Being that this is a comprehensive article, there is going to be a lot of references to studies. I will be doing this because a lot of my opinions are based in science.
I wanted to create this article to answer any and all questions you might have about veganism and health.
So take this as an invitation to the logic in my beliefs, I hope you enjoy the read!
Without any further adieu, here is the table of contents.
Table of Contents
- Lipid Profiles
- What exactly are Lipoproteins?
- Effects of Lipoproteins and Their Levels
- What Does This Have to do With A Vegan Diet Though?
- Dietary Effects on Lipids
- Further analysis of these findings
- Dietary Fat Composition
- Dyslipidemia and Saturated Fat
- What The Authorities Have To Say About Saturated Fat
- My Stance On Vegetable Oils
- LDL Cholesterol
- Animal Products, Cholesterol and Neurodegenerative diseases.
- Here Is Where We Have To Do Some Detective Work
- Why Triglycerides Associate with Cancer and CVD
- Nitrates and Nitrates – Formation of NOCs
- Heme Iron
- HCAs and POHs
- Effects of HCAs and POHs
- Insulin-like Growth Factor-1
Mostly when you hear people in the debate on eating animal products, veganism, and health, the topic of cholesterol and saturated fat arise. Not to say that these people are wrong in discussing this, but limiting the discussion to those alone is a large simplification.
When looking at cholesterol, it comprises of many subgroups. These include:
- LDL size
- HDL size
- Apolipoproteins (ApoA1, ApoB, etc.)
Working from the bottom up, I want to start with the Apolipoproteins because it seems to have lack of exposure in these discussions.
What Exactly are Apolipoproteins?
Apolipoproteins are proteins that bind lipids such as fat and cholesterol and transport it through your bloodstream. a common misconception is that cholesterol floats around in your blood on its own. However, cholesterol is just one of many things that apolipoproteins carry including but not limited to triglycerides.
ApoA1, ApoB and the ApoB/ApoA1 ratios are important because they are likely the strongest predictor of Cardiovascular Disease (CVD).
ApoA1 is the main protein component in HDL particles in plasma. It is responsible for helping clear fats and cholesterol including macrophages (white blood cells) within the walls of arteries which have become overloaded with ingested fats from oxidized LDL particles.
There are two different forms of ApoB. There is ApoB48 and ApoB100. For the sake of this article, when I mention ApoB, I am referring to ApoB100. The liver synthesizes this and is relevant to atherosclerosis.
Atherosclerosis is known as the building up of plaque and hardening of arteries. Therefore, atherogenic is process of atherosclerosis
ApoB is the main apolipoprotein in a few atherogenic particles, including LDL particles. It’s function is not entirely understood at this current point in time. However, it is known to be the primary organizing protein for these particles. There is also a lot of evidence that ApoB levels are superior indicators of CVD, heart disease, stroke, and other complications.
Only one ApoB molecule is present in an LDL particle. This means that ApoB measurements will yield an accurate LDL particle number measurement.
Effects of Apolipoproteins and Their Levels
According to this study, “high serum APOA1 levels significantly associated with better cancer-specific survival (CSS) … and Overall Survival (OS) … Similarly, high APOB levels associated with better CSS … and low APOB/APOA1 ratio showed association with better CSS … and OS.”
I have left out the numbers, but you can visit the study and see for yourself the magnitude of the associations.
Although, when researching other sources, it seems that having a lower ApoB level is more beneficial, as lower ApoB means there are less LDL Particles circulating in the bloodstream attaching to artery walls.
The optimal range for ApoB 40-125 mg/dL.
So we’ve learned having higher levels of ApoA1 and a lower ratio of ApoB/ApoA1 is ideal.
What Does This Have to do With a Vegan Diet Though?
Well, when we are analyzing level of total cholesterol, low-density cholesterol (LDL), HDL, apolipoprotein B (APOB), apolipoprotein A-1 (APOA1), triglycerides, glucose, haemoglobin A1c, and insulin level in blood, Vegetarians had higher ratios of total cholesterol/HDL, ApoB/ApoA1 ratios, LDL/HDL.
From multivariate linear regression analyses showed lower values of BMI, Total Cholesterol, LDL, ApoB, ApoA1 and insulin. However it is worth noting BMI similarly influences these factors.
It is also worth noting that, according to the materials and methods of the full study, “The subjects in vegetarian group had to be lacto-ovo-vegetarians or vegans for at least last 2 years.” They did not separate vegans from vegetarians.
Due to the fact that dairy has a lot of nutritional similarities to meat, I am guessing the reason that the higher ApoB/ApoA1 ratio is due to consumption of dairy. It is possible that the vegetarians had large amounts of dairy, as they tend to in efforts to make up for lost nutrients. However from this study alone I can not conclude for certain this is the reason.
I believe that a study conducted comparing vegans to omnivors would be optimal for displaying the differences in lipid profiles.
Why, you ask? Well, lets take a look at what this study had to show.
Dietary effects on Lipids
For the following information, it is important to understand a negative association means as one variable increases, the other decreases.
- Alcohol intake, Myristic acid and Folate positively associates with all HDL’s and ApoA1.
- Carbohydrate and iron intake negatively associates with all HDL’s and ApoA1.
- Animal Fat % negatively associates with HDL-C and ApoA1.
- HDL-2 negatively associates with Arachidonic acid, but positively associates with Eicosapentaenoic acid.
- Protein and fiber negatively associates with HDL-3 and Vitamin C positively associates with ApoA1.
There is some information I was not able to find in the study and feel it would be of importance. I was unable to determine if:
- Carbohydrates were separated into different groups based on
- Simple Carbs and refined sugars
- Complex Carbs
- Glycemic index and Glycemic load
- If heme iron was separated from non-heme iron
When searched on google, you can find that refined sugars and simple carbohydrates do in fact raise ApoB levels.
Nonetheless, there remains a lot of valuable information for us from the study and those charts.
Further Analysis of These Findings
From looking at the chart it seems that reducing carbohydrates has a negative-negative effect, thus increasing ApoA1 levels. I believe this would be one reason why this lowers the ApoB/ApoA1 ratio.
This is consisting with these findings stating that “A reduction in the ratio of apolipoprotein B100 to apolipoprotein A1 was observed in the low-carbohydrate compared with the low-fat group (P=0.001).”
This again is consistent with a study that concluded that “A self-selected low-carbohydrate vegan diet, containing increased protein and fat from gluten and soy products, nuts and vegetable oils, had lipid lowering advantages over a high-carbohydrate, low-fat weight loss diet, thus improving heart disease risk factors.”
So, basically, we should all consume less carbohydrates and more fat right? But what kinds of fat are good?
Dietary Fat Composition
When you think of fats, what do you think of?
You probably think of saturated fat first. Things like nuts and oils and butter. Before you go and start lathering this stuff all over your food, remember the charts earlier. They stated Animal Fats had a negative association with ApoA1 levels.
Well that must make vegetable sources of saturated fat okay, right?
Not necessarily. Consuming saturated fat is a risk factor for dyslipidemia which is a risk factor for CVD.
Dyslipidemia and Saturated Fat
Dyslipidemia is the state of having high total cholesterol and/or LDL cholesterol.
Coconut oil contains >80% SAFA. The idea that the medium-chain SAFA in coconut oil metabolizes differently than long-chain SAFA is a mistake. Coconut oil contains approximately 50% lauric acid and 15% myristic acid, both raising LDL and HDL. Scientific data disagrees with the popular belief of coconut oil being a healthy alternative.
It is also worth noting that diets high in coconut oil have been found to be only slightly lower in LDL-C and total cholesterol to those consuming fats from butter.
Another review of observational and intervention studies of partially replacing SAFA with PUFA found convincing evidence of lower blood LDL-C levels and a reduced risk of CVD, especially in men.
This study found that diets that were higher in linoleic acid (LA) decreased total cholesterol by 15% and LDL-C by 22%. This did not largely alter HDL-C after 6 weeks of dietary intervention in 11 healthy middle aged, male subjects. Apolipoprotein B decreased by 37% whereas apolipoprotein A-I increased by 24% in the group of individuals supplemented with this diet.
I found this study from another study that was discussing a dietary intervention of hemp, which is high in LA.
What The Authorities Have To Say About Saturated Fat
Though some is needed, here’s what the American Heart Association has to say in regards to saturated fat:
“Cardiovascular disease (CVD) is the leading global cause of death, accounting for 17.3 million deaths per year, comprising 31.5% of total global deaths in 2013. In 2014, nearly 808,000 people in the United States died of heart disease, stroke, and other CVDs, translating to about 1 of every 3 deaths. Lowering intake of dietary saturated fat and replacing it with monounsaturated and polyunsaturated vegetable oil reduced CVD by about 30%, similar to the reduction achieved by statin treatment.”
The AHA isn’t the only association that suggests limiting dietary saturated fat intake. Others include, but are not limited to:
- World Health Organization
- American Heart Association
- Health Canada
- The US Department of Health and Human Services
- The UK Food Standards Agency
- The Australian Department of Health and Aging
- The Singapore Government Health Promotion Board
- The Indian Government Citizens Health Portal
- The New Zealand Ministry of Health
- The Food and Drugs Board Ghana
- The Republic of Guyana Ministry of Health
- Hong Kong’s Centre for Food Safety
There was also a study conducted on spanish children, that concluded “The growth rate of children does not seem to be affected by the level of saturated fat intake. Furthermore, at the levels of intake observed in this study, diets with less saturated fat are associated with better alimentary, nutritional and plasma lipid profiles.”
My stance on Vegetable Oils
I currently disagree with AHA’s comments on replacing the saturated fat with vegetable oils. Even if it is polyunsaturated vegetable oils. Let me explain why.
I don’t want to advocate vegetable oils as they raise serum triglyceride levels. They cause acute endothelial (cells that line the inner blood vessels) impairment, decreasing flow-mediated vasodilation by 32.1%.
What that basically means is that it impairs artery function by reducing the dilation of your arteries. Scientists also believe that endothelial dysfunction links with atherosclerosis.
Due to my findings here, my suggestion is to avoid oils and replace saturated fats with whole foods that are polyunsaturated fats.
Cholesterol is a large, if not the leading cause of atherosclerosis. Some studies tell you there is no relationship between cholesterol and heart disease. Others also say that adding cholesterol to your diet don’taffect your serum cholesterol.
Understanding that these studies are either flawed by design (intentionally or unintentionally) is important. Members of boards whom the true results would be a conflict of interest (meat, dairy, egg, pharmaceutical, etc.) may also fund these studies.
With that out of the way, lets discuss cholesterol.
Remember what we learned earlier? About how cholesterol bonds to whats called Lipoproteins and these particles are what flow through our blood? Good.
We measure LDL in two ways. Concentration, and number of particles (LDL-C and LDL-P respectively). Numerous studies show that lowering LDL-C using statins, a residual risk for CVD remains.
This causes confusion (as the whole health and fitness industry tends to be). But, a study was conducted on a group of Japanese men who were free of clinical CVD by a group of scientists performing cross-sectional associations between lipid profiles and carotid intima-media thickness (cIMT) and coronary artery calcification (CAC).
What they found LDL-P significantly associates with cIMT and maintains this association after adjustments for LDL-C and other lipid measures.
Not surprisingly, Higher LDL-P associates with a significantly higher odds ratio of CAC and further adjustment for LDL-C did not affect this relationship. In contrast, the LDL-C association with CAC was no longer significant after adjustment for LDL-P.
So the take away from this, is in order to assess CVD risk in terms of cholesterol, LDL-P measurements are a significantly more accurate marker. Some remedies according to this study, include “Interventions that will lower LDL-C more than LDL-P include statins, estrogen replacement therapy, some antiretrovirals, and a low-fat, high-carbohydrate diet. Interventions that lower LDL-P more than LDL-C include fibrates, niacin, pioglitazone, omega-3 fatty acids, exercise, Mediterranean and low-carbohydrate diets.”
Not convinced? Heres a few more studies that illustrate the significance of LDL-P over LDL-C for CVD prediction.
Animal Products, Cholesterol, and Neurodegenerative Diseases.
Now when I first began my research for this article, I assumed that high levels of cholesterol cause alzheimers. Surprisingly, this is not true.
Circulating cholesterol in the blood can not get into the brain due to the blood brain barrier. The brain regulates its own cholesterol.
However Significant changes in brain cholesterol metabolism have also been observed in other conditions different from Alzheimers.
these include Huntington’s disease, Parkinson’s, depression, amyotrophic lateral sclerosis, stroke, head trauma, and also normal aging.
So Here Is Where We Have To Do Some Detective Work
If you notice, I mention changes in brain cholesterol metabolism associates with stroke. Well, Blood pressure is one of, if not the most prominent factor in stroke risk.
Blood Pressure has been strongly associated with Coronary Heart Disease (CHD). Finally, opting for a plant based diet has shown decreased blood pressure and lower rates of hypertension. So it is safe to conclude that consuming animal products raise blood pressure.
So to summarize, Cholesterol in the blood does not directly cause alzheimers.
However, consuming animal products raises blood pressure, which raises stroke risk directly and indirectly through CHD/CVD risk. Through higher blood pressure, damaged blood vessels and even strokes and CVD events, cholesterol metabolism in the brain can alter negatively.
Thus, consuming animal products will indirectly cause neurodegenerative diseases.
Just to really drive this point home, as stated before, we know animal products have high amounts of saturated fat.
With that in mind, you can look at this study which shows a 32% reduction of stroke events in those who replacing part of their SFA with PUFA.
There was 41 stroke events in >1700 participants.
I also was reading a meta analysis of SAFA intake and CHD which stated there was no correlation between the two. However in the footnotes, they mentioned this:
While this paper was in revision, re-analyses of these cohorts were unable to verify this finding. In contrast, a positive association between SAFA intake and CHD risk was observed.
Triglycerides are main parts of body fat in animals and humans but are also parts of vegetable fats. Their purpose is largely to transfer adipose fat and blood glucose from the liver.
High levels of triglycerides in the bloodstream associates with atherosclerosis and stroke.
A study conducted on Triglycerides and CVD events yield the following results.
The risks of CVDs and all-cause mortality were increased by 15.0% and 9.0% in the borderline hypertriglyceridemia group, and 25% and 20% in the hypertriglyceridemia group, respectively. Overall, the risks of CVDs and all-cause death were increased by 13% and 12% per 1-mmol/L increase in TG level…
Prospective studies have found that elevated TG levels increases the risk of non-CVDs mortality . A collaborative study of metabolic syndrome and cancer (Me-Can) involving 514,097 participants with a 13.4-year follow-up, demonstrated a positive association between serum TG and risk of cancer overall and at several sites.
Why Triglycerides Associate With Cancer and CVD.
According to the study, triglycerides associate with atherogenic remnant particles. TG rich Lipoproteins and their remnants promote inflammation among other things.
hypertriglycerideia associates with oxidative stress and reactive oxygen species. ROS directly influence rapid increases in cell numbers, contributing to the multistage carcinogenesis process.
This oxidative stress in fat appears to be an important pathogenic pathway in metabolic syndrome. Also, hypertriglyceridemia associates with increased cortisol levels.
In conclusion, elevated blood TG levels associate with a greater risk of both CVDs and all-cause mortality. The findings of this meta-analysis suggest that controlling TG can help to prevent CVDs and other causes of death.
Nitrites and nitrates – Formation of NOCs
Companies often add Nitrite to processed meat as an antibacterial agent against Clostridium botulinum. It also produces the characteristic red-pink color of cured meats. Nitrates and nitrites found in processed meats and smoked cheeses can lead to the formation of N-Nitroso compounds (NOCs).
Nitrites and nitrogen oxides reacting with secondary amines and N-alkylamides produce NOCs, a process that can happen within tissues and organs.
Nitrates are abundant in certain fruits and vegetables. This might make you think that veggies and fruit will also cause cancer right?
Well, you’d be wrong. The nitrates in fruits and veggies produce nitric oxide. This relaxes blood vessels, and the vitamin C prevents the production of nitrosamines.
In the NIH-AARP study, nitrate and nitrites from processed meats positively associate with gastric, esophageal, bladder, pancreatic, thyroid (in men only), advanced prostate, and ovarian cancer, as well as with chronic liver disease mortality, but not heptocellular carcinoma, glioma, or NHL.
NOCs form, however, by other dietary factors as well.
Heme iron, of which red meats are a rich source, can act as a catalyst in the formation of NOCs in the gut. There is also evidence to suggest that heme iron increases cell proliferation in the mucosa.
Recently, the NCI has developed a heme iron database. This bases measured values from meat samples cooked by different methods and to varying doneness levels.
In the NIH-AARP study, individuals in the highest category of heme iron intake also had an increased risk of cancers of the lung and prostate, as well as an increased risk of chronic liver disease mortality, but not hepatocellular carcinoma, NHL or breast cancer.
Heme iron absorbs significantly more effectively than iron found in vegetable sources. However there are a lot of bad associations with heme iron.
This study showed that men with a normal weight who consumed high amounts of heme iron had increased risk of stroke. Those who consume higher amounts of heme iron also have a 31% higher chance of CHD, and a higher risk of colorectal cancer.
HCAS and PAHs
HCAs stand for Heterocyclic amine. These amines, in terms of cooking, are carcinogenic.
PAHs stand for Polycyclic Aromatic Hydrocarbons. These are abundant in the universe and are considered to make up a large portion of the carbon. PAHs are also found in coal and tar.
Depending time and temperature when cooking, HCAs and PAHs form. Higher amounts of these compounds manifest with higher temperature and longer time.
HCAs form from the reaction between creatine or creatinine, amino acids, and sugars found in muscle meats at high cooking temperatures.
as of 2007, there were 17 identified HCAs formed during the meat cooking process. In 1993 the International Agency for Research on Cancer concluded that the evidence from animal studies was sufficient to claim two HCAs are carcinogenic: (MeIQx) and (PhIP).
Effects of HCAs and PAHs
PhIP is the most abundant HCA detected in the human diet followed by MeIQx and (DiMeIQx). The EPA designates 7 PAH compounds as probable human carcinogens. This includes benzo(a)pyrene, which is often used as a surrogate for total PAH exposure.
Colorectal adenomas link to PhIP intake in the PLCO trial, but not colorectal cancer in the NIH-AARP study. However, these compounds may largely correlate and it may not be possible to seperate their effects.
Diets high in grilled and barbecued meat, as well as breads, cereals, and grains make up most of your PAH exposure. In a control population of men and women at the National Naval Medical Center, Bread/cereal/grains and grilled/barbecued meat contributed 29% and 21% respectively to average daily intakes of benzo(a)pyrene.
Eating meat increases benzo(a)pyrene. Increased Benzo(a)pyrene intake raises colorectal adenoma occurrences. high Benzo(a)pyrene intake also raises occurrences of kidney and prostate cancer.
MeIQx intake increases levels of lung and pancreatic cancer in the NIH-AARP study and PLCO Trial. DiMeIQx consumption increases pancreatic and gastic cardia cancer.
It is worth mentioning both MeIQx and DiMeIQx deacrease risk of chronic lymphocytic leukemia and small lymphocytic lymphoma. PhIP also increase risk of renal cell carcinoma.
One of many things included in milk is estrone and estradiol.
These can be metabolized, creating whats called catechol estrogens.
From here, the catechol estrogens can change into whats called semiquinones or quinones.
In a series of complex processes, these metabolites associate with estrogen-linked cancers.
This study showed that these metabolites can act as tumour initiatiors in our tissues and organs.
The main source of animal-derived estrogens (60–70%) in the human diet is milk and dairy products. The distribution of estrogens especially 17β-oestradiol in fat or non-fat parts of milk still is controversial.
However, this study discovered there are no differences in 17β-oestradiol between organic and non-organic milk.
When cows were inseminated, it was found that concentrations of estrogens increased about 100 days after and remained elevated during the pregnancy. In fact, the levels of estrogens in the third trimester was more than 27 times higher than those in the first trimester.
This study looking at steroid hormones in cow’s and their milk concluded that Not only progesterone but also pregnenolone, androstenedione and estrone increase with the fat content.
Bovine feed regularly include phytoestrogens, including isoflavones. This brings concern as to if it travels up the food chain to humans.
Since phytoestrogens interact with alpha and beta oestrogen receptors, some believe they are endocrine disruptors. According to this study, isoflavanoids found in soybean products and other plants are changed to hormone-like compounds with estrogenic activity. Cows milk and breast milk also contain phytoestrogens.
Sounds scary right? Fear not. If you click the link and look at the study, they mention plant isoflavones along with possibly lignans from berries and nuts have strong natural anti-cancer properties.
Estrone and 17-beta estradiol however aren’t just in milk and milk products, they are also in the tissues of these animals.
Since almost all animal products contain 17 beta-estradiol and its metabolites, it is unavoidable in diets that contain animal products.
Large consumption of estrone has been linked to obesity and weight gain. The absorption of 17 beta estradiol and oestrone may be low, but prepubertal children have higher sensitivities to the residues in animal products. Claiming the amount of residues of these hormones being safe to consumers is not agreed upon. The methods of analyzing levels were conducted in the 1980’s when technology was less effective and animals were also treated differently than they are now.
Building further on this, Japanese men saw a 25-fold increase in not only prostate cancer, but death from it with an increase in milk, meat and egg consumption. Testicular cancer rates also increased largely.
Insulin like Growth Factor-1
Mainly the mammary gland and the liver produce IGF-1, insulin-like growth factor-1. The bioavalability of IGF-1 in milk is not entirely clear, but is definitely not null.
IGF-1 plays an important role in a few metabolic processes. Some include amino acid uptake, xellular glucose metabolism, lipogenesis, and more. However, It has been found the high levels of IGF-1 and insulin in humans promotes multiple different kinds of cancer.
I can not advocate a vegan diet enough.
Here are some of the leading causes of death in 2017 according to the CDC.
- Heart disease: 633,842
- Cancer: 595,930
- Stroke (cerebrovascular diseases): 140,323
- Diabetes: 79,535
It is my hope with this article to spread awareness of the benefits of a vegan diet and hopefully prolong not only peoples lives but their loved one’s lives as well. Don’t let yourself be a part of those numbers.
I plan to write more articles on different things surrounding vegan diets. Some of these will include optimizing testosterone, managing weight, and more. Make sure to visit back for more articles if this interested you!
What did you find most surprising?
What is your favourite part of this article?
Did i miss something, or is there something you want me to discuss?
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