20 June 2026Cardiovascular, Diabetes and Obesity, Inflammatory Bowel Disease, Kidney, Whole Food Plant Based Diets, Wise Nutrition Coaching

The Myth of Good and Bad Cholesterol

The Victor Change Institute recommendations for lipids are: ¹

HDL (“good cholesterol”): 0.9–2.1 mmol/L (35-80 mg/dL)
LDL (“bad cholesterol”): 1.7-3.5 mmol/L (65-135 mg/dL)
Triglycerides: 0.5–1.7 mmol/L (45-150 mg/dL)
Lipoprotein (a): <= 0.8 nmol/L (30 mg/dL)

Their conclusions include:

One in twelve (8.4% or 2.1 million) people had self-reported high cholesterol in 2022.
The prevalence of high cholesterol has increased since 2011–12 (6.8%).
Almost three in ten (29.0%) people aged 75 years and over had high cholesterol.

Harvad Health states that blood indicator goals are: ²

HDL (“good cholesterol”): >= 1 mmol/L (40 mg/dL)
LDL (“bad cholesterol”): < 1.8 mmol/L (< 70 mg/dL)
Triglycerides: < 1.7 mmol/L (< 150 mg/dL)
Lipoprotein (a): 0.75 mmol/L (< 30 mg/dL)

Harvad Health are include:

having enough “good cholesterol” (high density lipoprotein or HDL).
There is no consensus on the best diet. The most effective diet to lower total and LDL cholesterol is a vegetarian diet. However, this is not an easy diet to follow.

The claim that a vegetarian [vegan] diet is not an easy diet to follow is very subjective.

The Physicans Committee for Responsible Medicine produced a Vegan Starter KitOpens in a new window which is an excellent and gentle guide to shopping, preparing, eating as well as socialising on a healthy, animal-free diet.

The foods are low in saturated fat, free of cholesterol, and packed with vitamins, minerals, phytochemicals and fiber. People who eat a plant-based diet substanially lower their risk for heart disease, type 2 diabetes, obesity and many other health conditions.

These recommendations are significantly different to those of Dr. William Roberts. ³

William Roberts is a leading cardiovascular pathologist. He was the Editor-in-Chief editor of the American Journal of Cardiology from 1982 to 2022 (40 years). He has published over 1,500 articles. Roberts served as the first head of the pathology service at the National Heart, Lung, and Blood Institute at the National Institutes of Health from 1964 to 1993. He has been located at Baylor Heart and Vascular Institute and Baylor University Medical Center in Dallas, Texas since 1993. He has been advocating a whole-food, plant-based diet since 1982.

William Roberts died in June 1923 at the age of 90.

Vegan diet: If we did so, however, we would prevent the daily killing in the United States of 100,000 cows, of 300,000 pigs, and of 15 to 20 million chickens!

Thus, although not clearly established at this time, to prevent atherosclerotic plaques, the serum LDL cholesterol must be < 70 mg/dL [1.8 mmol/L], the serum total cholesterol certainly < 150 mg/dL [3.9 mmol/L], and the high-density lipoprotein. (HDL) cholesterol > 20 mg/dL [0.5 mmol/L].

The latter—surely a surprise to most readers—is in patients with a serum total cholesterol level about 130 mg/dL [3.4 mmol/L] and a LDL cholesterol level of about 60 mg/dL [1.6 mmol/L].

Exactly what HDL cholesterol level is required to prevent plaques is unclear at this time, but clearly if the LDL cholesterol is very low (eg, 50 mg/dL [1.3 mmol/L]), then a low HDL cholesterol — as long as it is > 20 mg/dL [0.5 mmpl/L] — appears not to be dangerous.

Ideal may be equal serum HDL and LDL cholesterol levels or an HDL cholesterol > LDL cholesterol.

In a 2010 journal article It’s the cholesterol, stupid!, Roberts writes:

Hypercholesterolemia [elevated srum cholesterol] is the only direct atherosclerotic risk factor; the others are indirect.

If, however, the total cholesterol level is > 150 mg/dL [3.9 mmol/L] and the LDL cholesterol is > 100 mg/dL [2.6 mmol/L], the other risk factors clearly accelerate atherosclerosis.

It’s the cholesterol, stupid. ⁴

No-one has produced atherosclerosis experimentally by increasing the arterial blood pressure or glucose levels or by blowing smoke in the faces of rabbits their entire lifetime or by stressing these animals. The only way to produce atherosclerosis experimentally is by feeding high-cholesterol and/or high-saturated-fat diets to herbivores.

Atherosclerosis is not a disease of carnivores, and it is not possible to produce atherosclerosis in carnivores [dogs, cats, tigers, lions, etc.] unless the thyroid gland is removed or made dysfunctional before a high-cholesterol or high-saturated fat diet is administered.

This is not to say that cigarette smoking, elevated blood pressure, diabetes mellitus, obesity, and inactivity are not harmful—of course they are — but if the serum LDL cholesterol is < 60 mg/dL [1.6 mmpl/L] or the serum total cholesterol is < 150 mg/dL [3.9 mmol/L], there is no evidence (with extremely rare exceptions) in my view that these other “risk factors” cause atherosclerosis.

The lower the LDL cholesterol the better, and this principle has been established repeatedly despite the voices of the anticholesterol, antistatin fallacy mongers! ⁵ ~ ⁶

What is the role of Cigarette Smoking?

Although it is incompatible with good health, cigarette smoking does not in and of itself produce atherosclerotic plaques. In populations where serum total cholesterol levels are less than 150/mg/dL [3.9 mmol/L], atherosclerotic events are rare, even when cigarette smoking is widespread.

In Japan cigarette smoking is common, but atherosclerotic events are relatively uncommon. The average serum total cholesterol in adults in Japan is approximately 170 mg/dL [4.4 mmol/L], which is not a level associated with a high frequency of atherosclerotic events. Many Japanese adults have serum total cholesterol levels less than 150 mg/dL [3.9 mmol/L].

In populations where the average serum total cholesterol level in adults is greater than 200 mg/dL [5.2 mmol/L], such as the United States, smoking cigarettes appears to accelerate atherosclerosis, but this acceleration appears to be a cholesterol-dependent phenomenon. ⁷

LDL Cholesterol, ApoE Gene and the Nigerian Paradox

ApoE is a protein with 299 amino acids that come in three varients (alleles). ⁸

ApoE2: has the amino acid cysteine at postions 112 and 158
ApoE3: has arginine in one of these postitions
ApoE4: has arginine at both of these positions

LDL cholesterol is 40 mg/dL [1 mmol/L] higher in those people with ApoE4 gene. This increase in cholesterol increases the risk of a heart attack and Alzheimer’s disease.

Nigeria has one of the highest prevalences of the APOE ε 4 allele globally. However, Nigeria lacks the strong association with Alzheimer’s disease – the “Nigerian Paradox”. ⁹

ApoE2: Prevalence 3%
ApoE3: Prevalence 68%
ApoE4: Prevalence 28%

Their diet is rich in rice, beans, plantains (cooking bananas), yams, cassava, tomatoes, onions, pepper and hot spices.

Perhaps their diet is significant.

We Act As If We Are Carnivores

In a 1991 paper, We think we are one, we act as if we are one, but we are not one, Roberts writes:

Natural carnivores live on meat. Natural herbivores live on vegetables, fruits, and starches (rice, corn, potatoes, beans, pasta). Carnivores and herbivores are made differently (Table 1). Carnivores have claws and sharp teeth for ripping meat apart; herbivores have hands {unless they have hooves} for gathering food and flat teeth for grinding the vegetables, fruits, and grains.

Carnivores have short bowels, rapidly digest flesh, and rapidly excrete the putrefying animal products. The time required for food to travel through their intestinal tract is short. Herbivores have long intestines so that there is plenty of time to digest the nutrients in the plants, fruits, and starches, and when these animals eat these foods, their transient times also are relatively short, despite their long intestinal tracts. Meat eaters pant to cool themselves and lap water; plant eaters, in contrast, sweat to cool and sip water.

Carnivores synthesize their own vitamin C, which is virtually absent in meat and dairy products; herbivores obtain their vitamin C from plant foods in which it is abundant.

Although human beings eat meat, we are not natural carnivores. We were intended to eat plants, fruits, and starches! No matter how much fat carnivores eat, they do not develop atherosclerosis. It is virtually impossible, for example, to produce atherosclerosis in a dog, even when 100 grams of cholesterol and 120 grams of butter fat are added to its meat ration. (This amount of cholesterol is approximately 200 times the average amount that human beings in the USA eat each day!)

Thus, although we think we are one and we act as if we are one, human beings are not natural carnivores. When we kill animals to eat them, they end up killing us because their flesh, which contains cholesterol and saturated fat, was never intended for human beings, who are natural herbivores. ¹⁰

Reversing Heart Disease with Diet

Dr. Esselstyn demonstrates that a plant-based, oil-free diet can not only prevent and stop the progression of heart disease but also reverses its effects.

A coronary angiogram examines the heart’s blood vessels using X-rays. Images of coronary angiograms of the circumflex artery in Dr Esselstyn’s books and website shows significant improvement following 32 months on a plant-based diet. The Hagen–Poiseuille equation shows that the flow rate of blood through the artery is proportional to the radius raised to the fourth power, meaning that a small increase in the internal diameter of the artery greatly increases the amount of blood that flows through the artery. ¹¹

Caldwell B. Esselstyn, Jr., M.D. Prevent and Reverse Heart Disease Avery Trade 2008

www.dresselstyn.com/site/Opens in a new window

Relevance of High-density Lipoproteins (HDL)

It is generally accepted that HDL Cholesterol absorbs cholesterol in the blood and carries it back to the liver where if is then flushed it from the body. High levels of HDL cholesterol can lower your risk for heart disease and stroke. ¹²

Consider the fact that excess cholesterol can only occur in herbivores AND ALL animals have HDL Cholesterol. The purpose of HDL Cholesterol is NOT to flush the excess from the blood.

While several lines of evidence prove that elevated concentrations of low-density lipoproteins (LDL) causally contribute to the development of atherosclerosis and its clinical consequences, high-density lipoproteins are still widely believed to exert atheroprotective effects.

Hence, HDL cholesterol (HDL-C) is in general still considered as “good cholesterol”. Recent research, however, suggests that this might not always be the case and that a fundamental reassessment of the clinical significance of HDL-C is warranted.

In contrast to LDL cholesterol (LDL-C), HDL-C correlates with [a decreased] cardiovascular risk only in healthy individuals.

An increase in HDL-C through lifestyle change (smoking cessation, physical exercise) has positive effects and is recommended. ¹³

Higher HDL cholesterol is associated with less heart disease ONLY when comparing people on a standard Western diet – which is nearly everyone. HDL cholesterol can be easily raised by eating all forms of an animal-based diet. This includes red meat, poulty, fish, eggs and diary. Not a great idea.

When total cholesterol is lowered all fractions of cholesterol are reduced which includes HDL-cholesterol. LDL Cholesterol occurs in the body about 3-4 times more than HDL Cholesterol. The LDL-cholesterol is reduced at a faster rate than the HDL-cholesterol. Cholesterol:HDL ratio is calculated by dividing your total cholesterol by your high-density lipoprotein (HDL) cholesterol. As your total cholestrol and LDL cholesterol is lowered then your Cholesterol:HDL ratio becomes lower and therefore “improves”.

There is a mistaken belief with the medical profession and their patients that “my LDL-cholesterol is high but so is my HDL-cholesterol so it’s all OK”. NOT SO.

What about Lipoprotein A [or Lp(a)]?

Lipoprotein(a) or Lp(a) is structurally similar to low-density lipoprotein (LDL), but it contains an additional protein called apolipoprotein(a) bound to the LDL particle. This protein alters its behavior making Lp(a) significantly more atherogenic (plaque-forming) and pro-thrombotic (clot-promoting) than standard LDL. ¹⁴

Lipoprotein(a) is an independent, genetic and causal factor for cardiovascular disease and heart attacks. At any level of LDL cholesterol, your risk of heart attacks and strokes is two to three-fold higher when Lp(a)is elevated. With a high enough level, atherosclerosis continues to progress, even if you get your LDL cholesterol way down, which may help explain why so many people continue to have heart attacks and strokes even under treatment for high cholesterol.

It is considered to be strongly determined by genetics. Levels stay constant throughout your life and are generally not lowered by diet or exercise. ¹⁵

What’s the point of checking it, though, if there’s not much we can do about it? To date, no drug to reduce circulating Lp(a) levels has ever been approved for clinical use.

Lp(a) is not found in typical lab animals, like rats and mice. It’s only found two places in nature: primates…and hedgehogs. How strange is that? No wonder Lp(a) is an enigmatic protein that has mystiﬁed medical scientists ever since it was first discovered a half century ago. But, who needs mice when you have men? The level in our bloodstream is primarily determined by genetics, and for the longest time, Lp(a) was NOT thought to be much inﬂuenced by things such as diet. Given its similarity to LDL, though, one might assume a healthy lifestyle would help. However, the evidence has been lacking––but maybe that’s because they have not yet tried a plant-based diet.

We’ve known for years that the trans fats found in meat and dairy are just as bad as the industrially-produced trans fat found in partially-hydrogenated oil junk food when it came to raising LDL cholesterol. When it comes to lipoprotein A, the meat and dairy trans fat appears to be even worse.

Just cutting out meat––putting people on a lacto-ovo-vegetarian diet does not appear to help, but put people on a whole food plant-based diet packed with a dozen servings of fruits and vegetables a day, and within four weeks, Lipoprotein A levels dropped 16%. Of course, in those 30 days, they also lost 15 pounds.

But weight loss does not appear to affect Lp(a) levels; so, you figure, it must have been due to the diet. ¹⁶

Impact of 4 Week Vegan Diet

Lipoprotein(a) [Lp(a)] is an atherogenic lipoprotein structurally similar to low-density lipoprotein cholesterol (LDL-C). The key differences is the presence of apolipoprotein B100 (Apo-B).

All of the 31 particpants had high blood pressure (systolic blood pressure ≥ 140 mmHg or diastolic blood pressure ≥ 90 mmHg), had elevated LDL-C at ≥ 100 mg/dL [2.6 mmol/L] and were overweight with BMI ≥ 25 kg/(m•m) at the start of the study. ¹⁷

Participants consmumed a plant-based diet for 4 weeks. Excluded were animal products, cooked foods, free oils, soda, alcohol and coffee. Raw fruits, vegetables, seeds, avocado and small amounts of raw buckwheat and oats were permitted. The particpants did not change their exercise routines.

Note: 1 tsp = 15 ml; 1 cup = 250 ml. ¹⁸

Food Group	Serving Size	Start	End	Change (%)
Fruits	½ cup chopped, ¼ cup dried, 1 medium piece	1.3	1.8	+808
• Avocado	½ sliced	0.1	0.9	+800
Vegetables	½ chopped or 1 cup raw leafy	2.7	16.0	+493
• Dark-green	½ chopped or 1 cup raw leafy	0.7	5.2	+643
• Deep-yellow	½ cup chopped	0.2	1.2	+500
• Tomatoes	½ cup chopped	0.4	1.7	+325
• Other vegetables	½ cup chopped	1.4	7.9	+464
White potatoes	½ cup chopped or 1 medium baked	0.3	0.0	-100
Fried potatoes	½ cup chopped or 70 g french fries	0.5	0.1	-80
Grains	1 slice bread or ½ cup cooked cereal	5.7	0.7	-88
• Refined grains	1 slice bread or ½ cup cooked cereal	3.8	0.2	-95
• Whole grains	1 slice bread or ½ cup cooked cereal	1.9	0.5	-74
Sweets	4 g sugar, 1 tsp honey, 2 tsp syrup	1.8	1.7	-5
Nuts/Seeds	½ oz [15 g]	1.2	1.4	+17
Added oils	1 tsp	3.2	0.1	-97
Added animal fats	1 tsp	1.3	0.0	-100
Animal products	1 oz [30 g]	7.9	0.4	-95
• Red meat	1 oz [30 g]	2.1	0.1	-95
• White meat	1 oz [30 g]	3.9	0.2	-95
• Eggs	1 large egg	0.5	0.0	-100
• Dairy	1 cup milk or yogurt or 1½ oz [45 g] cheese	1.5	0.1	-93

Significant reductions were observed for serum Lipoprotein(a), apolipoprotein B, low-density lipoprotein (LDL) particles and small-dense LDL cholesterol.

Inflammation markers serum interleukin-6 (IL-6), total white blood cells, lipoprotein associated phospholipase A2 (Lipoprotein-PLA2), high-sensitivity C-reactive protein (hs-CRP) and fibrinogen were significantly reduced.

Changes to serum Lipoprotein(a) are considered to be impossible. Not according to this study.

Criteria	Units	Start	End	Change (%)
Weight	kg	108.1	101.4	-6
BMI	kg/(m•m)	37.5	35.2	-6
Total Cholesterol	mmol/L	5.6	4.7	-16
LDL Cholesterol	mmol/L	3.7	3.1	-17
HDL Cholesterol	mmol/L	1.4	1.3	-9
Triglycerides	mmol/L	1.40	1.18	-16
Lipoprotein (a)	mmol/L	200.7	168.8	-16
Apo-B	mg/dL	115.2	101.9	-11
Apo-A1	mmol/L	189.7	160.2	-14

Other Dietary Studies Showing Changes to Lipoproteins

According to the American Heart Association, apolipoprotein B (ApoB) is the primary protein found in “bad” cholesterol particles such as LDL Cholesterol and Lipoprotein(a). High levels indicate an elevated risk of heart disease and stroke outperforming other tests in predicting cardiovascular events.

In a 2010 study, thirty healthy volunteer men (age 45 years and body–mass index 24.29 kg/(m•m)) with mild hyperlipidemia received 60g [50 almonds] almonds daily for 4 weeks. ¹⁹

After 4 weeks, almond supplementation significantly decreased LDL cholesterol, total cholesterol and apolipoprotein B100. Whilst Lipoprotein(a) was not measured, the relationship with apolipoprotein B100 is possibly significant.

Impact of Almonds on Coronary Risk Factors

A 2002 study showed the impact of almonds on blood lipids and lipoproteins. ²⁰

David Jenkins from Toronto, Canada and the developer of the Glycemic Index was the lead author.

Three 1-month diet phases with each phase separated by a minimum 2-week washout period were completed by 27 subjects. The 3 phases consisted of:

A muffin phase (control)
A full-dose almond phase – 73 g/day (60 almonds, ½ metric cup)
A half-dose almond plus half-dose muffin

Some observations from the study.

Average BMI was 25.7 kg/(m•m) – range 20.5 to 31.5 kg/(m•m). That is, on average the participants were overweight.
All subjects had elevated LDL chholesterol and triglycerides at recruitment.
None had clinical or biochemical evidence of diabetes, liver or renal disease.
The muffins were made from whole-wheat flour with corn oil sufficient to provide the same amount of SFA, PUFA, and fiber as the almonds and skim milk powder and egg white to provide a similar level of protein.
Muffin protein was 46% animal protein.
The participants’ diet was lacto-ova-vegetarian – that is, vegetarian with the addition of eggs and dairy.
The change measured is at the end of the 3 month study.
The background diet was kept constant across all 3 phases to allow direct comparison between the supplements.
There was no change to the BMI.
HDL Cholesterol was increased 3.6%.
All other indicators were decreased significantly.
This included Lipoprotein(a) which is supposedly strongly determined by genetics AND not lowered by diet or exercise.
Physical activity remained constant for the participants.
What caused these significant reductions if it was not diet?

Serum Lipid	Units	Start	End	Change	Change (%)
BMI	kg/(m•m)	71.2	71.0	-0.2	-0.3
Cholesterol, Total	mmol/L	6.60	6.21	-0.39	-5.9
Cholesterol, LDL	mmol/L	4.45	4.01	-0.44	-9.9
Cholesterol, HDL	mmol/L	1.40	1.45	+0.05	+3.6
Apolipoprotein, ApoB	g/L	1.31	1.21	-0.10	-7.6
Total cholesterol : HDL cholesterol	ratio	5.00	4.58	-0.42	-8.4
LDL cholesterol : HDL cholesterol	ratio	3.40	2.99	-0.41	-12.1
Lipoprotein(a)	mg/L	16.3	14.2	-2.1	-12.9
Pulmonary nitric oxide	ppm	22.3	17.4	-2.9	-13.0

The following studies indicate that a healthy, vegan diet would have much better results.

Seventh-day Adventists studies ²¹ ~ ²² ~ ²³ and the Taiwanese Buddhist Studies ²⁴ ~ ²⁵ ~ ²⁶

The following table shows the different fractions of lipoproteins in the blood.

Lipoprotein	Size (nm)	Lipids	Apoproteins	Description
Chylomicrons	75-1200	Triglycerides	Apo B-48, Apo C, Apo E, Apo A-I, A-II, A-IV	Made by the intestine. Involved in the transport of dietary triglycerides and cholesterol to peripheral tissues and liver.
Chylomicron Remnants	30-80	Triglycerides, cholesterol	Apo B-48, Apo E	The removal of triglyceride from chylomicrons results in smaller particles. Compared to chylomicrons these particles are enriched in cholesterol.
Very Low-Density Lipoproteins (VLDL)	30-80	Triglycerides	Apo B-100, Apo E, Apo C	Produced by the liver.
Low-Density Lipoproteins (LDL)	18-25	Cholesterol	Apo B-100	Results from the removal of triglycerides from VLDL by muscle and adipose tissue. Carries the majority of cholesterol in the blood.
High-Density Lipoproteins (HDL)	5-12	Cholesterol, phospholipids	Apo A-I, Apo A-II, Apo C, Apo E	Transport cholesterol from peripheral tissues to the liver. HDL particles contain cholesterol and phospholipids.
Lipoprotein (a)	30	Cholesterol	Apo B-100, Apo (a)	Significantly increases the risk of heart attack and stroke. It is considered to be strongly determined by genetics. *Levels stay constant throughout your life and are generally not lowered by diet or exercise.*

Where do You Get Your Protein?

Last updated on Tuesday 14 July 2026 at 20:18 by administrators

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Footnotes

Victor Chang Institute (2026) What is High Cholesterol. Available from: https://www.victorchang.edu.au/heart-disease/high-cholesterol.
Harvard Health Publications (2022) What is Cholesterol_ Levels, Diet, and Treatments – Harvard Health . Available from: https://www.health.harvard.edu/topics/cholesterol.
Roberts, W. C. (2008) The Cause of Atherosclerosis. Nutrition in Clinical Practice. 23 (5), 464–467.
Roberts, W. C. (2010) It’s the cholesterol, stupid! American Journal of Cardiology. 106 (9), 57–73.
Roberts – 2000 – Twenty questions on atherosclerosis.pdf
Roberts, W. C. (1992) Atherosclerotic risk factors—are there ten or is there only one? Atherosclerosis Supplements. 97 (Supplement), S5–S9.
Roberts, W. C. (1995) Preventing and arresting coronary atherosclerosis. American Heart Journal. 130 (3), 580–600.
Sebastiani, P. et al. (2019) APOE Alleles and Extreme Human Longevity. The Journals of Gerontology. Series A, Biological sciences and medical sciences. 74 (1), 44–51.
Olajide, T. et al. (2025) Genetics and environmental determinants of Alzheimer’s disease and related dementias in older Africans: a narrative review. Genes and Environment. 47 (1), 16.
Roberts, W. C. (1991) We think we are one, we act as if we are one, but we are not one. American Journal of Cardiology. 66 (10), 896.
Hagen-Poiseulle’s law states that the flow rate Q depends on the fluid viscosity η, pipe length L with a radius of r and the pressure difference between the two ends of P by: Q = (pi * ((r^4) * P) / (8 * η * L)
Centers for Disease Control and Prevention (2024) LDL and HDL Cholesterol and Triglycerides
März, W. et al. (2017) HDL cholesterol: reappraisal of its clinical relevance. Clinical Research in Cardiology. 106 (9), 663–675.
Tsimikas, S. & Bittner, V. (2024) Particle number and characteristics of lipoprotein (a), LDL, and apoB: perspectives on contributions to ASCVD. Journal of the American College of Cardiology. 83 (3), 396–400.
Feingold, K. R. (2000) Introduction to Lipids and Lipoproteins. Available from: http://europepmc.org/abstract/MED/26247089.
Greger, M. (2020) How to Lower Lp(a) with Diet. Available from: https://nutritionfacts.org/video/how-to-lower-lpa-with-diet/
Najjar, R. S. et al. (2018) Consumption of a defined, plant-based diet reduces lipoprotein(a), inflammation, and other atherogenic lipoproteins and particles within 4 weeks. Clinical cardiology. 41 (8), 1062–1068.
Coffee Cup Size NSW
120ml: Espresso, macchiato or piccolo.
180ml: Flat whites, cappuccinos and lattes.
240ml: The standard small takeaway size.
355ml: Large coffee cup.
475ml: Iced coffees.
Jalali-Khanabadi, B.-A. et al. (2010) Effects of almond dietary supplementation on coronary heart disease lipid risk factors and serum lipid oxidation parameters in men with mild hyperlipidemia. Journal of alternative and complementary medicine (New York, N.Y.). 16 (12), 1279–1283.
Jenkins, D. J. et al. (2002) Dose response of almonds on coronary heart disease risk factors: blood lipids, oxidized low-density lipoproteins, lipoprotein (a), homocysteine, and pulmonary nitric oxide: a randomized, controlled, crossover trial. Circulation. 106 (11), 1327–1332.
Fraser, G. E. & Shavlik, D. J. (2001) Ten Years of Life – Is It a Matter of Choice? Archives of Internal Medicine. 161 (13), 1645–1652.
Fraser, G. E. (1999) Associations between diet and cancer, ischemic heart disease, and all-cause mortality in non-Hispanic white California Seventh-day Adventists. The American journal of clinical nutrition. 70 (3), 532s–538s.
Tonstad, S. et al. (2009) Type of vegetarian diet, body weight, and prevalence of type 2 diabetes. Diabetes Care. 32 (5), 791–796.
Chiu, T. H. T. et al. (2014) Taiwanese Vegetarians and Omnivores: Dietary Composition, Prevalence of Diabetes and IFG Marià Alemany (ed.). PLoS ONE. 9 (2), e88547.
Chang, Yao-Jen et al. (2017) Is vegetarian diet associated with a lower risk of breast cancer in Taiwanese women? BMC Public Health. 17 (1), (Accessed 20 May 2018).
Chen, F.-M. et al. (2014) Analysis of α-lactalbumin-, β-lactoglobulin-, and casein-specific IgE among children with atopic diseases in a tertiary medical center in northern Taiwan. Journal of Microbiology, Immunology and Infection. 47 (2), 130–136.

Tags: cholesterol hdl cholesterol ldl cholesterol lipoproteins nigeria nuts roberts william roberts