Tackling Arguments Against Plant-Based Diets: A Response to T-Nation

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Vegan nutrition tips online

This article is a rebuttal to a T-Nation article and was compiled after a VBBN member shared this link:
https://www.t-nation.com/diet-fat-loss/10-things-vegetarians-get-wrong

Relevant Abbreviations
SFA – saturated fats
PUFA – polyunsaturated fats
MUFA – monounsaturated fats
EFA – essential fatty acids
LA – linoleic acid, an EFA found in plants
ALA – alpha-linolenic acid, an EFA found in plants
CVD – cardiovascular disease
CHD – myocardial infarction, cardiac death
IHD – ischemic heart disease
T2D – type 2 diabetes
HDL – high density lipoprotein (“good” cholesterol)
LDL – low density lipoprotein (“bad” cholesterol)

Claim #1 – Saturated fat does not clog arteries.

T-Nation: “2009 review in American Journal of Clinical Nutrition analyzed research from 21 studies with saturated fat intake from 350,000 people and found no association with heart disease.”

The study being cited is http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824152/

“A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.”

The cited study was published in 2009, but a 2012 Cochrane review found a different outcome.

“This updated review suggested that reducing saturated fat by reducing and/or modifying dietary fat reduced the risk of cardiovascular events by 14%.” In studies examining fat modification (not reduction of total intake, but switching fats in the diet), a reduction in CVD events was observed, but effects on mortality were unclear. The analysis is limited by few studies examining reduced vs modified fat intakes.

http://www.ncbi.nlm.nih.gov/pubmed/22592684

SFA affect the arterial wall and may promote stiffness in arteries due to low-grade inflammation. The anti-inflammatory potential of HDL is reduced after consumption of saturated fat-containing meals, impairing function of the arterial endothelial cells.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878127/

http://www.ncbi.nlm.nih.gov/pubmed/15580061

http://www.ncbi.nlm.nih.gov/pubmed/16904539

Counseling families to feed children low saturated fat diets results in lower rates of metabolic syndrome as teenagers and young adults (up to 20 years old).

http://www.ncbi.nlm.nih.gov/pubmed/25605660

Also, see point #4 about other adverse health outcomes associated with saturated fats.

Claim #2 – Dietary cholesterol does not raise serum cholesterol.

This does not appear to be in line with the evidence either. Dietary cholesterol can raise serum cholesterol, but the research currently questions the association between dietary cholesterol and CVD risk. It is worth noting that dietary cholesterol raises LDL cholesterol more than it raises HDL cholesterol (by a 2:1 ratio), and it is LDL levels that have been associated with CVD.

http://www.ncbi.nlm.nih.gov/pubmed/25815993

http://www.ncbi.nlm.nih.gov/pubmed/26282344

http://www.ncbi.nlm.nih.gov/pubmed/26298740

Of particular concern are small, dense LDL particles and oxidized LDL particles.

http://circ.ahajournals.org/content/95/1/69.abstract

http://jama.jamanetwork.com/article.aspx?articleid=374290

http://atvb.ahajournals.org/content/12/2/187.short

Adding eggs to the diet of men and women to increase dietary cholesterol are associated with small increases in serum cholesterol, and a dose-dependent effect is observed:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3292202/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3287065/

A hyperbolic shape has been suggested for the association between serum and dietary cholesterol levels.

http://ajcn.nutrition.org/content/55/6/1060.full.pdf

“Clinical feeding studies show that a 100 mg/day change in dietary cholesterol will on average change the plasma total cholesterol level by 2.2-2.5 mg/dl, with a 1.9 mg/dl change in low density lipoprotein (LDL) cholesterol and a 0.4 mg/dl change in high density lipoprotein (HDL) cholesterol.” However, the physiological significance of cholesterol in CVD risk is questioned in this article. http://www.ncbi.nlm.nih.gov/pubmed/11111098

This 2015 review shows that dietary cholesterol can raise serum cholesterol – total cholesterol by 11.2 mg/dL, LDL cholesterol by 6.7 mg/dL, and HDL cholesterol by 3.2 mg/dL. No association of cholesterol with coronary artery disease, ischemic stroke, or hemorrhagic stroke was detected. “Reviewed studies were heterogeneous and lacked the methodologic rigor to draw any conclusions regarding the effects of dietary cholesterol on CVD risk. Carefully adjusted and well-conducted cohort studies would be useful to identify the relative effects of dietary cholesterol on CVD risk.”

http://www.ncbi.nlm.nih.gov/pubmed/26109578

A good lay article summarizing the various studies on SFA and serum cholesterol are here, noting most do not find an association between SFA and cholesterol:

http://wholehealthsource.blogspot.com/2011/01/does-dietary-saturated-fat-increase.html

Claim #3 – Processed meats are not as healthy as unprocessed meats.

The reference list on T-Nation includes this study from the European Prospective Investigation into Cancer and Nutrition (EPIC study). http://www.ncbi.nlm.nih.gov/pubmed/23497300

“After multivariate adjustment, a high consumption of red meat was related to higher all-cause mortality (hazard ratio (HR) = 1.14, 95% confidence interval (CI) 1.01 to 1.28, 160+ versus 10 to 19.9 g/day), and the association was stronger for processed meat (HR = 1.44, 95% CI 1.24 to 1.66, 160+ versus 10 to 19.9 g/day). After correction for measurement error, higher all-cause mortality remained significant only for processed meat (HR = 1.18, 95% CI 1.11 to 1.25, per 50 g/d). We estimated that 3.3% (95% CI 1.5% to 5.0%) of deaths could be prevented if all participants had a processed meat consumption of less than 20 g/day. Significant associations with processed meat intake were observed for cardiovascular diseases, cancer, and ‘other causes of death’. The consumption of poultry was not related to all-cause mortality.”

There is evidence that processed red meats are associated with CVD, whereas red meats in other forms (not processed) are not as well associated with CVD.

http://www.ncbi.nlm.nih.gov/pubmed/24932617

http://circ.ahajournals.org/content/121/21/2271.full

Claim #4 – PUFA are associated with heart disease, but SFA are not.

The first part is not in line with the current evidence. For the second part, see point #1.

Replacement of SFA with PUFA for at least a year results in less CHD (myocardial infarction and/or cardiac death) risk, and longer duration increases benefits. When subjects ate 8-21% of energy from PUFA, the pooled risk reduction was 19% compared to subjects eating 4-6% of energy from PUFA. This corresponds to a 10% reduction in CHD risk for each 5% increase in PUFA consumption.

http://www.ncbi.nlm.nih.gov/pubmed/20351774

“Convincing evidence was found that partial replacement of saturated fat (SFA) with polyunsaturated fat (PUFA) or monounsaturated fat (MUFA) lowers fasting serum/plasma total and LDL cholesterol concentrations… Furthermore, there was convincing evidence that partial replacement of SFA with PUFA decreases the risk of CVD, especially in men.”

http://www.ncbi.nlm.nih.gov/pubmed/25045347

“Furthermore, there was convincing evidence that partial replacement of SFA with PUFA decreases the risk of CVD, especially in men. This finding was supported by an association with biomarkers of PUFA intake; the evidence of a beneficial effect of dietary total PUFA, n-6 PUFA, and linoleic acid (LA) on CVD mortality was limited suggestive. Evidence for a direct association between total fat intake and risk of T2DM was inconclusive, whereas there was limited-suggestive evidence from biomarker studies that LA is inversely associated with the risk of T2DM.” Note that LA is an essential fatty acid and is found in plants.

http://www.ncbi.nlm.nih.gov/pubmed/25045347

There may be specific SFA associated with disease risk. For CVD, palmitic and myristic acids were shown to be adversely associated with CVD risk factors in Alaskan Natives. For diabetes, higher circulating levels of palmitic and stearic acids in blood are associated with greater risk.

http://www.ncbi.nlm.nih.gov/pubmed/26274054

http://www.ncbi.nlm.nih.gov/pubmed/25527759

Higher SFA intake is associated with reduced bone mineral density, particularly in men. http://jn.nutrition.org/content/136/1/159.full

Over-feeding SFA palmitic acid produced more weight gain in visceral adipose and liver fat compared to PUFA linoleic acid.

“Both groups gained similar weight. SFAs, however, markedly increased liver fat compared with PUFAs and caused a twofold larger increase in visceral adipose tissue than PUFAs. Conversely, PUFAs caused a nearly threefold larger increase in lean tissue than SFAs. Increase in liver fat directly correlated with changes in plasma SFAs and inversely with PUFAs.”

http://diabetes.diabetesjournals.org/content/63/7/2356.long

There are other studies suggesting that other types of fats are more harmful than SFA, such as trans fat.

“Saturated fats are not associated with all cause mortality, CVD, CHD, ischemic stroke, or type 2 diabetes, but the evidence is heterogeneous with methodological limitations. Trans fats are associated with all cause mortality, total CHD, and CHD mortality, probably because of higher levels of intake of industrial trans fats than ruminant trans fats.”

http://www.ncbi.nlm.nih.gov/pubmed/26268692

Claim #5 – Lineolic acid is the dominant fat in vegetable oil, and consumption is linked to tumor growth. Conjugated lineolic acid found in animal fat has proven effective in preventing cancer.

Lineolic acid (LA) is not associated with tumor growth or CVD (see above).

“Large scale human epidemiological studies indicate that high intakes of linoleic acid protect against the development of cancer.”

http://www.ncbi.nlm.nih.gov/pubmed/9561154

“We reviewed the epidemiologic and experimental literature on linoleic acid intake and cancer risk and performed additional meta-analyses of risk estimates from case-control and prospective cohort studies. None of the combined estimates from within-population studies indicated a significantly increased risk of cancer with high compared with low intakes of linoleic acid or polyunsaturated fat.“

http://ajcn.nutrition.org/content/68/1/142.abstract

“It seems that no consistent result was observed even in similar studies conducted at different laboratories, this may be due to variations in age, gender, racial and geographical disparities, coupled with type and dose of CLA supplemented. Thus, supposed promising results reported in mechanistic and pre-clinical studies cannot be extrapolated with humans, mainly due to the lack of inconsistency in analyses, prolonged intervention studies, follow-up studies and international co-ordination of concerted studies. Briefly, clinical evidences accumulated thus far show that CLA is not eliciting significantly promising and consistent health effects so as to uphold it as neither a functional nor a medical food. “

http://www.ncbi.nlm.nih.gov/pubmed/25972911

Claim #6 – The China Study is a farce.

T-Nation mentions the Tuoli and Longxian populations, making the following claims:

– The Tuoli have 45% fat, 135 g animal protein, and lower heart disease and cancer.

– The Longxian have lowest amount of animal foods, but second highest death rate from heart disease.

– The data show a 7-fold greater cancer association with high carb and high sugar diet, as well as fewer cancer deaths with a high animal fat intake.

The 1989 China Study data is available online: http://www.ctsu.ox.ac.uk/%7Echina/monograph/

In the various tables, the Longxian population is marked as TD, whereas the Tuoli population is marked as WA. The Tuoli population were noted as consuming an atypical diet during a festival in 1983, and the cholesterol and milk/dairy intakes were much higher in 1983 than in 1989. For cholesterol intake by the Touli, the 1983 value was 678.3 mg/day and the 1989 value was 120.55 mg/day. The mean intake of 73 mg/day between the two years was largely unchanged. The average cholesterol intake in the UK was noted as 400 mg/day. The milk/dairy intake of the Tuoli was 856.5 g/day in 1983 and 94.15 g/day in 1989. The cholesterol and milk/dairy intakes of the Longxian were essentially zero.

From the 1989 data on the reference man (per day amounts, 65 kg body weight, light activity):

– The Longxian had 25.8 g total fat, 11.8% of calories from fat, and essentially zero animal protein intake.

– The Tuoli had 62.2 g total fat, 22.4% of their calories coming from fat, 13.1 g animal protein, and 19.1% of calories from protein.

– No county examined had 45% of their calories from fat, the highest county had 32.6%.

– No county examined had 135 g animal protein intake, the highest county was 27.6 g.

– For carbohydrate intakes, the Longxian had 392 g and the Tuoli had 420 g. This represents 77.4% of calories for the Longxian and 66.6% of calories for the Tuoli.

– White flour intakes were 499.8 g for the Longxian and 588.8 g for the Tuoli.

– Starchy tuber intakes were 132.6 g for the Longxian and 26 g for the Tuoli.

– For processed starch and sugar intakes, both groups had zero intake.

– For the Longxian, red meat and poultry intakes were essentially zero. For the Tuoli, red meat and poultry intake was 88.3 g, while milk and dairy was 94.2 g.

– For the Longxian, saturated fat intake is 5.5 g and cholesterol is 2 g. For the Tuoli, saturated fat intake is 23.83 g and cholesterol is 120.5 mg.

The mortality rates for all cause mortality, all cancer, all vascular, and IHD were different between the Longxian and the Tuoli. The numbers are reported as standardized rates per 1,000 people.

The all cause mortality includes causes of death unrelated to health, such as accidents, murder, and other causes. Medical mortality was also determined. The mortality in the 0 to 34 age group is dominated by infant and childhood deaths.

– For ages 0 to 34 years old, the all cause mortality rates are rural Chinese men 226, rural Chinese women 188, Longxian men 260, Longxian women 205, Tuoli men 363, Tuoli women 370. Compared to the rural Chinese averages, the Longxian are similar and the Tuoli have greater all cause mortality in the 0 to 34 age group. The Longxian had lower rates of all cause mortality than the Tuoli for the 0 to 34 age group.

– For ages 35 to 69 years old, the all cause mortality rates are rural Chinese men 16, rural Chinese women 10, Longxian men 23, Longxian women 22, Tuoli men 12, Tuoli women 8. Compared to the rural Chinese averages, the Longxian have a slightly higher (~50%) all cause mortality and the Tuoli have a slightly lower (~25%) all cause mortality in the 35 to 69 age group. The Longxian had 2- to 3-fold higher rates of all cause mortality than the Tuoli in the 35 to 69 age group.

– For ages 70 to 79 years old, the all cause mortality rates are rural Chinese men 82, rural Chinese women 56, Longxian men 178, Longxian women 135, Tuoli men 20, Tuoli women 21. Compared ot the rural Chinese averages, the Longxian have a ~2-fold higher all cause mortality and the Tuoli have a lower (~75%) all cause mortality in the 70 to 79 age group. The Longxian had a ~7 to 9-fold higher all cause mortality rate than the Tuoli in the 70 to 79 age group.

– For ages 0 to 34 years old, the medical mortality rates are rural Chinese men 147, rural Chinese women 134, Longxian men 183, Longxian women 175, Tuoli men 305, Tuoli women 341. Compared to the rural Chinese averages, the Longxian have similar rates of medical mortality and the Tuoli have ~2-fold higher rates of medical mortality in the 0 to 34 age group. The Longxian had a lower (~50%) medical mortality rate than the Tuoli in the 0 to 34 age group.

– For ages 35 to 69 years old, the medical mortality rates are rural Chinese men 15, rural Chinese women 10, Longxian men 21, Longxian women 21, Tuoli men 11, Tuoli women 8. Compared to the rural Chinese averages, the Longxian have 1.5- to 2-fold higher medical mortality rate and the Tuoli have a slightly lower (~20-30%) medical mortality rate in the 35 to 69 age group. The Longxian had 2- to 3-fold higher medical mortality rates than the Tuoli in the 35 to 69 age group.

The Longxian and the Tuoli had similar rates of all cancers in 0-34 and 35-69 years old.

– The all cancer mortality rates for ages 0-34 are rural Chinese men 18, rural Chinese women 12, Longxian men 7, Longxian women 15, Tuoli men 10, Tuoli women 7. Compared to the rural Chinese averages, the Longxian and the Tuoli had lower all cancer mortality in men, but the Longxian women had slightly higher (~25%) all cancer mortality and the Tuoli women had lower (~40%) all cancer mortality in the 0 to 34 age group.

– The all cancer mortality rates for ages 35-69 are rural Chinese men 6, rural Chinese women 3, Longxian men 4, Longxian women 3, Tuoli men 5, Tuoli women 3. Compared to the rural Chinese averages, the Longxian and the Tuoli had similar all cancer mortality in the 35-69 age group.

The Longxian had higher deaths from vascular causes and ischemic heart disease (IHD) for ages 35-69 years old than the Tuoli, and it is noted that the Longxian have a high incidence of stroke. For men, a portion of the IHD deaths are attributable to cigarette smoking (~15%). The rates have at least doubled for both men and women in China since 1974, but the rates are highly variable across the country. Rates in China are lower than in the US or UK.

– The vascular death mortality rates for ages 0 to 34 years old are rural Chinese men 7, rural Chinese women 7, Longxian men 14, Longxian women 16, Tuoli men 22, Tuoli women 0. Compared to rural Chinese averages, the Longxian have a ~2-fold higher vascular death mortality rate, the Tuoli men have a ~3-fold higher vascular death mortality rate, and the Tuoli women have a lower rate of vascular death mortality rate. The Longxian men had a lower vascular death mortality rate than the Tuoli men, but the Longxian women had a higher vascular death mortality rate than the Tuoli women, in the 0 to 34 age group.

– The vascular death mortality rates for ages 35 to 69 years old are rural Chinese men 3, rural Chinese women 3, Longxian men 10, Longxian women 12, Tuoli men 3, Tuoli women 3. Compared to the rural Chinese averages, the Longxian have a 3- to 4-fold higher vascular death mortality rate and the Tuoli had a similar vascular death mortality rate in the 35 to 69 age group. The Longxian had a 3- to 4-fold higher vascular death mortality rate than the Tuoli in the 35 to 69 age group.

– The IHD mortality rates for ages 35 to 69 years old are rural Chinese men 52, rural Chinese women 33, Longxian men 197, Longxian women 162, Tuoli men 43, Tuoli women 41. Compared to the rural Chinese averages, the Longxian had a 4- to 5-fold higher IHD mortality rate, the Tuoli men have a slightly lower (~20%) IHD mortality rate, and the Tuoli women had a slightly higher (~33%) IDH mortality rate in the 35 to 69 age group. The Longxian had a 4- to 5-fold higher IHD mortality rate than the Tuoli in the 35 to 69 age group.

Relating these differences in mortality solely to diet is complicated. T-Nation claimed the data show a 7-fold greater cancer association with high carb and high sugar diet, as well as fewer cancer deaths with a high animal fat intake. The Longxian and the Tuoli had similar all cancer rates.

– The Tuoli eat more total calories (500 more calories!), grams of carbohydrates, white flour, red meat, poultry, and dairy than the Longxian. However, the Tuoli’s higher calorie intake shifts the relative percentage of carbohydrate intakes: 420 g carbs = 67% of calories for the Tuoli, 392 g carbs = 77% of calories for the Longxian.

– The Tuoli’s intake of red meat and poultry was 88 g = 7 oz, or the equivalent of ~2 servings. The Tuoli’s dairy intake was 94 g = 0.4 cup = 6.4 tablespoons, or the equivalent of ~1/2 serving.

– Neither group ate processed starches or sugars, and the mean processed sugar intake in China was only 2 g/day.

– The Tuoli ate more carbohydrates and more white flour. The Longxian and the Tuoli had similar rates of cancer in the 35 to 69 age group.

– The Tuoli’s animal fat intake was only 8.5 g, although their total fat intake was 62.6 g. The Longxian and the Tuoli had similar rates of cancer in the 35 to 69 age group.

– The total protein intakes were similar: Longxian 56.1, Tuoli 68.4 g.

Also, in the methods section (page 3), “In contrast, ischaemic heart disease (IHD; which also shows ten-fold variation between one part of China and another) is, in every county, much less common than in the UK. Dietary factors might well account for much of this—average fat intake in rural China (18% of dietary calories) was less than half that in the UK, and average plasma cholesterol was only about two-thirds that in the UK (3.8 mmol/L, 148 mg/dL). Among the study counties, however, the variation in IHD mortality is not significantly correlated with the variation in fat intake, possibly because fat intake is correlated about as strongly with HDL cholesterol (which cardioprotective particles carry) as it is with non-HDL cholesterol.”

The comments on fat intake are interesting, as Drs. Hu and Willett suggested various aspects of fat intake may be more related to disease risk than protein intake. “In the Nurses’ Health Study, however, we identified several important dietary factors for risk of ischemic heart disease, including trans fatty acids (5), the ratio of polyunsaturated to saturated fat (5), α-linolenic acid (6), cereal fiber (7), nuts (8), whole-grain products (9), and fruit and vegetables (Kumudi unpublished observations, 2000).”

http://ajcn.nutrition.org/content/71/3/850.full

As for Campbell’s well-known experiments with aflatoxin-treated rodents fed casein, a similar study in rhesus monkeys did not replicate his results.

http://informahealthcare.com/doi/abs/10.3109/15569548909059756

Casein is ~80% of protein found in cow milk, but the evidence of milk being linked to cancers in humans is generally unclear, except for calcium and dairy with prostate cancer. http://www.milkfacts.info/Milk%20Composition/Protein.htm

http://www.ncbi.nlm.nih.gov/pubmed/24847855

http://www.ncbi.nlm.nih.gov/pubmed/24976856

http://www.ncbi.nlm.nih.gov/pubmed/25406801

Claim #7 – The myth is that meat causes cancer because it is acidic. An alkaline diet emphasizing fruits and veggies is beneficial, and omnivores can get benefits from eating fruits and veggies too.

The alkaline dietary theory suggests that “acidifying” and “alkalizing” foods should be consumed in “a balance” with an emphasis on consuming alkalizing foods. The acidifying foods include meats, dairy products, corn, wheat, and refined sugars. The alkalizing foods include fruits and vegetables. The alkaline dietary theory proposes that a diet of fruit and vegetables lowers the body’s acid load and reduces stress on the kidneys. The alkaline dietary theory recommends that approved foods are consumed in specific ways, called “food combining,” to reduce acidosis. There is no evidence for food combining principles to regulate acidosis in humans in the literature, although one study showed that food combining principles did not produce any additional weight loss when calories were reduced equally in a traditional diet and a food combining diet.

http://www.ncbi.nlm.nih.gov/pubmed/10805507

The hypothesis that meat causes cancer because meat is acidic is flawed. The alkaline diet was originally studied in the context of bone health, because an acidic load in the body would, in theory, leech calcium from the bones and reduce bone health. The data showed that acid load from meat did not harm bones, and similar results were obtained with milk. A 2009 meta-analysis concluded that, “This meta-analysis did not find evidence that phosphate intake contributes to demineralization of bone or to bone calcium excretion in the urine. Dietary advice that dairy products, meats, and grains are detrimental to bone health due to “acidic” phosphate content needs reassessment. There is no evidence that higher phosphate intakes are detrimental to bone health.”

http://www.ncbi.nlm.nih.gov/pubmed/19754972 (quoted)

http://www.ncbi.nlm.nih.gov/pubmed/21248199

http://www.ncbi.nlm.nih.gov/pubmed/22127335

http://www.ncbi.nlm.nih.gov/pubmed/15546911

http://www.ncbi.nlm.nih.gov/pubmed/19419322

http://www.ncbi.nlm.nih.gov/pubmed/18842807

http://www.ncbi.nlm.nih.gov/pubmed/20459740

http://www.ncbi.nlm.nih.gov/pubmed/24094472

http://www.ncbi.nlm.nih.gov/pubmed/22081694

Fruits and veggies are generally associated with reduced cancer risk, but there is no evidence they have to be consumed in any special pattern as proposed by the alkaline dietary theory. I have not seen any papers claiming food combining or other alkaline dietary principles are required for the health benefits of fruits and veggies. If an alkaline diet protects against cancer, then fruits and vegetables should both consistently show protective effects in studies examining cancer risk. Meat and dairy should be associated with increased cancer risk if the alkaline dietary theory is correct about a food’s acid load and its ability to promote undesirable health effects. For example, colon cancer is commonly associated with meat consumption, but dairy products and calcium appear protective. Both meat and dairy are considered acidic by the alkaline diet theory, but their influences on CRC risk are different. In hepatocellular carcinoma (HCC, liver cancer), it has been suggested that only vegetables have protective effects, but not fruits. In breast cancer, it has been suggested that fruits or the combination of fruits and vegetables are weakly protective, but not vegetables alone. Inconclusive data exists for the effects of fruits and vegetables on bladder cancer risk. Together, these reviews and meta-analyses question the validity of the alkaline diet theory when its two main food groups have different influences on the risk of various cancers.

http://www.ncbi.nlm.nih.gov/pubmed/25583132

http://www.ncbi.nlm.nih.gov/pubmed/25093007

http://www.ncbi.nlm.nih.gov/pubmed/25127680

http://www.ncbi.nlm.nih.gov/pubmed/22706630

http://www.ncbi.nlm.nih.gov/pubmed/25461441

http://www.ncbi.nlm.nih.gov/pubmed/26148912

http://www.ncbi.nlm.nih.gov/pubmed/25680825

http://www.ncbi.nlm.nih.gov/pubmed/26610570

http://www.ncbi.nlm.nih.gov/pubmed/26589974

http://www.ncbi.nlm.nih.gov/pubmed/26371287

A popular extension of the alkaline dietary theory is that it can be used as a treatment when someone is diagnosed with cancer. There is insufficient evidence for this claim, and more research is needed before the alkaline diet can be suggested as a component of treatment.

http://www.ncbi.nlm.nih.gov/pubmed/24403443

http://www.ncbi.nlm.nih.gov/pubmed/22013455

To address the last part of this claim, omnivores eating plenty of fruits and veggies with small portions of lean meats are likely to have positive health outcomes. This does not seem controversial. The standard American diet does not include much fruit and veggie consumption though. This would be where a whole foods vegan diet could have advantages, because vegans would be consuming fruits and veggies closer to the recommended amounts.

“However, during 2007–2010, half of the total U.S. population consumed <1 cup of fruit and <1.5 cups of vegetables daily; 76% did not meet fruit intake recommendations, and 87% did not meet vegetable intake recommendations (2). Median frequency of reported fruit intake across all respondents was once per day, ranging from 0.9 in Arkansas to 1.3 times per day in California (Table). Median frequency of reported vegetable intake was 1.7 times per day, ranging from 1.4 in Louisiana, Mississippi, and North Dakota to 1.9 times per day in California and Oregon. Based on prediction equations, 13.1% of respondents met fruit recommendations, and 8.9% met vegetable recommendations. The percentage of state populations meeting recommendations for fruits ranged from 7.5% in Tennessee to 17.7% in California, and for vegetables, from 5.5% in Mississippi to 13.0% in California.”

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6426a1.htm

Claim #8 – Vegans and vegetarians do not have lower rates of disease.

T-Nation mentioned Seventh Day Adventists (generally vegetarian) and Mormons (not vegetarian) as study populations. Both groups tend to avoid smoking and alcohol use, allowing potential associations with other lifestyle factors like diet to be studied. They cited 22% lower cancer rate and 34% lower mortality rate from colon cancer in the Mormons compared to the general American population.

It does appear Mormons have lower cancer rates and mortality rates compared to the general population.

http://www.ncbi.nlm.nih.gov/pubmed/15904509

http://www.ncbi.nlm.nih.gov/pubmed/17920112

http://www.ncbi.nlm.nih.gov/pubmed/6933238

Mormons were examined in a study looking at the connection between families and cancer risk. Familial factors were implicated in a substantial portion of cancer risk.

http://www.ncbi.nlm.nih.gov/pubmed/15779016

Mormons also have lower rates of cardiovascular disease deaths.

http://www.ncbi.nlm.nih.gov/pubmed/727204

“Accordingly, mortality rates of Mormons and Seventh-day Adventists show a significant lower level when compared with cancer data of lung, colon and rectum, and prostate from the best German cancer registry (Saarland). Some tumor rates are higher in Mormons, e.g. malignant melanoma, also all types of malignant lymphoma and myeloma. The life expectancy is generally elevated by 2-4 years in Mormons and Seventh-day Adventists.”

http://www.ncbi.nlm.nih.gov/pubmed/1449267

T-Nation: “Despite the Seventh Day Adventists’ low rate of colorectal cancer, they seem to be at a higher risk of other cancers – Hodgkin’s disease, malignant melanoma, brain, skin, uterine, prostate, endometrial, cervical, and ovarian cancer.”

The Adventist Health Studies in America started in 1960 and are still ongoing today. The initial study in 1960-1965 showed Adventists had 60-76% lower death rates from all cancers, and reduced incidence of lung, colorectal, and breast cancers, and lower coronary heart disease. The second study in 1974-1988 identified several dietary factors that were associated with reduced risk of heart disease and select cancers. The third study started in 2002. The studies are summarized here: http://publichealth.llu.edu/adventist-health-studies

In Danish Adventists, lower rates of cancer in the lung, buccal cavity, liver, cervix, rectum, and stomach were observed in a 2012 study. http://www.ncbi.nlm.nih.gov/pubmed/22910035

The rates of various cancers in vegetarians (vegetarian, pesco-vegetarian, vegan, and other categories) are well organized here, including the Adventist, EPIC-Oxford, and other similar studies: http://www.veganhealth.org/articles/cancer

There are lower rates of all cancers in vegetarians, plus lower incidence of the several specific cancers in vegetarians, including colorectal, prostate, breast, stomach, pancreatic, brain (meningioma), oral, bladder, and lymphatic & hematopoietic tissues (non-Hodgkin’s lymphoma, multiple myeloma). Not all studies separated vegans from other types of vegetarians, but it appears that not consuming meat provides a reduction in cancer risk.

Looking at this data, I would venture that the avoidance of smoking and alcohol use is likely a large contributor to the health outcomes measured. The connection between smoking and cardiovascular disease risk is well established, and there is also data on alcohol use and cancer risk. Another factor to consider is that Adventists emphasize maintaining a healthy body weight, and adiposity/obesity is associated with cancer risk. Vegetarians have a significant difference in BMI from non-vegetarians in the Adventist studies.

“The 5-unit BMI difference between vegans and nonvegetarians indicates a substantial potential of vegetarianism to protect against obesity. Increased conformity to vegetarian diets protected against risk of type 2 diabetes after lifestyle characteristics and BMI were taken into account. Pesco- and semi-vegetarian diets afforded intermediate protection.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2671114/

More on BMI and cancer risk, alcohol and cancer risk

http://www.nhlbi.nih.gov/health/health-topics/topics/smo

http://circ.ahajournals.org/content/96/9/3243.full

http://www.cancer.gov/about-cancer/causes-prevention/risk/alcohol/alcohol-fact-sheet

http://www.cancer.gov/about-cancer/causes-prevention/risk/obesity/obesity-fact-sheet

Claim #9 – Vegetarians do not live longer.

T-Nation: “Research from 1973 in the American Journal of Epidemiology found higher all-cause mortality rates in both vegetarian men (0.93%) and women (0.86%) compared to their non-vegetarian counterparts (men 0.89%, women 0.54%).”

I cannot find a study about vegetarian mortality in the American Journal of Epidemiology’s archive for 1973. The first study that comes up in the search feature is a 1974 paper that shows vegetarians have lower blood pressure.

Vegetarian mortality is about half that of the study populations in several large studies. http://www.veganhealth.org/articles/dxrates

Emphasizing a more plant-based diet (without having people commit to veganism) appears to offer protection in the PREDIMED study.

http://ajcn.nutrition.org/content/100/Supplement_1/320S.long

A recent meta-analysis using 7 studies containing nearly 125,000 people found lower mortality, disease, and cancer in vegetarians.

“Seven studies with a total of 124,706 participants were included in this analysis. All-cause mortality in vegetarians was 9% lower than in nonvegetarians (RR = 0.91; 95% CI, 0.66-1.16). The mortality from ischemic heart disease was significantly lower in vegetarians than in nonvegetarians (RR = 0.71; 95% CI, 0.56-0.87). We observed a 16% lower mortality from circulatory diseases (RR = 0.84; 95% CI, 0.54-1.14) and a 12% lower mortality from cerebrovascular disease (RR = 0.88; 95% CI, 0.70-1.06) in vegetarians compared with nonvegetarians. Vegetarians had a significantly lower cancer incidence than nonvegetarians (RR = 0.82; 95% CI, 0.67-0.97).” http://www.ncbi.nlm.nih.gov/pubmed/22677895

If vegetarians have lower mortality rates, they are likely living longer. J

http://ajcn.nutrition.org/content/78/3/526S.long

Many of the groups known for their longevity emphasize plant-based diets, not necessarily vegan diets. There are potential mechanisms for longevity extension in plant-based diets – methionine restriction, reduction of IGF-1, lower energy intakes (calorie restriction), and antioxidant consumption. Plant proteins are lower in methionine content than animal proteins.

http://www.ncbi.nlm.nih.gov/pubmed/18789600

http://www.ncbi.nlm.nih.gov/pubmed/12699704

http://www.ncbi.nlm.nih.gov/pubmed/23454735

http://www.ncbi.nlm.nih.gov/pubmed/24291541

http://www.ncbi.nlm.nih.gov/pubmed/10696634

http://www.ncbi.nlm.nih.gov/pubmed/17299498

Claim #10 – Myth of soy as a superfood.

T-Nation lists the following hazards of consuming soy: inhibits reproductive health, negatively alters brain function, suppresses thyroid hormone, endocrine disruption, increases breast and prostate cancer risk.

Reproductive function not affected by soy:

In several studies examining soy protein or isoflavone supplementation, men did not have significant changes in testosterone, free testosterone, estrogen, sex hormone binding globulin protein, or semen quality. A decrease in prostate specific antigen (PSA), which could be beneficial for prostate cancer, was seen in men consuming soy supplements. Interestingly, one study showed no changes in T levels, but decreased androgen receptor (AR) expression was observed; decreased AR could be beneficial in hormone-sensitive prostate cancer growth.

http://www.ncbi.nlm.nih.gov/pubmed/23874588

http://www.ncbi.nlm.nih.gov/pubmed/22066824

http://www.ncbi.nlm.nih.gov/pubmed/20378106

http://www.ncbi.nlm.nih.gov/pubmed/19524224

http://www.ncbi.nlm.nih.gov/pubmed/17585029

http://www.ncbi.nlm.nih.gov/pubmed/16775579

http://www.ncbi.nlm.nih.gov/pubmed/15351581

http://www.ncbi.nlm.nih.gov/pubmed/12094627

http://www.ncbi.nlm.nih.gov/pubmed/11880595

In women, soy does not appear to have a negative impact on fertility, endometrial health, or ovarian health. In a study examining women receiving fertility treatments, soy consumption was positively associated with having a live birth.

http://www.ncbi.nlm.nih.gov/pubmed/25577465

The Adventist studies link soy consumption with not having a child or becoming pregnant, but the difference in having a child was small. “In women with high (≥40 mg/day) isoflavone intake (12% of this group of women), the adjusted lifetime probability of giving birth to a live child was reduced by approximately 3% (95% CI: 0, 7) compared to women with low (<10 mg/day) intake.”

http://www.ncbi.nlm.nih.gov/pubmed/24741329

Brain function: T-Nation claims “a study from Journal of the American College of Nutrition found cognitive dysfunction and brain atrophy in men consuming two or more servings of tofu per week.”

The studies on soy and cognition are summarized here:

http://www.veganhealth.org/articles/soy_wth#cog

Most studies show neutral or positive associations between soy consumption and cognition. Negative associations originally observed in studies went away with time, and some concerns were raised about formaldehyde used in processing tofu in other countries.

Suppressed thyroid hormone or hypothyroidism: There is limited evidence that people with healthy thyroids and appropriate iodine intake are negatively affected by soy consumption [36]. Some hypothyroid patients may need to adjust their medicine’s dose to compensate for soy foods, as well as other foods that contain goitrogens (uncooked cruciferous vegetables, for example). Hypothyroid patients should discuss iodine intake and medications with their doctors.

http://www.ncbi.nlm.nih.gov/pubmed/16571087

“Vegan versus omnivorous diets tended to be associated with reduced risk (OR 0.89, 95% CI: 0.78–1.01, not statistically significant) while a lacto-ovo diet was associated with increased risk (OR 1.09, 95% CI: 1.01–1.18). In the incidence study, female gender, white ethnicity, higher education and BMI were predictors of hypothyroidism. Following a vegan diet tended to be protective (OR 0.78, 95% CI: 0.59–1.03, not statistically significant). In conclusion, a vegan diet tended to be associated with lower, not higher, risk of hypothyroid disease.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847753/?tool=pmcentrez

Endocrine disruption: The phytoestrogens are much weaker than estrogens produced by your body, and they also preferentially bind to the Estrogen Receptor Beta. The ERb is associated with anti-proliferative responses, whereas the other isoform ERa largely drives estrogen-responsive growth.

http://www.ncbi.nlm.nih.gov/pubmed/9751507

http://www.ncbi.nlm.nih.gov/pubmed/17700529

Breast cancer risk: Long-term observational data shows no harm from soy for breast cancer risk or recurrence. The traditional Japanese diet has 25-50 mg isoflavones per day in 2-3 servings of soy and may be protective. E2 and estrogen-responsive tissues do not appear to be affected by soy in human trials. In nearly 10,000 breast cancer survivors, those who ate more soy after diagnosis had a significant 25% reduction in recurrence at 7.4 years post-diagnosis.

http://www.ncbi.nlm.nih.gov/pubmed/24312387

http://www.ncbi.nlm.nih.gov/pubmed/24898224

Prostate cancer risk: There is some evidence for soy and its isoflavones to reduce prostate cancer risk, but the mechanism is unclear. Effects on hormones, prostate specific antigen (PSA), and sex hormone binding globulin (SHBG) protein could not be derived due to limitations of the reviewed data sets. In patients with localized prostate cancer, thyroid hormone and sex hormones were not significantly altered by the genistein treatments, and serum PSA was decreased.

http://www.ncbi.nlm.nih.gov/pubmed/24053483

http://www.ncbi.nlm.nih.gov/pubmed/21714686

Claim #11 – Soy is bad for athletic performance.

T-Nation: “And even if we look strictly at performance, soy protein has been shown to decrease muscular strength, lower testosterone and increase cortisol when consumed post-workout.”

I do not see a citation for this claim, but it appears to be a reference to this study of 10 resistance-trained men. http://www.ncbi.nlm.nih.gov/pubmed/24015701

“This investigation observed lower testosterone responses following supplementation with soy protein in addition to a positive blunted cortisol response with the use of whey protein at some recovery time points. Although sex hormone binding globulin (SHBG) was proposed as a possible mechanism for understanding changes in androgen content, SHBG did not differ between experimental treatments. Importantly, there were no significant differences between groups in changes in estradiol concentrations.”

When this paper’s data are examined, the soy consuming group’s T levels within an hour of exercise were 2-3 nmol/L lower than the non-soy consumers. Both values are still within the normal range of T levels, and the physiological relevance of such a small change is not well explained. Dr. Stu Phillips questions the role of transient increases in hormones in hypertrophy responses, and lists the following factors in order of importance for muscle hypertrophy: exogenous T (steroid usage, greatest effect) > muscle fiber recruitment and exercise volume > protein source and timing > exercise load and local androgen metabolism > exercise-induced hormones and growth hormone (least effect). http://www.ncbi.nlm.nih.gov/pubmed/20959702

This review from Brad Schoenfeld covers that various hormones implicated in hypertrophy responses, and concludes that effects are likely modest for endogenous hormones with caveats for training experience and genetic variability between subjects.

http://www.ncbi.nlm.nih.gov/pubmed/23442269

Soy does not reduce strength in new exercisers compared to whey or placebo across age groups from 18 to 70 years old in either men or women. Body composition improvements were noted in several of these studies.

http://www.ncbi.nlm.nih.gov/pubmed/22066824

http://www.ncbi.nlm.nih.gov/pubmed/12197993

http://www.ncbi.nlm.nih.gov/pubmed/23488651

http://www.ncbi.nlm.nih.gov/pubmed/16948480

http://www.ncbi.nlm.nih.gov/pubmed/22876725

66 Romanian Olympians in endurance sports increased lean body mass and strength with additional soy supplement: http://www.ncbi.nlm.nih.gov/pubmed/1306084

You can read an exchange with Dr. Stu Phillips about using soy as a protein supplement in training HERE. We discussed if soy could produce a similar response in muscle protein synthesis if leucine content was controlled for in studies, as it had not been controlled for in earlier studies, and he said that soy could work as a protein supplement if sufficient leucine content maximizes MPS. He also pointed out that more calories would need to be consumed to hit the leucine threshold, but Dr. Jose Antonio’s protein over-feeding study suggests that excess calories from protein are unlikely to contribute to body fat gain.

https://www.facebook.com/groups/VeganNutrition/843022429126666/

In pre- and post-menopausal women, soy isoflavones do not alter cortisol levels.

http://www.ncbi.nlm.nih.gov/pubmed/9920082

http://www.ncbi.nlm.nih.gov/pubmed/10522983

http://www.ncbi.nlm.nih.gov/pubmed/11756072

In young adults, soy supplementation did not affect cortisol in students undergoing a moderate endurance exercise protocol.

http://www.ncbi.nlm.nih.gov/pubmed/22876725

Claim #12 – The brain needs saturated fat and cholesterol, and lower levels of these lipids are associated with cognitive impairment, Alzheimer’s, and Parkinson’s.

T-Nation mentions that breast milk contains high amounts of saturated fat to nourish our developing brains, and that brain support from cholesterol is one reason why cholesterol levels increase as we age.

In general, higher saturated and trans fat intakes are associated with reduced cognition. This appears to be related to the hippocampus, and not the frontal cortex.

http://www.ncbi.nlm.nih.gov/pubmed/23291218

http://www.ncbi.nlm.nih.gov/pubmed/22023100

http://www.ncbi.nlm.nih.gov/pubmed/21167850

Saturated fats may increase neurodegenerative responses to dietary copper.

http://www.ncbi.nlm.nih.gov/pubmed/16908733

There is evidence that high fat diets are associated with inflammation in the brain, including in the hypothalamus before weight gain is apparent.

http://diabetes.diabetesjournals.org/content/62/8/2629.full

http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0005045

http://www.ncbi.nlm.nih.gov/pubmed/24075847 (in rodents)

Studies in rodents suggest the mechanism is a transfer of inflammatory signals from the gut to the hypothalamus through the nodose ganglion.

http://www.sciencedirect.com/science/article/pii/S0006291X15303272

We are unable to do experiments where we try to give people neurodegenerative diseases, but observational studies and rodent models suggest that dietary fat, particularly saturated and trans fat, are associated with the development of neurodegenerative diseases.

Review of human observational studies:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4107296/

http://www.ncbi.nlm.nih.gov/pubmed/24916582

Insulin resistance is associated with Alzheimer’s. See above for discussion on various SFA and diabetes.

http://www.ncbi.nlm.nih.gov/pubmed/26159189

http://www.ncbi.nlm.nih.gov/pubmed/26003667

http://www.ncbi.nlm.nih.gov/pubmed/24998414

http://www.ncbi.nlm.nih.gov/pubmed/23790682

It appears that high fat diet promotes Alzheimer’s, potentially independently of tau and amyloid protein pathways. (These are the proteins that form tangles/clusters in AD brains that can cause symptoms.)

http://www.ncbi.nlm.nih.gov/pubmed/24269929

http://www.ncbi.nlm.nih.gov/pubmed/24630364

http://www.ncbi.nlm.nih.gov/pubmed/24205258

Claim #13: Consumption of animal foods increased human brain size.

T-Nation: “The incorporation of increasingly greater amounts of animal products into the diet was essential in the development of the large human brain.” – Aiello and Wheeler, Current Anthropology, 1995

While the inclusion of calorie-rich animal foods likely did contribute to development of the human brain, there are other contributors as well, including cooking and social interaction.

Cooking increases the available calorie content of food, and also makes some nutrients more bioavailability. The combination of modest amounts of animal foods and cooking (both plants and meat) produced a shift in calorie intake to support brain development.

“Mechanisms contributing to energy being gained from cooking include increased digestibility of starch and protein, reduced costs of digestion for cooked versus raw meat, and reduced energetic costs of detoxification and defence against pathogens. If cooking consistently improves the energetic value of foods through such mechanisms, its evolutionary impact depends partly on the relative energetic benefits of non-thermal processing methods used prior to cooking.”

http://www.ncbi.nlm.nih.gov/pubmed/19732938

“This limitation was probably overcome in Homo erectus with the shift to a cooked diet. Absent the requirement to spend most available hours of the day feeding, the combination of newly freed time and a large number of brain neurons affordable on a cooked diet may thus have been a major positive driving force to the rapid increased in brain size in human evolution.”

http://www.ncbi.nlm.nih.gov/pubmed/23090991

“These changes in diet and foraging behavior did not turn our hominid ancestors into carnivores; however, the addition of modest amounts of meat to the diet combined with the sharing of resources that is typical of hunter-gatherer groups would have significantly increased the quality and stability of hominid diets. These changes in dietary quality appear to have been critical in promoting the rapid brain evolution seen with the evolution of H. erectus. While dietary change alone cannot explain the evolution of large hominid brains, a sufficiently high quality diet was probably necessary for supporting the increased energy demands of larger brains.”

http://www.ncbi.nlm.nih.gov/pubmed/14527625

Processing social cues and interacting with others may have also helped drive human brain development, as time was available for more social interactions in early humans who were not foraging all day.

“In the spirit of these objectives, we present here a new theoretical proposal, the Inferential Brain Hypothesis, whereby the human brain is thought to be characterized by a shift from perceptual processing to inferential computation, particularly within the social realm. This shift is believed to be a driving force for the evolution of the large human cortex.”

http://www.ncbi.nlm.nih.gov/pubmed/22459075

“Thus, humans have evolved towards increased collaboration and mutual support. This kind of evolutionary pressure may have provided the basis for the development of the human brain with its unique functions.”

http://www.ncbi.nlm.nih.gov/pubmed/23414685

“Focusing on recent research from nonhuman primates, we describe how the primate brain might implement social functions by coopting and extending preexisting mechanisms that previously supported nonsocial functions. This approach reveals that highly specialized mechanisms have evolved to decipher the immediate social context, and parallel circuits have evolved to translate social perceptual signals and nonsocial perceptual signals into partially integrated social and nonsocial motivational signals, which together inform general-purpose mechanisms that command behavior.”

http://www.ncbi.nlm.nih.gov/pubmed/23754410

Claim #14: The myth is that meatless diets contain essential nutrients.

T-Nation lists deficiencies in B12, omega 3 fats, and iron in vegetarians and vegans.

(a) B12 deficiency – “Research from 2003 in the American Journal of Clinical Nutrition determined that B12 deficiency in vegetarians and vegans is as high as 70-80%.”

The study is here: http://ajcn.nutrition.org/content/78/1/131.long

An editorial on the study is here: http://ajcn.nutrition.org/content/78/1/3.short

The Hermann et al study is very small with only 29 vegans included, but older studies show similar trends as discussed in the editorial. It’s worth noting that the Hermann study abstract says, “In subjects who did not consume vitamins, low holotranscobalamin II (< 35 pmol/L) was found in 11% of the omnivores, 77% of the LV-LOV group, and 92% of the vegans.” It is well known that plant foods are not good sources of vitamin B-12. To examine non-users of supplements is likely not representative of all vegans. In the methods section, “Seventeen vegans (59%) and 13 LV-LOV subjects (20%) supplemented their diet with B vitamins. Not all vitamin users provided details about the dose and the frequency of vitamins used.” Of the 29 vegans, 17 were using B vitamin supplements, whereas 11 of the 12 non-users had B12 deficiency. As the editorial points out, there is cause for concern about people eating mostly vegetarian diets due to poverty, as this population likely does not have access to supplements or fortified foods.

In the general population, vitamin B12 deficiency has been estimated to affect between 1.5 and 15% of the population. The Framingham study found people using B12 supplements or consuming 4+ servings of fortified foods were much less likely to have vitamin B12 deficiency. Vegetarians are ~5% of the population, whereas vegans are ~1% of the population. Since plant foods do not contain B12 (unless fortified), supplementation is recommended for vegetarians.

http://www.ncbi.nlm.nih.gov/pubmed/16034940?dopt=Abstract

http://www.ncbi.nlm.nih.gov/pubmed/16585128?dopt=Abstract

http://www.ncbi.nlm.nih.gov/pubmed/8875026?dopt=Abstract

http://www.ncbi.nlm.nih.gov/pubmed/10648266

(b) Omega-3 fats deficiency:

– T-Nation: “Short-chain omega-3’s (ALA), which have an extremely weak conversion rate (2-10%) to the long-chain essential fatty acids usable by humans (EPA and DHA). There’s some evidence suggesting that attempting to raise blood DHA status with strictly an ALA omega-3 source is nearly impossible.”

Yes, the conversion of ALA to DHA and EPA is very inefficient. “There are small increases in EPA after ALA supplementation (r2 = 0.49, P = 0.052); however, plasma phospholipid DHA concentrations do not detectably increase after ALA supplementation with doses up to 14 g/d.”

http://ajcn.nutrition.org/content/83/6/S1467 (see Figure 3)

However, ~10% of DHA can be converted to EPA in humans. When 1.62 g DHA was provided per day for 6 weeks, a significant increase in EPA levels was observed.

http://www.ncbi.nlm.nih.gov/pubmed/9076673

Therefore, direct supplement of DHA and possibly EPA is recommended. Microalgae oil appears to be a viable omega-3 source for humans.

“Ten key papers published over the last 10 years were identified with seven intervention studies reporting that ALA from nut and seed oils was not converted to DHA at all. Three studies showed that ingestion of micro-algae oil led to significant increases in blood erythrocyte and plasma DHA.”

http://www.ncbi.nlm.nih.gov/pubmed/24261532

“Oil from the micro-algae Nannochloropsis oculata contains a significant amount of EPA conjugated to phospholipids and glycolipids and no DHA… The concentration of EPA was higher with algal oil than with krill oil at several time points… This study in healthy young men given a single dose of oil indicates that the polar-lipid rich oil from the algae Nannochloropis oculata is a good source of EPA in humans.”

http://www.ncbi.nlm.nih.gov/pubmed/23855409

2.14 g algae-derived DHA per day for 6 weeks increased DHA and EPA in postmenopausal vegetarian women. http://www.ncbi.nlm.nih.gov/pubmed/16278686

1.62 g algae-derived DHA per day for 6 weeks increased DHA and EPA in vegetarian men and women. “Consumption of DHA capsules increased DHA levels in serum phospholipid by 246% (from 2.4 to 8.3 g/100 g fatty acids) and in platelet phospholipid by 225% (from 1.2 to 3.9 g/100 g fatty acids). EPA levels increased in serum phospholipid by 117% (from 0.57 to 1.3 g/100 g fatty acids) and in platelet phospholipid by 176% (0.21 to 0.58 g/100 g fatty acids) via metabolic retroconversion; the estimated extent of DHA retroconversion to EPA was 11.3 and 12.0%, based on the serum and platelet analyses, respectively.”

http://www.ncbi.nlm.nih.gov/pubmed/9001371

“Plasma phospholipid DHA concentrations are highly sensitive to dietary intake of this fatty acid at doses up to ≈ 2 g/d. At doses above this amount, plasma DHA concentrations approach saturation and increase only incrementally. DHA supplementation also results in an apparent linear increase in EPA concentrations, presumably through retroconversion, with EPA concentrations increasing by ≈0.4 g/100 g fatty acid for each 1 g of DHA intake.” http://ajcn.nutrition.org/content/83/6/S1467 (see Figure 4)

The EFSA lists a combined intake of EPA and DHA at 5 g/day, EPA at 1.8 g/day, and DHA at 1 g/day as safe. http://www.efsa.europa.eu/en/efsajournal/pub/2815

(c) T-Nation: “a lack of saturated fat, iron and zinc also appear to inhibit our ability to convert ALA.”

I was unable to find evidence for the lack of saturated fat and zinc claims, but iron may reduce the activity of the enzyme that helps convert ALA.

The conversion of ALA to DHA requires an enzyme known as delta-6-desaturase (also known as FADS2) to catalyze the first step of the reaction.

http://www.ncbi.nlm.nih.gov/pubmed/8386433

Gene expression of FADS2 in adipose (fat) tissue does not appear to be affected by SFA intake in humans when 9% or 15% of fat intake was SFA.

http://ajcn.nutrition.org/content/86/3/759.long#sec-2

I was unable to find data on low zinc affecting omega-3 production in humans, but the enzyme may be influenced by zinc status when producing other molecules. “Other factors important in regulating D6D and the conversion of GLA to PGE1 are zinc, pyridoxine, ascorbic acid, the pineal hormone, melatonin, and possibly vitamin B3.”

http://www.ncbi.nlm.nih.gov/pubmed/6270521

Iron is part of the enzyme complex, and low iron and B vitamin levels may affect enzymatic activity.

“Iron is present in end proteins of the delta6-desaturase enzyme complex, and vitamin B6 deficiency can affect the transmethylation reaction of proteins… In groups of subjects with low vitamin B6 and low iron levels, delta6-desaturase activity together with delta5-desaturase activity (conversion of alpha-linolenic/18:3,n-3/ into eicosapentaenoic acid/20:5,n-3/) as well as the conversion index of docosahexaenoic acid formation (22:6,n-3) from 22:5,n-3 (second delta6-desaturase activity) were significantly reduced. The inhibition effect on fatty acid synthesis was more pronounced in subjects with low iron levels than in those with low vitamin B6 levels.”

http://www.ncbi.nlm.nih.gov/pubmed/14988642

(d) T-Nation: “Compared to omnivores, vegetarians have approximately 30% less EPA and DHA and vegans 50-60% less.”

http://ajcn.nutrition.org/content/82/2/327.full.pdf+html

In a cohort from the EPIC-Oxford study, the vegetarians and vegans did have lower EPA and DHA levels in the serum. They also have lower levels of saturated fats. The authors note that time on the diet did not affect levels, so endogenous production is likely low but stable. The inverse correlation between LA (found in vegetable oils) and DHA and EPA is worth noting, and the authors suggest reduction of LA-rich oils might help vegetarians/vegans boost DHA and EPA with this caveat: “However, our analyses are based on proportions of plasma fatty acids rather than absolute amounts of fatty acids, and the results should therefore be interpreted with caution.”

Claim #15: Anti-nutrients reduce absorption of important minerals.

T-Nation: Phytates reduce Mg, Ca, Fe, Zn, B12; they are only 50% removed from an 18 hr soak; and none are removed from soy. Lectins promote inflammation in the gut and cannot be destroyed by heat.

Phytates are a stored form of phosphorous in plants. They can interfere with mineral absorption in the GI tract. In reading several studies, the concern over phytates appears to be for people in the developing world, where they need to optimize mineral uptake on a limited calorie intake. As example is here: https://www.mja.com.au/journal/2013/199/4/zinc-and-vegetarian-diets

Magnesium: In one study with phytic acid-free white bread, the investigators added two different amounts of phytic acid to the bread at levels similar to brown bread and whole wheat bread to see if radiolabeled Mg was absorbed. They found that phytic acid did reduce the Mg absorption in their study, more for whole wheat than brown bread. They noted, “However, the absolute amounts of magnesium absorbed from whole-meal and brown bread can be expected to be higher than those from white bread because of the 2-3-fold higher magnesium content, unless other components in whole-meal and brown bread (such as dietary fiber, minerals, and trace elements) influence magnesium absorption or modify to a great extent the effect of phytic acid on magnesium absorption.” This suggests that the higher total Mg content in wheat breads would compensate for the loss of some Mg by phytates.

www.ncbi.nlm.nih.gov/pubmed/14985216

Calcium: A similar study with radiolabeled Ca and sodium phytate added to phytate-free white bread found that higher concentrations of phytate reduced Ca and Zn absorption. They noted, “The results of this study cannot be extrapolated directly to the effect of native phytate in cereals and legumes.”

http://www.ncbi.nlm.nih.gov/pubmed/16632176

Iron: Habitual high phytate consumption reduces the impact on non-heme (plant) iron absorption, and combining vitamin C with iron sources containing phytates improve Fe absorption more than phytase enzyme treatment.

http://www.ncbi.nlm.nih.gov/pubmed/26041677

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2266880/

Zinc: As mentioned above, the addition of phytate can reduce Zn absorption. Another study showed only 5% decrease in zinc in the bloodstream, but this was still within the normal range. This study said the inclusion of whole grains and beans can help lacto-ovo-vegetarians meet zinc intakes and maintain zinc balance.

http://www.ncbi.nlm.nih.gov/pubmed/9497185

Vitamin B12: I couldn’t find anything on pubmed for phytates reducing B12 absorption. The absorption of B12 is limited by the amount of intrinsic factor protein available to carry B12 into the intestines, and also stomach acid to release B12 from food. High dose supplements of B12 are not efficiently absorbed due to limiting intrinsic factor protein.

Phytate content of foods can be reduced by soaking, sprouting, and other methods. T-Nation said 50% of less of phytate could be removed from food. For lupin seeds, the debittering processed removed up to 71% of phytic acid. Soaking in warm water and longer soak times were the most effective methods. Rice had a 77% reduction with warm water soaking and extrusion. Chickpea bulgur soaked up to 12 hours reduced phytic acid up to 55%.

http://www.ncbi.nlm.nih.gov/pubmed/26396330

http://www.ncbi.nlm.nih.gov/pubmed/25666413

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4062680/

Phytates can be removed from soy. Soymilk has a very low phytate content, so fortification with calcium is a viable strategy. Sprouting reduced phytic acid by 55-60% in soybeans used for soymilk and tofu production. Soy foods with moderate phytate concentrations, as well as low oxalate concentrations, may be beneficial for kidney stone patients or persons at risk of developing kidney stones.

http://www.ncbi.nlm.nih.gov/pubmed/16177199

http://www.ncbi.nlm.nih.gov/pubmed/24803698

http://www.ncbi.nlm.nih.gov/pubmed/15998131

T-Nation claimed lectins are inflammatory by binding gut cells, and are resistant to heating. I could not find anything on Pubmed to support this claim. Consumption of whole grains and low glycemic index foods is associated with reduced inflammation in women with Type 2 diabetes. General dietary patterns that include whole grains are associated with positive health outcomes, and lower incidence of diseases associated with inflammation. In dwarf elder berries, 5 minutes of boiling water bath sensitized lectins to digestion by pepsin enzyme.

http://www.ncbi.nlm.nih.gov/pubmed/16443861

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705319/ (see section 6 for inflammation)

http://www.ncbi.nlm.nih.gov/pubmed/24793353

About The AuthorChristine

Christine Crumbley has a PhD in molecular biology. Her research interests include nuclear receptors, regulatory mechanisms of transcription, metabolism, and circadian rhythms. As a scientist and an ethical vegan, she feels she is uniquely positioned to discuss health-related topics. She helps moderate an evidence-based vegan nutrition and fitness group on facebook (VBBN), and enjoys researching members’ questions to produce new content for the site. Her hobbies include powerlifting, Olympic lifting, Crossfit, baking, and talking to cats. Her favorite inspirational quote is, “Use your strength to help others.”

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