Month: March 2024

VP: We already talked about coronary artery disease in the chapter on that subject. But to briefly summarize: elective stenting and CABG have only a minimal benefit, and usually do not decrease the risk of future myocardial infarction, or all cause mortality.

Pmp: High tech is great for computers, and great for radiology machines, but the human body prefers low tech approaches like diet and exercise.

Ding dong! The old monarchs of stents and surgeries are dead!

Long live the new monarchs of Vegan diet and exercise!

SR: Hold on a second. Interventional cardiologists save lots of lives by reopening arteries during acute myocardial infarctions (MI).

VP: Yes. For acute MI, cardiac cath with stent placement saves lives.

Pmp: But most patients have chronic symptoms.

SR: And cardiac surgery saves lots of lives.

VP: Yes. There are some patients who greatly benefit from cardiac surgery. Cardiac patients are often complex, with combined arterial, and valvular disease.

Pmp: Granted. There are a lot of patients who benefit from stents, and surgery. However, the VAST MAJORITY of patients would obtain optimal results by becoming health vegans.

In a health vegan population – following an Esselstyn equivalent diet – coronary artery disease does not exist.

Obesity does not exist.

VP: When one also makes the diet “low sodium,” then hypertension usually does not exist.

Pmp: And when eating plant foods, there is adequate potassium, and magnesium, and fiber; so cognitive function is improved, and abdominal pressure syndrome is minimized, and autoimmune disease is rare.

Paradise regained!

VP: You only get one life on this planet. Make it healthy. Choose Vegan: the only diet proven to prevent atherosclerosis, obesity, hypertension, and diabetes.

SR: What about the difference between grass fed cattle versus factory farm cattle?

VP: Yeah, sure. Factory farm cattle that are fed a diet high in omega 6 fats, are going to have more omega 6 fats.

But the point is moot. People should not eat any meat. You can’t polish a turd. Meat is a metabolic poison. Even the best possible meat is high in animal protein and saturated fat; poison for humans.

The only exception is human breast milk, during infancy. That’s it.

SR: How much fat is ideal for adult humans?

VP: Less than 5%. Ideally, I would like my dietary fat to be about 5%, but that’s hard to achieve.

A low fat, low sodium, 100% plant based, starch based diet will probably lead to about 10% fat, 10% protein, and 80% carbohydrate.

Kempner’s rice diet was about 5% fat, 5% protein, and 90% carbohydrate.

The lower that fat content, the skinnier the population; the lower the cancer rates.

Pmp: Most people do not know that meat has tons of fat, especially saturated fat. Butter is about 55% sat fat. Beef has about 50% sat fat. Pork has about 40% sat fat. Chicken has about 30% sat fat.

SR: How does fatty acid nomenclature work?

VP: Fatty acids are long chain carboxylic acids. In organic chemistry nomenclature, numbering of fatty acid carbons begins with the carbonyl carbon (also known as the carboxylic carbon). The carboxylic acid is polar. The fatty acid “tail” is nonpolar, hydrophobic.

In the biochemistry and nutritional literature, the numbering begins with the METHYL end carbon which is also called the OMEGA end. TheMETHYL method is better for nutrition and biochemistry because the omega end remains constant. With the METHYL method, when there is an elongation reaction, the double bond stays in the same numerical place; like for making a C18:3, w-3 fatty acid, into a longer fatty acid, like EPA C20:5, or DHA C22:6.

The “w” designation is for the location of the double bond, based on counting from the METHYL end carbon, which is also called the OMEGA end carbon.

SR: What is saturated fat?

VP: Saturated fat has no double bonds. Saturated fat is usually solid at room temperature. Butter is a good example of saturated fat. The fat in steak is primarily saturated fat.

Saturated fat causes a big increase in LDL cholesterol, which is quite atherogenic. Saturated fat accumulation in RBC plasma membranes, causes stiffening of those membranes. Stiff RBC membranes means increased blood viscosity.

Increased blood viscosity means increased blood pressure. Increased blood pressure means increased atherosclerosis. Increased atherosclerosis means increased myocardial infarction.

SR: What are common examples of saturated fat?

C16:0 is palmitic acid. PALMitic acid is the most common form of saturated fat. PALMitic oil is of course very common in PALM oil. Palmitic is also the most common type of saturated fat in beef, chicken, pork, and milk.

C18:0 is stearic acid. Stearic acid is the second most common form of saturated fat.

SR: What about omega 3 fats?

VP: Omega 3 fats have a double bond at the number 3 position, which is listed as w-3.

SR: What are common examples of omega 3 fats?

VP: C18:3 w-3 is alpha linoleNic acid (ALA) which is present in plant foods.

C20:5 w-3 is EPA (EicosaPenaenoic Acid); especially present in ocean plants, and cold water fish.

C22:6 w-3 is DHA (DocosaHexaenoic Acid); especially present in ocean plants, and cold water fish.

SR: Why do all the common fatty acids have an even number of carbons?

VP: Because they are built up from 2 carbon units, called acetyl units. Palmitic acid C16:0 is the most common fatty acid, made in mammals, by fatty acid synthase.

SR: Are omega 3 fats good for you?

VP: No. Omega 3 fats are still an oil. All oils are bad for health. It is difficult to purify fish oil, and there is concern about risk of contamination.121314

Pmp: Omega 3 oil is a highly processed food. All oils promote obesity.

VP: Increased dietary omega 3 oil is associated with possible increased insulin resistance and diabetes, and possibly increased risk of prostate cancer.

SR: What are common examples of omega 6 fats?

VP: C18:2 w-6 is Linoleic acid.

SR: What are common examples of MUFA’s (MonoUnsaturated Fatty Acids)?

VP: C18:1 w-9 is oleic acid. Oleic acid is the main type of oil in olive oil, comprising about 73% of olive oil.

SR: What other oils are found in olive oil?

VP: It depends on the type of olive oil. Olive oil may contain saturated fat like palmitic oil up to at least 11%, and omega 6 oil like Linoleic acid C18:2 w-6, up to 9%, and omega 3 fat like alpha linolenic acid up to .8%.15 Notice that these numbers show a significant amount of saturated fat, and a ratio of omega 6 fat >> omega 3 fat.

SR: What is the significance of the omega 6 to omega 3 ratio?

VP: Our ancestors are thought to have eaten a ratio of omega 6 to omega 3 of about 1:1. Nowadays, MOFFUUC’S PP eaters get a huge excess of omega 6 fats >>> omega 3; and this causes inflammation.

SR: What is a triglyceride?

VP: Triglycerides (TG’s) are also called TriAcyl Glycerides (TAG’s). Acyl means fatty acid group, as in fatty acid being part of a larger molecule, like a TAG.

Glycerol is the “backbone” of TAG’s. Glycerol is the same thing as “propane-triol,” which is a 3 carbon alkane with a hydroxyl group – (hydroxyl group is same thing as an alcohol group) – on each carbon.

The vast majority of dietary fat is triglycerides. When someone says “fat,” they usually mean triglyceride, unless otherwise specified.

SR: What is the difference between a fatty acyl group, and a free fatty acid?

VP:An “acyl group” usually refers to a fatty acid group on a bigger molecule, like a TAG.

A free fatty acid is by itself. Free fatty acids are sometimes called NEFA’s (Non-Esterified Fatty Acids). Most fatty acids in the typical fat person, are in storage form, which means esterified to a glycerol molecule, as part of a TAG, in adipose tissues.

GO TO PART 3

SR: What determines the solubility of a fatty acid?

VP: Saturated fatty acids tend to be solid at room temperature, because their carbon tails have a standard, monotonous, up and down pattern, that enables them to interdigitate closely, with each other.

Double bonds are normally in cis configuration. Cis double bonds cause a BIG BEND in the carbon tail. This big bend “pushes away” other fatty acids – like in a plasma membrane fatty acid bilayer – so that the membrane is “fluidized.”

The more double bonds, the more likely the fatty acid is oil = liquid.

The longer the fatty acid – ie. the more carbons in the tail – the more likely it is solid.

The effect of double bonds can “overpower” the effect of fatty acid length; EPA and DHA are liquid at body temperature. That’s how “fish oil” helps prevent the fish from freezing in cold temperatures.

SR: What is a phospholipid?

VP: A phospho-lipid contains phosphate and lipid. The phosphate is just a phosphate. The lipid is a Di-Acyl Glycerol. Phospholipids are the second most common type of dietary fat.

Pmp: Di-Acyl Glycerol (DAG) + Phosphate is called Phospha-Tidic Acid (PTA). PTA is the “building block” for most phospholipids.

Membrane phospholipids are made by starting with PTA and adding a “head group” like choline, or serine, or inositol, or ethanolamine.

For example: PhosphaTidic Acid + Choline = PhosphaTidyl Choline. PhosphaTidyl Choline is the most common membrane phospholipid in mammals.

SR: What is CARDIOLIPIN?

VP: Cardiolipin is a unique fatty acid. Cardiolipin is a “giant size” phospholipid. Cardiolipin consists of 2 PTA’s connected by a glycerol. Cardiolipin is mostly found in the inner mitochondrial membrane.

The fatty acid tails on cardiolipin are often PUFA’s. The fact that cardiolipin has several PUFA type fatty acid tails, and it is located on the inner mitochondrial membrane – the hot spot in the human body for the production of reactive oxygen, free radicals – makes it obvious that cardiolipin is highly vulnerable to lipid peroxidation!!16

SR: What about lipid peroxidation?

VP: Lipid peroxidation is a major problem with PUFA’s (PolyUnsaturated Fatty Acids). A PUFA is any fatty acid with two or more double bonds.

A methylene group is a CH2 group. The methylene bridge carbon – the single bonded carbon, between a pair of double bonds – has only a “weak” grip on its hydrogen – and is vulnerable to lipid peroxidation.

Lipid peroxidation is a chain reaction that progresses like a stack of dominoes, to destroy lots of other lipids.

Lipid peroxidation can be very damaging to plasma membranes, and to mitochondrial membranes. Cardiolipin is especially vulnerable to lipid peroxidation. The brain has a relatively large amount of PUFA’s in its cell membranes, and this makes the brain more vulnerable to oxidative stress, and lipid peroxidation.

Pmp: With lipids, there’s always more details to talk about.

VP: The key point is to minimize dietary lipids! There are no “good fats.” FAT IS BAD! The way to minimize dietary lipids is to eat a low fat, plant based diet.

SR: What is the difference between cholesterol and a steroid?

VP: Cholesterol has 4 rings of carbon – labeled A, B, C, D – and a total of 27 carbons. Cholester-OL has a hydroxy group at the C3 position (on the A ring).

The steroid nucleus also has 4 rings of carbon, based on the 4 rings of cholesterol.

GO TO PART 4

SR: How does the steroid nucleus relate to steroid hormones, and estrogen?

VP: In general, the steroid hormones are made by starting with cholesterol, then removing the alkane chain attached to C17, then adding some hydroxy groups, alcohol groups, or ketones.

SR: Why is estrogen unique?

VP: Estrogen is unique, because it’s the only one with a benzene ring. The A ring of estrogen is a “benzene.”

SR: What is the characteristic feature of bile acids?

VP: Like the name says, the bile ACIDS are based on an ACID. To make a primary bile ACID, a carboxylic acid is added to a cholesterol molecule. Then a couple of hydroxyl groups are added. Primary bile acids are made in the liver.

This combination of nonpolar (hydrophobic), and polar (hydrophilic) regions, enables bile acids to function as EMULSIFIERS, for digestion of fats.

Pmp: The liver then “conjugates” the primary bile acids. Conjugation consists of adding an amino acid to the bile acid. Typically, glycine or taurine is added to the primary bile acid. The new chemical is called a “conjugated” bile acid.

SR: What about bile salts?

VP: The conjugated bile acid becomes deprotonated, so it carries a negative charge. The negative charge attracts a positive charge. Ions like sodium and potassium will bind to the deprotonated bile acid. The combination of deprotonated bile acid combined with sodium or potassium is called a bile salt.

Pmp: The terms bile acid and bile salt are often used interchangeably.

SR: What happens to the bile acids?

VP: About 95% of bile acids are reabsorbed – mostly in the ileum. The reabsorbed bile salts travel through the portal vein so they can return to the liver.

SR: What about secondary bile acids?

VP: Some gut bacteria in the colon will remove a “hydroxyl group,” from a conjugated primary bile acid, at carbon number seven.

The resultant molecule is called a “secondary” bile acid.

SR: What is the significance of secondary bile acids?

VP: Secondary bile acids are unique in the sense that they are in the COLON. The higher the concentration of secondary bile acids in the colon, the higher the risk of colon cancer.17

Pmp: The MORE FAT A PERSON EATS, THE MORE BILE GETS SECRETED; and the more bile reaches the colon; and the more colon cancer.

Rvw:Rural Africans who eat a plant based diet hardly ever get colon cancer. African Americans commonly get colon cancer.

This is old information. Denis Burkitt and Nathan Pritikin knew all this stuff about fiber and colon cancer back in the 1960’s and 1970’s.

SR: Why does meat increase the risk of colon cancer?

VP: Meat increases the risk of colon cancer because:

High fat content leads to MORE SECONDARY BILE ACIDS in colon. All dietary fat – beyond the small amount in low fat plant foods – is bad for the colon. Even PUFA’s (PolyUnsaturated Fatty Acids) cause increased risk of colon carcinoma in animal studies.

High fat associated with insulin resistance, and higher insulin levels, and insulin is a growth factor.

Meat has more leucine & methionine which causes more activation of mTOR

Meat leads to higher blood levels of insulin like growth factor (ILGF).

Meat has no fiber. Lack of fiber leads to proliferation of bad gut bacteria.

Promotion of bad gut bacteria that produce hydrogen sulfide, and are associated with inflammatory bowel disease.

Saturated fat leads to RBC rouleaux, and relative hypoxia of tissues; which can lead to the Warburg effect, causing cells to transform into cancer.

Increased Polycyclic Aromatic Hydrocarbons (PAH).

Increased herbicides.

Increased pesticides.

Increased antibiotics in the meat which kills good gut bacteria.

Increased estrogen.

Increased N-Nitroso compounds.

Increased TMAO.

Increased sulfur containing amino acids like methionine, and cysteine with resultant low grade metabolic acidosis.

Increased AGE’s.

Increased Heterocyclic Aromatic Amines.

Increased atherosclerosis which can lead to tissue hypoxia.

GO TO CITATIONS

1  Penelope questioned Oddyseus about the olive tree to confirm his identity, when he returned after twenty years, in the Oddysey.

2  Silva et al. “Olive, soybean, palm oil have similar acute detrimental effect on endothelial function in healthy young subjects” Nutr Metab Cardiovasc dis 2007;17:50.

3 “Postprandial effects of components of Mediterranean diet on endothelial function.” Robert Vogel et al. J am coll cardiology, vol 36, no 5, 2000. Olive oil caused reduced dilation of brachial artery, indicating decreased function of endothelical cells, and decreased nitric oxide production.

4 Angina pectoris induced by fat ingestion in pt’s with coronary artery disease.” Peter Kuo MD, JAMA 1955 July. Great paper. Chest pain occurred at peak lipemia at about 5 hours. Peak lipemia was at about 4-6 hours!! Therefore after a high fat meal, a person has high blood lipids from at about 2-8 hours.

5  Takahash et al. “High MUFA diet induced obesity & diabetes in mice” Metabolism 1998, Jun; 47 (6): 724.

6  Wilson et al. “Dietary MUFA’s promote atherosclerosis in mice” Arterioscler Thromb Vasc Biol. 1998; 18; 1818.

7  Blankenhorn et al. “Influence of diet on the appearance of new lesions in human coronary arteries” Jama, 1990; 263(12):1646. Atherosclerotic plaques progressed just as much eating a diet high in MUFA’s as a diet high in sat fat.

8  Rudel et al. “Compared with dietary MUFA & sat fat, PUFA protects African green monkeys from coronary artherosclerosis” Arterioscl thromb vasc biol. 1995;15:2101.

9 “Effects of dietary fat on postproandial activation of blood coagulation factor 7” Arterioscler thromb vasc biol, 1997, Nov; 17 (11) 2904. Larsen et al

10  Esselstyn et al.” A way to reverse CAD? J Fam Practice. 2014;63:356-364.

11 “Prevent and reverse heart disease” book by Caldwell Esselstyn MD.

12 “Dietary PUFAS and composition of human aortic plaques.” Lancet, 1994, Oct 29, 344 (8931): 1195.

13 “Dietary fat intake and early age related lens opacities” Am j clin jutr. 2005, Apr; 81 (4):773. Gail Rogers et al. Increased dietary inatke of C18 PUFA’s linoleic acid and linolenic acid was associated with increased risk of cataracts.

14 Griffini, P. “Dietary omega 3 PUFA’s promote colon carcinoma metastases in rat liver.” Cancer res, 1998, Aug 1; 58 (15) 3312

15 “Advanced nutrition and Human metabolism” book by Sareen Gropper p. 129.

16  Douglas Kell. “Iron behaving badly.” 2009. Great paper! Douglas Kell is a from England and he is the most entertaining speaker on the topic of iron metabolism. He claims that excess, unliganded-free iron can cause an autocatalytic chain reaction of reactive oxygen species via Fenton and Haber Weiss reactions leading to cellular death from lipid peroxidation (cell membrane damage) and DNA damage. He also claims that excess free iron can “reawaken” dormant bacteria. This paper has an interesting diagram of iron metabolism.

17  “Fat, fibre, and cancer risk in African Americans, and rural Africans” Nat commun, Apr 2015, 6:6342.