Author: Sharon

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.