Scientific literature describes with great detail an
involvement of B12, B9 and Vitamin D deficiencies, as well as, an impact
of sugar consumption on our body's healing mechanism.
All
these deficiencies are prevalent on a diet deprived of animal protein
& fat, also known as a vegan diet. B12, B9 and vitamin D are found
in adequate amounts in a human being's evolutionary diet of an omnivore
origin. Due to probiotic bacteria's abilities to synthesis B12 and B9,
as well as, synthesis of vitamin D on the skin following exposure to UVB
light, a meatless diet is debatable. Yet, there are other factors in
meat, that make it necessary for DNA repair and other healing processes.
The
goal of this article is to describe what is known, via presentation of
references to clinical studies as well as references to sources of
literature, that can expand the investigators confidence in the
knowledge presented.
Links in the body of the article will send you to Wikipedia articles, or other sources.
Study references can be found throughout the article, and the list is found at the end of the article.
Sugar Disease: Atherosclerosis
Hardening of the arteries is accomplished by a few contributing factors.
These factors include;
The Homocysteine Connection
B12** and
B9*** are essential in converting
Homocysteine into a stable compound
[1]*.
Homocysteine irritates the blood vessels walls, causing injury to the cell membrane
[2].
Cell membrane injury accompanies an
inflammatory response.
This response sends signals to brain.
The brain, in turn, tells Liver to create cholesterol and ship it to injured site.
The molecular machine that ships cholesterol from Liver to injured site is
LDL.
On a high sugar diet,
glucose is toxic.
It has been observed to accelerate oxidation of LDL particles
[3].
Insulin innate role
Insulin defends the whole system by accomplishing a few tasks;
- Shutdown of Liver's mechanism of converting amino acids into glucose[4][5][6][7],
- Shuttling all glucose present in the bloodstream into cells[7],
- Shuttling remaining glucose into fat cells (glucose converted into fatty acids for storage)[7].
The Liver is capable of creating glucose (for energy) by converting amino acids into glucose
[8].
Clearly,
the mechanism of shutting down glucose production in the liver by insulin is an
innate mechanism in place for taking care of existing high glucose
levels from the diet.
Glucose toxicity has been linked to pancreas beta-cell degradation
[9][10].
Clearly, sugar is harming insulin creating cells, leading to development of
Diabetes type 1.
Type 1 Diabetics MUST inject insulin when they eat sugar, otherwise heavy damage occurs.
When cells can't accept anymore glucose, insulin shuttles them into
fat cells, where they are converted into
fatty acids. Also, Insulin reduces the breakdown of fats into fatty acids, thus preventing the usage of stored energy for energy usage.
Consequently, fat cells become fatter, because of sugar.
LDL
particles and their cholesterol are oxidized due to the unstable nature
of the bloodstream; promoted by Homocysteine levels and sugar levels.
Note: LDL particles have an armor; antioxidants like CoQ10 and Vitamin E
[11][12]. Both are fat soluble, so they require fat to embed themselves in the LDL outer layer.
Macrophage Connection
As a defense mechanism accompanying the inflammatory response,
white blood cells are sent to the area of inflammation in order to deal with any potential
microbial/
viral/
fungal threat, neutralize it and clean the area up.
Monocytes, that come to the area, turn into
Macrophages[13][14].
Macrophages are like garbage trucks, they can grab the oxidized cholesterol and collect it.
The mechanism of transporting cholesterol back to the liver, for recycling, is accomplished by
HDL.
This particle has developed a mechanism with Macrophages called "
Reverse Cholesterol Transport".
This mechanism describes a transfer from macrophages to HDL particles
[15].
Essentially, this is how the Macrophages get rid of the accumulating cholesterol they grab and store.
Impairment of this mechanism causes Macrophages to self-destruct (
Apoptosis),
and the accumulated cholesterol hardens and forms
Foam cells.
Vitamin D Connection
Macrophages require Vitamin D to function properly.
This includes cholesterol metabolism
[16] by preventing cholesterol uptake by macrophages[17].
Vitamin
D's role has to do with relieving stress on the Macrophage. When stress
increases the macrophage changes expression and overeats oxidized
cholesterol LDL's, which leads to foam cell formation[18].
Supplementation with vitamin D2 (
1,25(OH)(2)D) has
clinically been observed to improve suppression of foam cell formation
by increasing cholesterol efflux from stressed Macrophages.
Vitamin D has an important role in managing the cholesterol uptake and egress in Macrophages.
This vitamin suppresses foam cell formation, thus suppressing plaque formation in the arteries.
Cause and Effect Chart
Deficiency in B9 and B12 >>> Increase in Homocysteine
Homocysteine >>> Inflammatory response
Inflammation >>> Cholesterol transport to site
High sugar in diet >>> Cholesterol oxidation
Deficiency in Vitmain D >>> Impaired Immune cell clean up of cholesterol
Macrophages accumulate cholesterol >>> Formation of Foam cells
*Some studies imply that B6 is necessary to reduce homocysteine. However, one study
[19]
has found not such effect. B6 contribution can be associated with the
cells requirements of that vitamin in order to synthesis Coenzyme Q10
[20]. CoQ10 can protect against homocysteine-induced toxicity.
**B12
deficiency can be a result of imbalance in the microbial population in
the gastrointestinal tract. Pathogenic bacteria destroy specialized
cells, that produce Intrinsic Factor - an enzyme that carries B12 across
the gut lining into the bloodstream
[21][22]. Probiotic supplementation resolves this issue
[23].
***Infection by
Helicobactor Pylori not only inhibits B12 absorption but also B9
[24]. This also found an increase in Homocysteine.
