurine and ethanol in the central nervous system

This purpose of this review will be to summarize the interactions between the endogenous amino acid taurine and ethyl alcohol (ethanol) in the central nervous system (CNS). Taurine is one of the most abundant amino acids in the CNS and plays an integral role in physiological processes such as osmoregulation, neuroprotection and neuromodulation. Both taurine and ethanol exert positive allosteric modulatory effects on neuronal ligand-gated chloride channels (i.e., GABA(A) and glycine receptors) as well as inhibitory effects on other ligand- and voltage-gated cation channels (i.e., NMDA and Ca(2+) channels). Behavioral evidence suggests that taurine can alter the locomotor stimulatory, sedating, and motivational effects of ethanol in a strongly dose-dependent manner. Microdialysis studies have revealed that ethanol elevates extracellular levels of taurine in numerous brain regions, although the functional consequences of this phenomenon are currently unknown. Finally, taurine and several related molecules including the homotaurine derivative acamprosate (calcium acetylhomotaurinate) can reduce ethanol self-administration and relapse to drinking in both animals and humans. Taken together, these data suggest that the endogenous taurine system may be an important modulator of effects of ethanol on the nervous system, and may represent a novel therapeutic avenue for the development of medications to treat alcohol abuse and alcoholism.

https://pubmed.ncbi.nlm.nih.gov/12436202/

The Effects of Taurine on Alcohol-Associated Liver Disease are Dose-Dependent Associated with Alterations of Taurine-Conjugated Bile Acids and FXR-FGF15 Signaling (in mice)

Our results demonstrate that the effects of taurine supplementation on ALD are dose dependent. Low dose of taurine suppresses, while high dose of taurine exacerbated, alcohol-induce steatosis and liver injury. Low dose taurine supplementation enhances Fxr-Fgf15 signaling in the setting of alcohol exposure in mice, while the mechanisms underlying the detrimental effects of high dose taurine on ALD warrant further investigation.

https://jpet.aspetjournals.org/content/389/S3/408

Taurine Accelerates Alcohol and Fat Metabolism of Rats with Alcoholic Fatty Liver Disease

Liver is considered to be the main organ capable of oxidizing alcohol and fat. Chronic consumption of alcohol is the major cause of liver injury and the development of alcoholic fatty liver disease (AFLD). Liver is also the main organ capable of synthesizing taurine, and the effects of taurine on liver disease have aroused great attention. In the present study, alcohol and pyrazole were administered to male Wistar rats by way of intragastric administration and combined with a high fat diet in order to establish the AFLD model. Taurine was administered in the drinking water during and after the establishment of the AFLD model. The preventive experiment lasted for 12 weeks. The curative experiment was divided into 4 and 8 weeks. Hepatic activities of ADH, ALDH, serum ALT, AST, TC, TG, HDL-C, LDL-C, NEFA and hepatic NEFA were measured. The results showed that hepatic ADH and ALDH in AFLD rats were significantly lower while serum ALT, AST, TC, TG, LDL-C, NEFA and hepatic NEFA in model group were significantly higher than normal rats (P < 0.05), and serum HDL-C was obviously lower. Serum ALT, AST, TC, TG, LDL-C, NEFA, and hepatic NEFA were decreased in taurine preventive and curative groups (P < 0.05), while hepatic activities of ADH and ALDH, serum HDL-C were significantly increased in taurine groups (P < 0.05). Observation of the pathological sections showed that taurine can significantly attenuate fatty degeneration and the deposition of the liver caused by alcohol. The results indicated that taurine presumably accelerates the metabolism of alcohol and fat in the liver, thereby inhibiting and reversing hepatic fatty degeneration in AFLD rats.

https://link.springer.com/chapter/10.1007/978-3-319-15126-7_64

Oral Taurine Supplementation Prevents the Development of Ethanol-Induced Hypertension in Rats

https://www.jstage.jst.go.jp/article/hypres1992/23/3/23_3_277/_article/-char/ja/kkkkkklkp

Taurine reverses alcohol-induced fatty liver in rats in only two days

https://academic.oup.com/alcalc/article/34/4/529/188043?login=false

Liver Damage seems to be PUFA+Alcohol rather than just alcohol. And no, this isn't a seed oil thing. It's seems to be PUFA in general, including Omega3s.

Dietary Fat and Alcoholic Liver Disease (review)

Although the amount of dietary fat and its accumulation in the liver plays a role in alcohol-induced liver injury, the type of fat ingested may also be an important factor. Comparison of dietary fat intakes in various countries with similar per capita alcohol consumption indicates that a high intake of saturated fat is associated with a lower mortality from alcoholic cirrhosis, whereas a high intake of unsaturated fat is associated with a higher mortality from cirrhosis.9 F

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.510280401

Dietary linoleic acid is required for development of experimentally induced alcoholic liver injury (rat study)

We had previously hypothesized that linoleic acid (LA) was essential for development of alcoholic induced liver injury in our rat model. Male Wistar rats were fed a nutritionally adequate diet (25% calories as fat) with ethanol (8-17 g/kg/day). The source of fat was tallow (0.7% LA), lard (2.5% LA) or tallow supplemented with linoleic acid (2.5%). Liver damage was followed monthly by obtaining blood for alanine aminotransferase assay and liver biopsy for assessment of morphologic changes. Enzyme and histologic changes (fatty liver, necrosis and inflammation) in the tallow-linoleic acid-ethanol fed animals were more severe than in the lard-ethanol group. The tallow ethanol group did not show any evidence of liver injury. Our results strongly support our hypothesis that LA is essential for development of alcoholic liver disease in our rat model.

https://pubmed.ncbi.nlm.nih.gov/2915600/

Effect Of Coconut Oil On Alcohol-Induced Liver Disease In Male Rats (rat study)

The potential attenuating effect of dietary coconut oil on ethanol-induced liver disease was determined in this study. Alcoholic liver disease was induced in rats for six weeks, and was treated with diets enriched in coconut oil, palm oil, and soybean oil. Severity of liver injury was based on the occurrence and degree of necrosis, steatosis, and fibrosis. Histopathological scores showed a significant difference among the five treatment groups. In groups fed with diets enriched in saturated fatty acids, i.e. coconut oil and palm oil, established alcoholic liver disease was attenuated to near normalization. Coconut oil in the diet, in place of unsaturated fatty acids, is a potential therapeutic intervention in alcohol- induced liver disease.

http://cas.upm.edu.ph:8080/xmlui/handle/123456789/2194

Oxidation of fish oil exacerbates alcoholic liver disease by enhancing intestinal dysbiosis in mice (Mouse Study)

https://www.nature.com/articles/s42003-020-01213-8

We know alcohol is addictive, we know it leads to a lot of death with drunk driving, it's often an element of domestic abuse, and can even play a role in suicide.

I'm going to make a series of threads to generate discussion on alcohol. This one will explore benefits of low-moderate dose of alcohol. The next one will be on alcohol paired with various dietary fats and liver harm. The two after that will explore glycine+alcohol, and taurine+alcohol.

I try to note mouse studies when it's a mouse study. There's some meta analysis and some observational studies as well.

What happens when we don't exceed 1-2 drinks a day? What happens if it's less? Then we start to see benefit - especially of red wine. Lets dig in

TOTAL MORTALITY

Alcohol dosing and total mortality in men and women: an updated meta-analysis of 34 prospective studies

A J-shaped relationship between alcohol and total mortality was confirmed in adjusted studies, in both men and women. Consumption of alcohol, up to 4 drinks per day in men and 2 drinks per day in women, was inversely associated with total mortality, maximum protection being 18% in women (99% confidence interval, 13%-22%) and 17% in men (99% confidence interval, 15%-19%)

https://pubmed.ncbi.nlm.nih.gov/17159008/

CVD

Alcohol consumption and the risk of heart failure: the Suita Study and meta-analysis of prospective cohort studies

https://pubmed.ncbi.nlm.nih.gov/37150604/

J-Curve effects on blood pressure.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8130994/

Red Wine Prevents the Acute Negative Vascular Effects of Smoking

"Markers of endothelial damage, inflammation, and cellular aging were completely attenuated by red wine consumption."

https://www.sciencedirect.com/science/article/abs/pii/S0002934316309123

Alcohol and red wine consumption, but not fruit, vegetables, fish or dairy products, are associated with less endothelial dysfunction and less low-grade inflammation

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5959974/

Wine consumption (~2.5 glasses/d for men) for 4 weeks was associated with a 11-16% increase in HDL and 8-15% decrease in fibrinogen relative to not drinking wine.

https://pubmed.ncbi.nlm.nih.gov/15674304/

A Note on Polyphenols in Wine

Much of the beneficial health effects of polyphenols may be due to binding of free iron.

https://link.springer.com/article/10.1007/s12013-009-9043-x

Wine drunk in regions of France and Sardinia with an especially high rate of male longevity are higher in polyphenols than other wines.

These polyphenols block a blood vessel constricting protein.

https://www.nature.com/articles/444566a

Cognitive Function

Findings In this cohort study of 19 887 participants from the Health and Retirement Study, with a mean follow-up of 9.1 years, when compared with never drinking, low to moderate drinking was associated with significantly better trajectories of higher cognition scores for mental status, word recall, and vocabulary and with lower rates of decline in each of these cognition domains.

https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2767693

The above is particularly interesting as alcohol reduces grey and white matter in the brain:

https://www.nature.com/articles/s41467-022-28735-5

Diabetes / Metabolic Syndrome

Increases insulin sensitivity

https://link.springer.com/article/10.1007/s00125-008-1031-y

Inverse association between alcohol consumption and diabetes risk in ~47,000 U.S. male health professionals.

https://pubmed.ncbi.nlm.nih.gov/11574424/

Long-term low-dose alcohol intake promotes white adipose tissue browning and reduces obesity in mice

https://pubs.rsc.org/en/content/articlelanding/2022/fo/d2fo00743f

Speaks to longstanding puzzle of lower obesity rates and BMI among moderate drinkers.

https://pubs.rsc.org/en/content/articlelanding/2022/fo/d2fo00743f

Cancer

Cancer-free men who consumed alcohol had a slightly lower risk of lethal prostate cancer compared with abstainers.

Among men with prostate cancer, red wine was associated with a lower risk of progression to lethal disease.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6599404/

Lymphoma

Compared to never drinkers, wine drinkers experienced better overall survival (75% vs. 69% five-year survival rates, p-value for log-rank test=0.030) and better disease free survival (70% vs. 67% five-year disease-free survival rates, p-value for log-rank test=0.049). Analysis by NHL subtype shows that the favorable effect of wine consumption was mainly seen for patients diagnosed with diffuse large B-cell lymphoma (DLBCL) (wine drinkers for more than 25 years vs. never drinkers: HR=0.36, 95% CI 0.14–0.94 for overall survival; HR=0.38, 95% CI 0.16–0.94 for disease-free survival), and the adverse effect of liquor consumption was also observed among DLBCL patients (liquor drinkers vs. never drinkers: HR=2.49, 95% CI 1.26–4.93 for disease-free survival).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3141078/

Those patients with large B-cell lymphoma had about 60 percent reduced risk of death, relapse or secondary cancer if they had been drinking wine for at least the previous 25 years before diagnosis.

https://www.sciencedaily.com/releases/2009/04/090421154322.htm#:~:text=Those%20patients%20with%20large%20B,affect%20outcome%2C%22%20said%20Han.

However, chronic exposure of lymphoma cells to 0.1% ethanol (slightly above the legal limit for operating a motor vehicle) for 10 days led to the inhibition of mTORC1. And moderate levels of alcohol in the drinking water of mice suppressed tumor growth.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2957519/

https://pubmed.ncbi.nlm.nih.gov/19293424/

Association between wine consumption and cancer: a systematic review and meta-analysis

Seventy-three studies were included in the systematic review, and 26 were included in the meta-analysis. The pooled RR for the effect of wine consumption on the risk of gynecological cancers was 1.03 (95% CI: 0.99, 1.08), that for colorectal cancer was 0.92 (95% CI: 0.82, 1.03), and that for renal cancer was 0.92 (95% CI: 0.81, 1.04). In general, the heterogeneity was substantial.

Conclusion The study findings reveal no association between wine consumption and the risk of developing any type of cancer. Moreover, wine drinking demonstrated a protective trend regarding the risk of developing pancreatic, skin, lung, and brain cancer as well as cancer in general.

https://pmc.ncbi.nlm.nih.gov/articles/PMC10507274/

Liver

Moderate wine drinking was associated with 85% lower risk of NAFLD (non-alcoholic fatty liver disease)

https://aasldpubs.onlinelibrary.wiley.com/doi/full/10.1002/hep.22292

https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-022-02525-8

^(Participants (age = 51 years; 88% men; body mass index = 31.2 kg/m2; 29% VAT) had an 89.8% retention rate and 79.3% completed eligible MRIs. While both MED diets reached similar moderate weight (MED: − 2.7%, green-MED: − 3.9%) and waist circumference (MED: − 4.7%, green-MED: − 5.7%) loss, the green-MED dieters doubled the VAT loss (HDG: − 4.2%, MED: − 6.0%, green-MED: − 14.1%; p < 0.05, independent of age, sex, waist circumference, or weight loss). Higher dietary consumption of green tea, walnuts, and Wolffia globosa; lower red meat intake; higher total plasma polyphenols (mainly hippuric acid), and elevated urine urolithin A polyphenol were significantly related to greater VAT loss (p < 0.05, multivariate models).)

What doesn't seem achievable in this is the Wolffia globosa. An equivalent is needed. To make matters worse, I have a heard a claim that entire countries are unable to create their own Urolithin A because their microbiome formed in the first 1000 days of being alive. There must be a way around this. I have also heard a claim that most people regardless of where they are simply cannot create Urolithin A. Therefore even walnut or pomegranate consumption is a nearly pointless act for them.

Looking for clarification on calcium after reading the following:

“Calcium inhibits the absorption of iron. Vitamin C helps the absorption of calcium.

“Calcium affecting your vitamin/minerals absorption applies to only supplements/fortified foods not calcium obtained through food sources”

I find this confusing because most paediatricians blame overconsumption of milk (calcium) for any iron deficiency a child has.

How does it work in a toddlers body?

Loss of proteostasis is a hallmark of aging and Alzheimer disease (AD). We identify β-hydroxybutyrate (βHB), a ketone body, as a regulator of protein solubility. βHB primarily provides ATP substrate during periods of reduced glucose availability, and regulates other cellular processes through protein interactions. We demonstrate βHB-induced protein insolubility is not dependent on covalent protein modification, pH, or solute load, and is observable in mouse brain in vivo after delivery of a ketone ester. This mechanism is selective for pathological proteins such as amyloid-β, and exogenous βHB ameliorates pathology in nematode models of amyloid-β aggregation toxicity. We generate libraries of the βHB-induced protein insolublome using mass spectrometry proteomics, and identify common protein domains and upstream regulators. We show enrichment of neurodegeneration-related proteins among βHB targets and the clearance of these targets from mouse brain. These data indicate a metabolically regulated mechanism of proteostasis relevant to aging and AD.

https://www.cell.com/cell-chemical-biology/fulltext/S2451-9456(24)00459-8

The study researchers found that ketone bodies cleared damaged proteins from the brains of mice.

An article published in the journal Neuropsychobiolgy reported that the frequency of Seasonal Affective Disorder was four times higher among Finnish vegetarians and three times higher in Dutch vegetarians than in meat eaters.

https://www.karger.com/Article/Abstract/477247

A study of 140 women found that the odds of depression were twice as great in women consuming less than the recommended intake of meat per week. (The researchers also found that women eating more than recommended amount were also likely to be depressed.).

https://www.karger.com/article/Abstract/334910

In 2014, Austrian researchers published an elegant study of individuals who varied in their diets—330 vegetarians, 330 people who consumed a lot of meat, 330 omnivores who ate less meat, and 330 people who consumed a little meat but ate mostly fruits and veggies. The subjects were carefully matched for sex, age, and socio-economic status. The vegetarians were about twice as likely as the other groups to suffer from a mental illness such as anxiety and depression.

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0088278

Investigators from the College of William and Mary examined depression among 6,422 college students. Vegetarian and semi-vegetarian students scored significantly higher than the omnivores on the Center for Epidemiologic Depression Scale.

https://www.tandfonline.com/doi/abs/10.1080/03670244.2018.1455675

In a 2018 study of 90,000 adults, French researchers examined the impact of giving up various food groups on depressive symptoms among meat eaters, vegans, true vegetarians, and vegetarians who ate fish. The incidence of depression increased with each food group that was given up. People who had given up at least three of four animal-related food groups (red meat, poultry, fish, and dairy) were at nearly two-and-a-half times greater risk to suffer from depression.

https://www.mdpi.com/2072-6643/10/11/1695

In a British study, 9,668 men who were partners of pregnant women took the Edinburgh Postnatal Depression Scale. Seven percent of the vegetarians obtained scores indicating severe depression compared to four percent of non-vegetarians.

https://www-sciencedirect-com.proxy195.nclive.org/science/article/pii/S0165032716323916

Researchers examined mental health issues among a representative sample of 4,116 Germans including vegetarians, predominantly vegetarians, and non-vegetarians. The subjects were matched on demographic and socioeconomic variables. More vegetarians than meat eaters suffered from depressive disorders in the previous month, the previous year, and over their lifetimes.

https://ijbnpa.biomedcentral.com/articles/10.1186/1479-5868-9-67

A longitudinal study of 14,247 young women found that 30 percent of vegetarians and semi-vegetarians had experienced depression in the previous 12 months, compared to 20 percent of non-vegetarian women. (Baines, 2007)

https://www.semanticscholar.org/paper/How-does-the-health-and-well-being-of-young-and-Baines-Powers/a69ed25438f1c9f2d4211bfa52ac53f387efd87e

Depressive episodes are more prevalent in individuals who do not eat meat, independently of socioeconomic and lifestyle factors. Nutrient deficiencies do not explain this association. The nature of the association remains unclear, and longitudinal data are needed to clarify causal relationship.

https://www.sciencedirect.com/science/article/abs/pii/S0165032722010643

(meta) Vegetarians show higher depression scores than non-vegetarians. However, due to high heterogeneity of published studies, more empirical research is needed before any final conclusions can be drawn. Also, empirical studies from a higher number of different countries would be desirable.

https://www.sciencedirect.com/science/article/abs/pii/S0165032721007771

According to the book Brain Energy, there seems a bi-directional relationship between every mental disorder (anxiety, depression, bipolar, schizophrenia, etc.) and every neurological disorder (Alzheimer's, ADHD, autism, parkinsons, epilepsy). Having any one of these disorders makes you 2 - 20x more likely to develop another over the population that has none of these disorders.

Vegetarian/Vegan diets (typically) are typically lower LDL due to less intake of saturated fat.

We have good information that HIGHER LDL is protective of both the brain and neurological system at large:

Low LDL cholesterol and increased risk of Parkinson's disease: prospective results from Honolulu-Asia Aging Study

https://pubmed.ncbi.nlm.nih.gov/18381649/

low LDL/ApoB might increase risk of Parkinsons Disease

https://pubmed.ncbi.nlm.nih.gov/31382822/

High Low-Density Lipoprotein Cholesterol Inversely Relates to Dementia in Community-Dwelling Older Adults: The Shanghai Aging Study

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6240682/

High total cholesterol levels in late life associated with a reduced risk of dementia

https://n.neurology.org/content/64/10/1689.short

We even see cholesterol's impact on cognition itself:

Serum cholesterol and cognitive performance in the Framingham Heart Study. High cognitive functioning is correlated with High Cholesterol

https://pubmed.ncbi.nlm.nih.gov/15673620/

My opinion: B12, choline, creatine (proven to have effect on depression and mitochondrial health), K2 (proven to improve depression scores in the insulin resistant), and even increased LDL, to a point, all play a role in neurological and thus psychological health.

2017: Vegetarian diet and all-cause mortality: Evidence from a large population-based Australian cohort - the 45 and Up Study

This 2017 study on a quarter million people showed that a PLANT BASED DIET conferred NO BENEFIT with regards to mortality! In fact the plant based group engaged in less harmful health behaviors and still did not do better

They found no significant difference in total mortality between vegetarians and omnivores. There was also no difference in mortality between vegetarians, pesco-vegetarians, and semi-vegetarians.

https://pubmed.ncbi.nlm.nih.gov/28040519/

https://www.ncbi.nlm.nih.gov/pubmed/28040519

Risk of death from cancer and ischaemic heart disease in meat and non-meat eaters

both vegetarians and health-conscious omnivores had lower risk of early death than the general population, but there was no difference in lifespan between the two groups.

https://www.bmj.com/content/308/6945/1667

Mortality in British vegetarians: results from the European Prospective Investigation into Cancer and Nutrition (EPIC-Oxford)

researchers found that the risk of death for both vegetarians/vegans & omnivores was 52% lower than in the general population—similar to findings from the two studies above. However, there was no difference in mortality between vegetarians & omnivores

https://academic.oup.com/ajcn/article/89/5/1613S/4596950

Debunking the vegan myth: The case for a plant-forward omnivorous whole-foods diet

"vegan or vegetarian diets are not associated with reduction in all-cause mortality rates"

https://www.sciencedirect.com/science/article/pii/S0033062022000834?via=ihub

Mortality in vegetarians and comparable nonvegetarians in the United Kingdom

no difference

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4691673/

Dietary habits and mortality in 11,000 vegetarians and health conscious people: results of a 17 year follow up

both vegetarians and omnivores in the health food store group lived longer than people in the general population—not surprising given their higher level of health consciousness—but there was no survival difference between vegetarians or omnivores

https://www.ncbi.nlm.nih.gov/pubmed/8842068

Vegetarian, vegan diets and multiple health outcomes: A systematic review with meta-analysis of observational studies

Meta-analysis:

Although they found slight relative reductions in death from heart disease and cancer in vegetarians and vegans compared with omnivores, they found no difference in total mortality.

https://www.ncbi.nlm.nih.gov/pubmed/26853923

Vegetarian diet, Seventh Day Adventists and risk of cardiovascular mortality: A systematic review

Meta Analysis

found no difference in total mortality between vegetarians/vegans and omnivores.

https://www.sciencedirect.com/science/article/pii/S016752731401290X

Lifestyle Determinants and Mortality in German Vegetarians and Health-Conscious Persons: Results of a 21-Year Follow-up

This study found that vegetarians had slightly higher (10 percent) total mortality than healthy omnivores. What’s more, the data suggested that non-dietary factors played a much greater role in predicting lifespan than diet: smoking, exercise, etc..

http://cebp.aacrjournals.org/content/14/4/963.long

Abstract

The popularity of vegetarian diets has increased the need for studies on long-term health outcomes. A limited number of studies, including only one study from a non-vegetarian population, investigated the risk of mortality with self-identified vegetarianism and reported inconsistent results. This study evaluated prospective associations between vegetarian diets and all-cause mortality among 117,673 participants from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial cohort study. Vegetarian diet status was self-identified on the questionnaire. Deaths were ascertained from follow-up questionnaires and the National Death Index database. Multivariable Cox regression models were used to estimate the risk of all-cause mortality in hazard ratio (HR) and 95% confidence intervals (CI). By diet group, there were 116,894 omnivores (whose diet does not exclude animal products), 329 lacto- and/or ovo-vegetarians (whose diet excludes meat, but includes dairy and/or eggs), 310 pesco-vegetarians (whose diet excludes meat except for fish and seafood) and 140 vegans (whose diet excludes all animal products). After an average follow-up of 18 years, 39,763 participants were deceased. The risk of all-cause mortality did not statistically significantly differ among the four diet groups. Comparing with the omnivore group, the HR (95% CI) were 0.81 (0.64-1.03) for pesco-vegetarian group, 0.99 (0.80-1.22) for lacto- and/or ovo-vegetarian group and 1.27 (0.99-1.63) for vegan group, respectively. Similarly, mortality risk did not differ when comparing lacto- and/or ovo-vegetarians plus vegans with meat/fish eaters (omnivores and pesco-vegetarians) (HR [95% CI] = 1.09 [0.93-1.28]). As this study is one of the two studies of vegetarianism and mortality in non-vegetarian populations, further investigation is warranted.

https://pmc.ncbi.nlm.nih.gov/articles/PMC10666432/